Compiled by Zakiyah Ebrahim | Health24

New information about the new coronavirus (SARS-CoV-2) is constantly emerging, which is critical in the race to develop a vaccine and treatment for Covid-19. In a recent discovery, scientists found that a patients genes may provide clarity on why one young, healthy individual can be almost unaffected by the virus, while another can become seriously ill and end up in the intensive care unit (ICU).

In looking for rare, silent (hidden) gene mutations that are triggered by the virus, researchers are hoping it will take them one step closer to potential treatments.

At risk: Not just older people with underlying illnesses

Its agreed that the Covid-19 virus causes severe disease and kills older people with chronic illness; those with underlying medical conditions such as diabetes and lung disease; and men, at a greater rate than young people.

However, in an unexpected twist, were seeing a minority of patients who are under 50 take up space in ICUs around the world as well without any underlying medical conditions.

Speaking to AFP, and quoted in aScienceAlert article, geneticist Jean-Laurent Casanova director of the human genetics of infectious diseases laboratory jointly based at the Imagine Institute in Paris and Rockefeller University in New York revealed thatthis amounts to roughly five percent of patients:"Someone who could have run the marathon in October 2019, and yet in April 2020 is in intensive care, intubated and ventilated."

Casanovas goal is to find out if these patients may possibly have rare genetic mutations. "The assumption is that these patients have genetic variations that are silent until the virus is encountered," he explained.

The geneticist also co-founded the Covid Human Genetics Effort, which will analyse the genome of younger Covid-19 patients with severe illness in China and Europe, and also hopes to find out why certain people do not become infected, in spite of repeated exposure.

Earlier this month, HealthDay reported on this international study, led by Casanova. It will enrol 500 patients under the age of 50 with no underlying health conditions, and who have been diagnosed with Covid-19 and admitted to ICU.

Gene mutations can also offer protection

Gene mutations may be given a bad rap for making certain people more susceptible to a number of viral infectious diseases, such as influenza, but there is also a positive side.

According to ScienceAlert, researchers found a particularly rare mutation of a single gene, named CCR5, in the 1990s. This mutation actually offered protection against disease in that it stopped people from contracting HIV, laying the foundation for the development of treatments.

How may this help in Covid-19 treatment?

Mark Daly, director of the Institute for Molecular Medicine Finland, told AFP that with a very large sample and collaboration, and the ability to repeat the observation to be confident about the results, as well as recruitment of at least 10 000 patients, their project will hopefully help to develop a treatment.

"There are a huge number of medicines available that target specific genes. If we find a genetic clue that points us to a gene that already has a medication developed, then we could simply repurpose the drug," he said. However, in the event that mutations in genes are found and there arent currently medications available for them, it might make the process more complex.

On 12 May, the virus has infected more than 4.1 million people and killed over 286 000 worldwide, according to a report by theJohns Hopkins Coronavirus Resource Centre.

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Why can two young and healthy individuals be affected so differently by coronavirus? - Health24

THOUSAND OAKS, Calif., May 12, 2020 /PRNewswire/ --Amgen(NASDAQ:AMGN) will present at the Bank of America Merrill Lynch Virtual Global Healthcare Conference at 1:40 p.m. ET on Thursday, May 14. Peter H. Griffith, executive vice president and chief financial officer, and Murdo Gordon, executive vice president of Global Commercial Operations at Amgen will present.

Live audio of the presentation can be accessed from the Events Calendar on Amgen's website,www.amgen.com, under Investors.A replay of the webcast will also be available on Amgen's website forat least90 days following the event.

About AmgenAmgen is committed to unlocking the potential of biology for patients suffering from serious illnesses by discovering, developing, manufacturing and delivering innovative human therapeutics. This approach begins by using tools like advanced human genetics to unravel the complexities of disease and understand the fundamentals of human biology.

Amgen focuses on areas of high unmet medical need and leverages its expertise to strive for solutions that improve health outcomes and dramatically improve people's lives. A biotechnology pioneer since 1980, Amgen has grown to be one of the world's leading independent biotechnology companies, has reached millions of patients around the world and is developing a pipeline of medicines with breakaway potential.

For more information, visit http://www.amgen.comand follow us on http://www.twitter.com/amgen.

CONTACT: Amgen, Thousand OaksMegan Fox, 805-447-1423 (media)Trish Rowland, 805-447-5631 (media)Arvind Sood, 805-447-1060 (investors)

View original content to download multimedia:http://www.prnewswire.com/news-releases/amgen-to-present-at-the-bank-of-america-merrill-lynch-virtual-global-healthcare-conference-301057141.html

SOURCE Amgen

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Amgen To Present At The Bank Of America Merrill Lynch Virtual Global Healthcare Conference - BioSpace

Charles Darwins Descent of Man is full of unexpected delights such as the trio of hard drinking, chain-smoking koalas that appear within its first few pages to illustrate our affinity to animals.

Yet Darwins great treatise on human origins is also, in parts, deeply disturbing.

Published a century and a half ago as of February, 2021 many of the opinions expressed in this seminal text (koalas aside) are still pertinent today. Indeed, despite (or rather, because of) the recent revolution in our understanding of genetics, the Descent is more relevant than ever.

Darwins wider musings on mankind have had an immense and lasting influence on our beliefs about human nature and behavior, not just scientifically, but socially and politically as well. And while the more reprehensible later applications of evolutionary theory to human society were not truly Darwinian at all, many troubling arguments about race, class, eugenics and the like can nonetheless be discerned within his Descent of Man.

Darwins intellectual legacy is part of the DNA of modern genetics, within which still lurk like malignant metaphorical retroviruses liable to revival and resurgence many of the odious beliefs that plagued its past.

What follows, therefore, are a few brief illustrative examples of problematic passages in the Descent of Man. The point is not as is common with many of Darwins detractors to simply cherry-pick quotes to make Darwin look bad (although, unfortunately, this is easy to do); rather it is to highlight how Darwin himself struggled with the social implications of his theory and this despite the many decades he had to dwell on these questions. Indeed, the rapid, recent explosion in our knowledge of genetics has not made the situation clearer, but rather more confused.

But lets begin with the contrast of some of the more captivating aspects of the Descent those which provide a glimpse of Darwin as an actual human being. (The on-going fascination with Darwin and the impetus for the seemingly inexhaustible Darwin Industry is not just due to his ideas and his genius, but also because he was a fascinating individual.)

Within the first few pages of Chapter 1, for example, Darwin notes that [m]any kinds of monkeys have a strong taste for tea, coffee, and spirituous liquors: they will also, as I have seen, smoke tobacco with pleasure. Not content with this as a single amusing anecdote of animals addictive affinities to mankind, he proceeds to discuss the three koalas mentioned above ones that acquired a strong taste for rum, and for smoking tobacco and an American Ateles monkey that, after getting drunk on brandy, would never touch it again, and thus was wiser than many men. He also delights in describing the consequences for a group of African baboons of over-indulgence in strong beer:

On the following morning they were very cross and dismal; they held their aching heads with both hands, and wore a most pitiful expression: when beer or wine was offered them, they turned away with disgust

Similar endearing animal anecdotes pepper the rest of the text, culminating after chapter upon chapter of detailed argument and speculation on the evolutionary origins of mankind (plus an extended interlude of the theory of sexual selection) with the rousing conclusion that we should not feel much shame, if forced to acknowledge that the blood of some more humble creature flows in [our] veins.

For my own part I would as soon be descended from that heroic little monkey, who braved his dreaded enemy in order to save the life of his keeper; or from that old baboon, who, descending from the mountains, carried away in triumph his young comrade from a crowd of astonished dogsas from a savage who delights to torture his enemies, offers up bloody sacrifices, practices infanticide without remorse, treats his wives like slaves, knows no decency, and is haunted by the grossest superstitions.

Darwin clearly liked animals better than people. Less facetiously, it is lurid passages such as these that make modern readers uncomfortable. Admittedly, this particular quotation does come straight after another glimpse of Darwin as an actual person; already in his sixties when he wrote these words, he evokes the memories of his 20-something self, aboard the Beagle, on first seeing a party of Fuegians on a wild and broken shore:

The astonishment which I felt will never be forgotten by me for the reflection at once rushed into my mindsuch were our ancestors. These men were absolutely naked and bedaubed with paint, their long hair was tangled, their mouths frothed with excitement, and their expression was wild, startled, and distrustful.

Given a modern appreciation of the manifold horrors of colonialism, it is a thorny question how we should deal with descriptions that clearly reflect the prejudices of their author. Does such obvious subjective opinion, for example, undermine the purportedly objective arguments that accompany it?

In this instance at least we can perhaps make allowances; after all, the first encounter between Darwin a wealthy young man from what was then the most technologically-advanced nation in the world and the Stone Age inhabitants of Tierra del Fuego must indeed have been astonishing. Moreover, unlike his cousin Francis Galton (who both coined and promoted the concept of eugenics), Darwin was not an explicit racist. (His loathing of slavery, for instance, comes across particularly strongly in the Journal of the Voyage of the Beagle.) Yet Darwin was also a product of a time when it seemed patently obvious that the English (and possibly the Scots) were the first among the civilized races. Further, the Descent also reflects the prevailing concept of a human hierarchy, descending from Europeans through the various barbarous, savage or lower races to mankinds closest living relatives amongst the anthropomorphous apes.

In a now-notorious passage, Darwin ranks the native inhabitants of Africa and Australia as just above the gorilla in the natural scale. At the same time, he callously concludes that the civilised races of man will almost certainly exterminate, and replace, the savage races throughout the world.

Nor was Darwins chauvinism confined simply to other races the lower classes of his own society were equally a target for his blatant prejudice. Indeed, as he remarks, at least [w]ith savages, the weak in body or mind are soon eliminated; and those that survive commonly exhibit a vigorous state of health.

We civilised men, on the other hand, do our utmost to check the process of elimination; we build asylums for the imbecile, the maimed, and the sick; we institute poor-laws; and our medical men exert their utmost skill to save the life of every one to the last moment. Thus the weak members of civilised societies propagate their kind. No one who has attended to the breeding of domestic animals will doubt that this must be highly injurious to the race of man.

And it is perhaps here that Darwins legacy even if distorted and exaggerated by the likes of Galton is most worrying in the modern age of embryonic screening, genetic manipulation and, potentially, genetically-enhanced designer babies. Today we are increasingly able to use genetic techniques to eliminate deleterious genes such as those for Huntingtons disease from future generations. But where is the line between an obviously harmful trait and an undesirable one? Is termination of fetuses with Down syndrome actually eugenics? Or what about those screened as having autism?

In Darwins pre-genetic age, these were questions that could not yet be asked, let alone answered. Of more relevance, however, was Darwins personal concern, having married his first cousin, Emma Wedgewood, with the possible inherited ill-effects of inbreeding on his own children. But even here, as he confidently asserts in the Descent, science would eventually come up with an answer:

When the principles of breeding and inheritance are better understood, we shall not hear ignorant members of our legislature rejecting with scorn a plan for ascertaining whether or not consanguineous marriages are injurious to man.

Yet while science can certainly inform our moral (or, in this case, legal) decisions, it cannot decide them facts do not determine values. Darwin half-heartedly acknowledges this when he concedes we ought not check our sympathy [for the weak], even at the urging of hard reason, without deterioration in the noblest part of our nature.

In the concluding paragraph to the Descent of Man, he goes on to claim, we are not here concerned with hopes or fears, only with the truth as far as our reason allows us to discover it. And while many of Darwins own hopes and fears appear inextricably tangled with his subjective version of the truth, it is his final closing description of humankinds noble qualities and exalted powers that perhaps shows the way beyond these ethical dilemmas: the sympathy which feels for the most debased, the benevolence which extends not only to other men but to the humblest living creature, and our godlike intellect which has penetrated into the movements and constitution of the solar system.

Modern genetics now allows us to penetrate into the very constitution of life itself. Informed by the history of what Darwin and his followers got right and what they got wrong, surely we can extend our sympathy, our benevolence and our godlike intellect to confront the moral demons that this new exalted power has conjured in our path.

Patrick Whittle has a PhD in philosophy and is a freelance writer with a particular interest in the social and political implications of modern biological science. Follow him on his website patrickmichaelwhittle.com or on Twitter @WhittlePM

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Viewpoint: Darwin's 'Descent of Man' is both deeply disturbing and more relevant than ever - Genetic Literacy Project

With sporadic reports in recent weeks of cats infected with the coronavirus that causes Covid-19, a group of researchers set out to determine whether cats can transmit the pathogen to one another.

The answer, the scientists said: They can. The question now is whether felines can transmit SARS-CoV-2 back to people.

Researchers from the University of Wisconsin-Madison and the University of Tokyo noted that none of the cats in their study was visibly ailing, but they shed the virus from their nasal passages for about six days.

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Considering the amount of virus we found coming out of the noses of the cats there is the possibility that these cats are shedding, fomites are being released in a persons household or at cat shelters or human societies and that somehow people could possibly pick up the virus. I think its something people should be aware of, said Peter Halfmann, a research professor at the University of Wisconsin and first author of the study, published as a letter in the New England Journal of Medicine.

It depends on the household and the cat, but there could be a lot of close contact with your pet cat on occasion, Halfmann said.

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The researchers, led by virologist Yoshihiro Kawaoka, experimentally infected three cats, and then placed an uninfected cat into each of the cages housing the infected animals a day later. The three uninfected cats were all infected within five days.

Halfmann said uninfected cats were also put into cages a foot away from the cages containing the infected cats. None of those felines became infected with the virus.

In early April, Chinese researchers reported that cats and ferrets were susceptible to infection. A few weeks later the U.S. Department of Agriculture announced that two pet cats in New York state had tested positive for the virus. At least eight big cats at the Bronx Zoo tigers and lions were also infected with the virus.

Many research groups have reported on virus shedding with Covid-19 by simply conducting testing by polymerase chain reaction, or PCR. A positive PCR hit tells you that the human or animal is shedding something, but it doesnt reveal if they are emitting viral debris which poses no risk of infection or actual infectious viruses.

The researchers responsible for this work did attempt to grow viruses from swabs taken from the noses and rectums of the cats; they found that all the animals were emitting infectious viruses from their noses. None of the rectal swabs produced infectious virus.

Halfmann said there was quite a lot of virus between 30,000 and 50,000 virus particles per swab. But what that means isnt clear, he said. Its not known how big a dose of virus is needed to infect a person. And theres no ethically acceptable way to construct a trial to see if cats can infect people.

Still the researchers suggested people should be aware of the possibility of transmission from cats to people, and keep cats away from anyone in a household who is suspected of being sick with Covid-19. I think its good practice to have this in peoples minds, Halfmann said. He and his co-authors also urged people not to abandon cats or give them up for adoption because of such concerns.

They also advised cat owners to keep their cats indoors.

Cats are still much more likely to get Covid-19 from you, rather than you get it from a cat, Keith Poulsen, director of the Wisconsin Veterinary Diagnostic Laboratory, said in a statement.

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Cats can catch Covid-19 from other cats. The question is: Can we? - STAT

A study analyzing data from the Rhode Island Consortium for Autism Research and Treatment (RI-CART) found that only 3% of individuals diagnosed with autism spectrum disorder reported having fully received clinical genetic tests recommended by medical professional societies.

The results bring to light a dissonance between professional recommendations and clinical practice, the researchers behind the study say.

Autism spectrum disorder is one of the most strongly genetic neuropsychiatric conditions. Medical professional societies -- such as the American Academy of Pediatrics, the American College of Medical Genetics, and the American Academy of Child and Adolescent Psychiatry -- recommend offering chromosomal microarray testing and Fragile X testing for patients diagnosed with autism. The tests can identify or rule out genetic abnormalities that could have implications in a patient's diagnosis and clinical care.

The study, published in JAMA Psychiatry on May 13, analyzed 1,280 participants with autism spectrum disorder based on medical records and self-reported data from the time period of April 2013 to April 2019. The participants are enrolled with RI-CART, a public-private-academic collaborative focused on advancing research and building community among individuals with autism spectrum disorder in Rhode Island and their families. The study's goal was to determine the current state of clinical genetic testing for autism in this cohort, said authors Dr. Daniel Moreno De Luca and Dr. Eric Morrow.

Of the 1,280 participants, 16.5% reported having received some genetic testing, with 13.2% stating they received Fragile X testing, and 4.5% reporting that they received chromosomal microarray testing. However, only 3% of participants reported having received both recommended tests.

"I had the impression that the frequency of recommended genetic testing was not going to be very high based on the patients I encounter clinically, but 3% is actually lower than I thought it would be," said Moreno De Luca, an assistant professor of psychiatry and human behavior at Brown University, who is affiliated with the Carney Institute for Brain Science, and a psychiatrist at Bradley Hospital. "A higher proportion has had either test individually, and the proportion of people with chromosomal microarray is higher in recent calendar years, which is a hopeful glimpse for people who are being diagnosed recently and who may be younger. However, this underscores that there is still significant work to be done, especially for adults on the autism spectrum."

In the study, researchers examine possible reasons for the gap between clinical practice and the recommendations from medical professional societies. Age was among the most prominent, as people with autism in older age groups are less likely to be tested. According to the study, adults with autism were generally unlikely to have undergone the clinical genetic tests.

The researchers also found that patients diagnosed by subspecialist pediatricians were more likely to report genetic testing as compared to those diagnosed by psychiatrists and psychologists.

"This paper is really about how you implement clinical genetic tests in the clinical diagnostic setting," said Dr. Eric Morrow, an associate professor of biology at Brown and director of the Developmental Disorders Genetics Research Program at Bradley Hospital. "There is rapid progress from research, and then there's the doctor and health systems that need to translate that to clinical practice. The clinics need to set up more support to educate clinicians and families about genetics and autism. Generally, this is done by genetic counselors who may be rare in autism clinics."

Furthermore, the researchers found that nearly 10% of participants who received an autism spectrum disorder diagnosis between 2010 and 2014 reported receiving chromosomal microarray testing, one of the more modern genetic tests. Compared to those in the study who received a diagnosis in years before 2010, this showed an increase in self-reported testing.

"There is a more hopeful message that conveys that the success in implementing clinical genetic testing is increasing," said Morrow, who is affiliated with the Carney Institute, co-leads the Autism Initiative at the Hassenfeld Child Health Innovation Institute at Brown and directs the University's Center for Translational Neuroscience.

Based at Bradley Hospital in East Providence, the team behind RI-CART represents a partnership between researchers at Brown, Bradley Hospital and Women and Infants that also involves nearly every site of service for people on the autism spectrum and their families in Rhode Island.

As a next step, the researchers behind the JAMA Psychiatry study are conducting a separate study to understand in greater detail the factors that could be influencing the rate of genetic testing.

"Challenges can be found on the patient and families side, on the physician side, and on the systemic side with institutional requirements and many other potential barriers," said Moreno De Luca. "We want to address each of those factors independently."

Reference:Moreno-De-Luca, D., Kavanaugh, B. C., Best, C. R., Sheinkopf, S. J., Phornphutkul, C., & Morrow, E. M. (2020). Clinical Genetic Testing in Autism Spectrum Disorder in a Large Community-Based Population Sample. JAMA Psychiatry. doi:10.1001/jamapsychiatry.2020.0950

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Study Finds Low Proportion of Individuals With Autism Receive Recommended Genetic Tests - Technology Networks

Emad Babakhanzadeh,1,2,* Ali Khodadadian,1,* Majid Nazari,1 Masoud Dehghan Tezerjani,1 Seyed Mohsen Aghaei,1 Sina Ghasemifar,1 Mehdi Hosseinnia,3 Mahta Mazaheri1,4

1Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran; 2Medical Genetics Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran; 3Department of Biology, Faculty of Science, University of Guilan, Rasht, Iran; 4Mother and Newborn Health Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran

*These authors contributed equally to this work

Correspondence: Mahta Mazaheri Email mahta.mazaheri2019@gmail.com

Introduction: DiGeorge syndrome critical region gene 8 (DGCR8) contributes to miRNA biogenesis, and defects in its expression could lead to defects in spermatogenesis.Methods: Here, we assess gene and protein expression levels of DGCR8 in the testicular biopsy specimens obtained from men with obstructive azoospermia (OA, n = 19) and various types of non-obstructive azoospermia (NOA) including maturation arrest (MA, n = 17), Sertoli cell-only syndrome (SCOS, n = 20) and hypospermatogenesis (HYPO, 18). Also, samples of men with NOA were divided into two groups based on successful and unsuccessful sperm recovery, NOA+ in 21 patients and NOA in 34 patients.Results: Examinations disclosed a severe decrease in DGCR8 in samples with MA and SCOS in comparison to OA samples (P < 0.001). Also, the results showed DGCR8 has significantly lower expression in testis tissues of NOA group in comparison to NOA+ group (p< 0.05). Western blot analysis confirmed that the DGCR8 protein was not expressed in SCOS samples and had a very low expression in MA and HYPO samples.Discussion: The results of this survey showed that DGCR8 is an important gene for the entire spermatogenesis pathway. Moreover, DGCR8 gene plays an important role in the diagnosis of NOA subgroups, and also the expression changes in it might contribute to SCOS or MA phenotypes. This gene with considering other related genes can also be a predictor of sperm retrieval.

Keywords: DGCR8, obstructive azoospermia, non-obstructive azoospermia, spermatogenesis

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Deficient Expression of DGCR8 in Human Testis is Related to Spermatoge | IJGM - Dove Medical Press

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Fulcrum Therapeutics, Inc.(NASDAQ:FULC)Q12020 Earnings CallMay 13, 2020, 8:00 a.m. ET

Operator

Good morning, and welcome to Fulcrum Therapeutics first-quarter 2020 conference call. [Operator instructions] I would now like to turn the call over to Christi Waarich, director of investor relations and corporate communications at Fulcrum. Please proceed.

Christi Waarich -- Director of Investor Relations and Corporate Communications

Thank you, Dmitria. Good morning, and welcome to the Fulcrum Therapeutics conference call to discuss our first-quarter 2020 financial results and recent corporate highlights. Earlier today, we issued a press release outlining our recent progress. For those of you who don't have a copy, you can access it in the investor relations section of our website fulcrumtx.com.

Please be reminded that remarks made during this call may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These may include statements about our future expectations and plans, clinical development time lines and financial projections. While these forward-looking statements represent our views as of today, they should not be relied upon as representing our views in the future. We may update these statements in the future but we are not taking on an obligation to do so.

Please refer to our most recent filings with the Securities and Exchange Commission for a discussion of certain risks and uncertainties associated with our business. With me on today's call are Robert Gould, president and chief executive officer; Diego Cadavid, senior vice president of clinical development; Owen Wallace, chief scientific officer; and Bryan Stuart, chief operating officer. Let me quickly run through this morning's agenda. Robert will begin the call with an overview of our recent progress.

Diego will discuss our FSHD program. Owen will discuss our sickle cell program and research efforts, and Bryan will cover our financials before opening the call for Q&A. With that, it's my pleasure to turn the call over to Robert. Robert?

Robert Gould -- President and Chief Executive Officer

Thank you, Christi. Good morning, everyone, and thank you for joining us today. I first want to thank the healthcare workers, investigators and caregivers for their courage and passion as they continue to support so many during the challenges of COVID-19. Our hearts go out to everyone who's been impacted.

To all of our friends, colleagues and the patient communities we serve, we hope you are keeping safe and healthy. Fulcrum's mission and purpose remain unchanged as we work to discover and develop therapeutics to treat genetically defined diseases by addressing their root cause. I'm proud of how our employees have risen to the evolving challenges of the COVID-19 pandemic. I would like to begin by highlighting some of our recent updates and accomplishments.

Today, we announced an amendment to ReDUX4, our Phase 2b trial with losmapimod in patients with facioscapulohumeral muscular dystrophy or FSHD. Diego will go over the amendment in more detail. These changes will extend the patient treatment from the original trial design and we believe will provide a more robust data set while addressing the challenges presented by COVID-19. Early in the quarter, we received orphan drug designation from the U.S.

Food and Drug Administration for losmapimod in FSHD. I'm pleased to report that we have also received orphan designation from the European Commission for losmapimod for the treatment of FSHD. Like in the U.S., orphan designation is granted by the European Commission to drugs that are intended for the treatment, prevention or diagnosis of life-threatening or chronically debilitating rare diseases. We are extremely pleased to have received this designation, further supporting the advancement of losmapimod's FSHD program.

We recently presented dose-dependent target engagement data in skeletal muscle from our Phase 1 trial with losmapimod during a virtual clinical trial session of the muscular dystrophy association meeting. We continue to make progress with FTX-6058, an oral small-molecule therapeutic designed to induce expression of fetal hemoglobin in select hemoglobinopathies. You'll hear about our sickle cell program from Owen later in the call. We also continue to make progress on our early research-stage activities, including building out FulcrumSeek, our proprietary product engine designed to identify drug targets, programs and clinical development candidates in a broad range of genetically defined diseases.

And we initiated research activities under our collaboration with Acceleron. I would now like to turn the call over to Diego for an update on the FSHD program. Diego?

Diego Cadavid -- Senior Vice President of Clinical Development

Thanks, Robert. As a reminder, FSHD is a progressive disease characterized by severe muscular degeneration that occurs as skeletal muscle is replaced by fat. We estimate there are approximately 16,000 to 38,000 patients in the U.S. and similar incidents worldwide.

There are currently no approved drugs for FSHD and we are advancing the only known industry-sponsored clinical trial evaluating a potential treatment. Unlike other diseases that can be characterized by the lack of a gene, FSHD is characterized by the aberrant expression of the gene DUX4, the root cause of the disease. We at Fulcrum discovered that losmapimod, a selective p38 MAP kinase inhibitor, reduced the expression of DUX4 in preclinical studies. We therefore believe losmapimod represents a potential novel therapeutic option for FSHD patients.

Our own evidence, as well as independent evidence suggests that we do not have to turn DUX4 off completely to provide benefit. There is a spectrum of DUX4 expression and FSHD presentation that suggests that even an incremental reduction may be beneficial to patients. Thus, we believe, as do independent researchers, that any reduction in DUX4-driven gene expression has the potential for benefit to patients. ReDUX4 is our international Phase 2b, double-blind placebo-controlled trial of losmapimod in patients with genetically confirmed FSHD.

We completed enrollment of 80 patients at the end of February, which exceeded the 66 we had originally planned. The primary endpoint of the trial is the change from baseline in DUX4-driven gene expression in affected skeletal muscle. We also completed enrollment in our Phase 2 single-site open-label trial which has been impacted by COVID-19, and we are considering next steps. Fulcrum is dedicated to maintaining the highest standards in patient and clinician safety in the planning and execution of our clinical research programs.

The safety of our clinical trial participants and their healthcare providers, as well as the integrity of the data we collect remains paramount. In the wake of COVID-19, a number of our clinical trial sites postponed trial-related activities, and we quickly implemented plans to limit the potential disruption to our FSHD program. The original design of the ReDUX4 included a pretreatment biopsy followed by a second biopsy at week 16 of the 24-week treatment period. Following the 24-week trial, patients had the opportunity to roll into an open-label extension.

Prior to the COVID-19 pandemic, 12 of the 80 patients completed their 24 weeks of treatment, including their week 16 biopsy and all enrolled in the open-label extension. As the COVID-19 pandemic continues, our team, in collaboration with our investigators, extended the ReDUX4 trial from 24 to 48 weeks. This allows approximately 67 subjects currently continuing in the trial to receive a biopsy at either week 16 or under the amended protocol at week 36 and after completing the 48-week treatment period, rolling to the open-label extension. To summarize, the ReDUX4 trial has been extended from 24 to 48 weeks with an open-label extension to follow.

Patients will receive a muscle biopsy at either 16 or 36 weeks. This extension will apply to the approximately 67 patients still enrolled in the trial while 12 have already completed and have been rolled into the open-label extension. As part of the modification to the trial, we will also conduct an interim analysis of approximately 25 subjects who have completed their 16-week biopsy. We anticipate sharing data from this interim analysis of subjects' DUX4-driven gene expression signature in the third quarter of this year, and we expect to report top-line data on the primary endpoint in the first quarter of 2021.

The extension from 24 to 48 weeks also allows for a longer assessment in a placebo-controlled design of the skeletal muscle MRI secondary endpoint and the various exploratory clinical endpoints such as reachable workspace, FSHD Timed Up and Go, muscle function measures and patient-reported outcomes. From both independent researchers, as well as our own preparatory studies, we know the DUX4 gene signature is stable over time in this population, and we believe that the longer we are able to treat patients, the greater the potential benefit losmapimod may have on the root cause of the disease. We strongly believe these changes to the ReDUX4 study are in the best interest of the patient community and provide the best opportunity to advance this important development effort as we work to address the challenges presented by COVID-19. All of these changes are designed to enable patients and investigators to continue participation in ReDUX4 and will allow us to collect essential data to support continued dialogue with regulators.

I'll now turn the call over to Owen. Owen?

Owen Wallace -- Chief Scientific Officer

Thanks, Diego. At Fulcrum, we pursue targeted indications where we believe we can develop safe and effective small-molecule therapies to rebalance gene expression. In our work across various indications, we consistently aim to address the root causes of disease to increase the potential efficacy of these treatments and, more broadly, transform the way these diseases are being treated. In spite of the challenges posed by COVID-19, we have continued to make progress on our research and early clinical portfolio.

As an essential business, we continue lab operations, albeit on a more limited basis. As a result, we continue to advance the collaboration with Acceleron, as well as our internal portfolio. We have also advanced our work on FulcrumSeek, our proprietary product engine designed to identify drug targets, programs and clinical development candidates in a broad range of genetically defined diseases. By combining high-throughput RNA sequencing, cellular imaging data and large-scale machine learning, we are monitoring more than 10,000 molecular and cellular features generated by the small-molecule probe and CRISPR perturbagen libraries.

Understanding their effects on gene expression is fundamental to our therapeutic strategy to modulate the genetic root cause of disease. FulcrumSeek is not only the core of our target identification strategy. It also provides us with a unique understanding of how cellular function is altered in human disease. I would like to thank our employees who have continued to work diligently through the COVID-19 crisis to advance our research programs, especially those who are coming into the lab working under social distancing and enhanced health and safety guidelines.

Likewise, our hemoglobinopathy program has continued to advance toward the IND filing. Our approach has focused on the up-regulation of fetal hemoglobin, which could be beneficial for both sickle cell disease and beta-thalassemia. By increasing levels of HbF to compensate for the mutated hemoglobin in sickle cell patients, we believe that we can develop and deliver a potent, effective and selective therapy for patients. This therapeutic strategy is supported by human genetics and pharmacology data where increasing levels of HbF have been shown to be associated with improved prognosis and outcomes, suggesting that HbF may be a surrogate endpoint in future clinical trials.

We're very pleased with our recent progress. Our clinical candidate FCX-6058 has been profiled broadly in preclinical in-vitro and in-vivo models of sickle cell disease, and we have seen robust elevation of HbF at drug concentrations that we believe will be readily achieved in humans based on pharmacokinetic profiling of the compound. We've had an abstract accepted for oral presentation at the 14th Annual Sickle Cell Disease Research & Educational Symposium scheduled for September of this year. We have also filed our non-provisional patent application, and we've completed our IND-enabling studies and toxicology work with FTX-6058.

We plan to submit the IND in sickle cell disease in the second half of 2020 and initiate our Phase 1 trial by the end of the year.With that, I will now turn the call over to Bryan for an update on our financial results for the quarter. Bryan?

Bryan Stuart -- Chief Operating Officer

Thanks, Owen. In these unprecedented times, Fulcrum is committed to making a difference for patients with FSHD and select hemoglobinopathies such as sickle cell disease. We are proceeding with a great sense of urgency to bring these potentially transformative therapies to patients. We ended the first-quarter 2020 with $81.2 million in cash, cash equivalents and marketable securities.

Based on our current operating plan and projections, we believe this will support our operations into the third quarter of 2021, allowing us to advance losmapimod in FSHD and bring FTX-6058 into the clinic while continuing to invest in our discovery-stage efforts. Research and development expenses for the quarter ended March 31, 2020, were $14.5 million, compared to $34.6 million in the first quarter of 2019. Included in that $34.6 million was $25.6 million of onetime costs associated with the issuance of series B convertible preferred stock under the company's license agreement with GSK for the rights to losmapimod. Excluding these onetime costs, the increase of $5.5 million was primarily due to increased costs related to the advancement of losmapimod for the treatment of FSHD, as well as increased personnel-related costs to support the growth of Fulcrum's research and development organization.

General and administrative expenses for the first quarter of 2020 were $5.1 million as compared to $2.6 million for the first quarter of 2019. This increase was primarily due to increased personnel-related costs to support the growth of our organization, as well as increased costs associated with operating as a public company. Overall, we remain undeterred in our mission and continue to expect several upcoming catalysts. We'll report the interim analysis from ReDUX4 in the third quarter of this year.

We'll initiate the Phase 1 trial with FTX-6058 in sickle cell disease and disclose the biochemical drug target by the end of the year, and we'll continue to advance our discovery programs from our product engine while making progress with our partners at Acceleron. We're excited about the work ahead and we continue -- as we continue to execute on our plans, and we look forward to keeping you updated on our progress in the months ahead. Operator, you may now open the line for questions.

Christi Waarich -- Director of Investor Relations and Corporate Communications

Operator, we're now ready for questions.

Operator

[Operator instructions] And our first question comes from Matthew Harrison with Morgan Stanley. You may proceed.

Kostas Biliouris -- Morgan Stanley -- Analyst

This is Kostas on for Matthew. A couple of questions from my side. The first one is whether you guys expect to lose any power given that you will only have 25 subjects in the first interim analysis. Do you think you will have enough power to see a signal there? Or do you expect the data only to be directional, to show you an improvement or not?

Diego Cadavid -- Senior Vice President of Clinical Development

Yeah. Thank you for the question. This is Diego Cadavid. The sample size of 80 subjects is -- we believe has appropriate power to answer the question at the end of the trial.

25 subjects, we believe, will give us an initial opportunity to look at the data and help us prepare and make some early insights into Phase 3 planning.

Kostas Biliouris -- Morgan Stanley -- Analyst

OK, thank you. And a follow-up question. Will you need to recruit additional subjects or you believe you have all the subjects you need at this point?

Diego Cadavid -- Senior Vice President of Clinical Development

We have completed recruitment. We believe we have all the subjects we needed.

Kostas Biliouris -- Morgan Stanley -- Analyst

OK. And then finally, I was wondering whether -- in the second part, when you expect all the subjects to have a biopsy at 16 or 36 weeks, given that there might be a second wave of the pandemic, of additional -- a second wave of infections, how certain you are you can have all the subjects complete the second biopsy at 36 weeks and whether there is any actions you are taking to mitigate this risk of losing some patients there again? Thank you.

Diego Cadavid -- Senior Vice President of Clinical Development

Yeah. When we amended the protocol, we carefully considered exactly what you're referring to. So we've built some windows -- time windows around the 36th week and sites have flexibility, as well as patients. So right now, we anticipate that we will get the data either at week 16 or at week 36 regardless.

Kostas Biliouris -- Morgan Stanley -- Analyst

OK. Thank you very much.

Operator

And our next question comes from Joseph Schwartz with SVB Leerink. You may proceed.

Joseph Schwartz -- SVB Leerink -- Analyst

My question would be, can you talk about how you arrived at a doubling in duration for the ReDUX protocol with respect to the clinical endpoints? Will patients in ReDUX still be evaluated at 24 weeks? And how many patients are hitting this time point in the second half of this year when it seems like social distancing might relax? And then when would most patients be hitting the 48-week time point? Have you done an analysis there to consider that this is in your best interest given -- however this pandemic might evolve with respect to its different waves based on where you're enrolling these patients?

Diego Cadavid -- Senior Vice President of Clinical Development

Yeah. The ReDUX4 trial completed enrollment in about six months between August of last year and February of this year. Therefore, the patients are moving across all the visits over a period of six months. We decided to extend the study by an additional 24 weeks because we believe, based on what is happening and what we expect to happen with COVID-19, this will give flexibility for the patients to collect data across a much longer period, where we expect the clinics to be open even if intermittently.

So overall, we believe that even if some 24-week visits are missed, patients would come back later. And as you know, FSHD is a slowly progressive disease. We are not counting acute events. So as long as we are collecting the data over time, we believe we'll be able to answer the efficacy questions.

Especially, many sites are still open. The impact of the pandemic is not affecting every site.

Joseph Schwartz -- SVB Leerink -- Analyst

And are you able to bring patients in and just strike while the iron is a little bit warmer in this period we seem to be entering as we speak now? Could you bring patients in for an evaluation? Can you talk about -- is it just at 24 and 48 weeks that the clinical assessments are being performed? Or do you have any ability to sneak in some additional sites without making additional protocol adjustments that might require you to take alpha hits?

Diego Cadavid -- Senior Vice President of Clinical Development

Yeah. This amendment builds flexibility. So all the visits of the original protocol over 24 weeks are open -- sites that are open, patients are coming. And the amendment provides additional opportunities at week 36, week 48 with extended windows.

So we really give opportunities to capture as much data regardless of what happens with COVID-19. We're very fortunate that not only the sites but the patients are very committed, and that's reflected in the high subject retention we have on the trial.

Joseph Schwartz -- SVB Leerink -- Analyst

That's very helpful. And then have you been able to garner any insights to date from the open-label trial? It sounds like you suggested it's been impacted from COVID-19, and I heard you're evaluating the next steps there. So why has that been impacted more, it sounds, than ReDUX4? Can you provide any color on that front?

Diego Cadavid -- Senior Vice President of Clinical Development

Yes. The open-label study is single site so you don't have this opportunity we have in ReDUX4 where we have many sites. And therefore, if one region that happens to be where this site is, is heavily affected, of course, the impact will be larger. That site is in the Netherlands.

We have always considered that a learning trial. The trial began in August. So obviously, we've had valuable learnings from that trial, which has always been the goal to inform what we do in ReDUX4. So in that sense, we believe this trial has been helpful.

Joseph Schwartz -- SVB Leerink -- Analyst

That's helpful. Thanks for the color.

Operator

And our next question comes from Tazeen Ahmad with Bank of America. You may proceed.

Tazeen Ahmad -- Bank of America Merrill Lynch -- Analyst

I just wanted to clarify your powering assumptions. So you previously said that the study would be powered to show a 50% reduction of DUX4 at week 16. Just based on the changes that you're talking about, how does that affect the potential path to accelerated approval? And have you spoken with FDA about this particular item?

Robert Gould -- President and Chief Executive Officer

Hi, Tazeen. This is Robert. Just a slight correction on -- I don't believe that we did power the study for a 50% reduction in the DUX4. That was not one of the original assumptions.

But I'll let Diego speak to the powering assumptions we made.

Diego Cadavid -- Senior Vice President of Clinical Development

Yeah. Robert is correct. We have never disclosed what the assumptions are for the power. This amendment is not impacting the power.

The sample size is the same. It only adds some flexibility. Because they're on treatment, muscle biopsy can be at week 16 or week 36, and we don't really expect a loss of subjects based on this amendment. Therefore, nothing has changed about the power assumptions.

Tazeen Ahmad -- Bank of America Merrill Lynch -- Analyst

OK. And how are you taking into account -- you're effectively increasing the length of the study to a year. What are you seeing in compliance rates for the study so far? And does this increase -- do you have any buffer, if you will, for potential dropouts in the study with the extended time of observation?

Robert Gould -- President and Chief Executive Officer

Yeah. Thanks, Tazeen. This is Robert again. One of the things that we've really been struck with is the cooperation of the patients and their willingness to take losmapimod.

Just to remind you, as you know, it's an oral drug taken twice daily, 7.5 milligram tablets, so two tablets in the morning, two tablets in the evening. And we just had not only a high retention rate of the patients, but we believe high compliance as well. And so the original trial was enrolling 66 patients. And because of the response we had from the patient community and the opportunity we had, we actually increased that to 80 patients.

So even if things were to change with the patients, we do believe that we're still going to be able to have the original 66 patients. But at this point in time, we believe we're going to be able to retain most of the patients that are currently in the study, if not all of them that are currently in the study.

Tazeen Ahmad -- Bank of America Merrill Lynch -- Analyst

OK. And my last question is about taking the biopsy at 16 weeks or 36. How did you come up with 36? And how do you feel confident in the integrity of the readings of both time periods? Because there's a big gap between the two.

Diego Cadavid -- Senior Vice President of Clinical Development

Yeah. This is Diego. So we have done our own preparatory study to look at the stability and variability of the DUX4 gene signature and the natural history, and that was done about six, eight weeks apart. The academic group of the Wellstone collaboration had done it over a year apart, and they were very generous and shared all their data with us.

So we know from these two studies that these DUX4 signature at the population level is very stable. So this interval between eight weeks or a year apart basically gives us a good argument that as long as you -- we collect repeated biopsies within that interval, we don't expect any impact on greater variability or loss of signature. So 36 really came in terms of building flexibility for patients and sites who had not obtained a 16-week biopsy as the pandemic moves, assuming that over time there will be a decrease of peaks and sites will be able to reopen and bring the patients in to obtain these biopsies. It's 36 weeks but we have a window so sites and patients can be flexible, and we believe that is the best chance to collecting the efficacy endpoint without losing power and keeping the quality.

Operator

[Operator instructions] And our next question comes from Ted Tenthoff with Piper Sandler. You may proceed.

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Fulcrum Therapeutics, Inc. (FULC) Q1 2020 Earnings Call Transcript - The Motley Fool

Phase 1/2 Trial of PR001 for Parkinsons Disease with GBA1 Mutations Ongoing; Study Startup ActivitiesProgressing for Phase 1/2 Trials of PR001 for Type 2 NeuronopathicGaucher Disease and PR006 forFrontotemporal Dementia with GRN Mutations

Data Presentations Highlight Potential of AAV Gene Therapy Approach toSlow or Stop Neurodegenerative Disease Progression in Preclinical Models

NEW YORK, May 14, 2020 (GLOBE NEWSWIRE) -- Prevail Therapeutics Inc. (Nasdaq: PRVL), a biotechnology company developing potentially disease-modifying AAV-based gene therapies for patients with neurodegenerative diseases, today reviewed recent business highlights and reported financial results for the first quarter ended March 31, 2020.

We are excited to continue the clinical development of PR001 and are on track to report interim data for a subset of patients from our Phase 1/2 clinical trial of PR001 for Parkinsons disease with GBA1 mutations (PD-GBA) later this year. In addition, we are advancing our AAV gene therapy-based pipeline, with the planned mid-year initiation of Phase 1/2 clinical trials of PR001 for Type 2 neuronopathic Gaucher disease (nGD) and PR006 for frontotemporal dementia with GRN mutations (FTD-GRN), said Asa Abeliovich, M.D., Ph.D., Founder and Chief Executive Officer of Prevail. In addition, at ASGCT and AAT-AD/PD, we presented or will present data that validate the potential of these products for neurodegenerative disease patients with urgent unmet needs, and detailed our ongoing and planned clinical trials.

Recent Business Highlights and Updates:

In addition, study startup activities are continuing for the PROVIDE Phase 1/2 clinical trial of PR001 for Type 2 nGD, and the Company intends to initiate dosing in mid-2020. Prevail also continues to expect to initiate the PROGRESS Phase 1/2 clinical trial of PR001 for Type 3 nGD in the second half of 2020. The timelines for PR001 are subject to any delays related to the COVID-19 pandemic.

Clinical Development of PR006: Study startup activities are also underway for the PROCLAIM Phase 1/2 clinical trial of PR006 for FTD-GRN patients, which is planned to initiate in mid-2020, subject to any delays related to the COVID-19 pandemic.

First Quarter 2020 Financial Results

About Prevail TherapeuticsPrevail is a gene therapy company leveraging breakthroughs in human genetics with the goal of developing and commercializing disease-modifying AAV-based gene therapies for patients with neurodegenerative diseases. The company is developing PR001 for patients with Parkinsons disease with GBA1 mutations (PD-GBA) and neuronopathic Gaucher disease; PR006 for patients with frontotemporal dementia with GRN mutations (FTD-GRN); and PR004 for patients with certain synucleinopathies.

Prevail was founded by Dr. Asa Abeliovich in 2017, through a collaborative effort with The Silverstein Foundation for Parkinsons with GBA and OrbiMed, and is headquartered in New York, NY.

Forward-Looking Statements Related to PrevailStatements contained in this press release regarding matters that are not historical facts are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Examples of these forward-looking statements include statements concerning: the potential impact of COVID-19 on Prevails ongoing and planned clinical trials, business and operations; the potential of Prevails gene therapies to modify the course of neurodegenerative diseases; the anticipated timing of Prevails clinical trials of PR001 in PD-GBA and in nGD and Prevails clinical trial of PR006, including resuming of delayed trials and initiation of new trials; the expected timing of reporting of interim data for a subset of patients from Prevails Phase 1/2 clinical trial of PR001; and expectations regarding Prevails cash runway. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. These risks and uncertainties include, among others: Prevails novel approach to gene therapy makes it difficult to predict the time, cost and potential success of product candidate development or regulatory approval; Prevails gene therapy programs may not meet safety and efficacy levels needed to support ongoing clinical development or regulatory approval; the regulatory landscape for gene therapy is rigorous, complex, uncertain and subject to change; the fact that gene therapies are novel, complex and difficult to manufacture; and risks relating to the impact on our business of the COVID-19 pandemic or similar public health crises.

These and other risks are described more fully in Prevails filings with the Securities and Exchange Commission (SEC), including the Risk Factors section of the Companys Quarterly Report on Form 10-Q for the period ended March 31, 2020, filed with the SEC on or about May 14, 2020, the Companys Annual Report on Form 10-K for the fiscal year ended December 31, 2019, filed with the SEC on March 26, 2020, and its other documents subsequently filed with or furnished to the SEC. All forward-looking statements contained in this press release speak only as of the date on which they were made. Except to the extent required by law, Prevail undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.

Prevail Therapeutics Inc.Statements of Operations(Unaudited)(in thousands, except share and per share data)

Balance Sheets(in thousands, except share and per share data)

Media Contact:Mary CarmichaelTen Bridge Communicationsmary@tenbridgecommunications.com617-413-3543

Investor Contact:investors@prevailtherapeutics.com

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Prevail Therapeutics Reports First Quarter 2020 Financial Results and Business Highlights - GlobeNewswire

Scientists have found evidence for mutations in some strains of the coronavirus that suggest the pathogen may be adapting to humans after spilling over from bats.

The analysis of more than 5,300 coronavirus genomes from 62 countries shows that while the virus is fairly stable, some have gained mutations, including two genetic changes that alter the critical spike protein the virus uses to infect human cells.

Researchers at the London School of Hygiene and Tropical Medicine stress that it is unclear how the mutations affects the virus, but since the changes arose independently in different countries they may help the virus spread more easily.

The spike mutations are rare at the moment but Martin Hibberd, professor of emerging infectious diseases and a senior author on the study, said their emergence highlights the need for global surveillance of the virus so that more worrying changes are picked up fast.

This is exactly what we need to look out for, Hibberd said. People are making vaccines and other therapies against this spike protein because it seems a very good target. We need to keep an eye on it and make sure that any mutations dont invalidate any of these approaches.

Studies of the virus revealed early on that the shape of its spike protein allowed it to bind to human cells more efficiently than Sars, a related virus that sparked an outbreak in 2002. The difference may have helped the latest coronavirus infect more people and spread rapidly around the world.

Scientists will be concerned if more extensive mutations in the spike protein arise, not only because they may alter how the virus behaves. The spike protein is the main target of leading vaccines around the world, and if it changes too much those vaccines may no longer work. Other potential therapies, such as synthetic antibodies that home in on the spike protein, could be less effective, too.

This is an early warning, Hibberd said. Even if these mutations are not important for vaccines, other mutations might be and we need to maintain our surveillance so we are not caught out by deploying a vaccine that only works against some strains.

The scientists analysed 5,349 coronavirus genomes that have been uploaded to two major genetics databases since the outbreak began. By studying the genetic makeup of the viruses, the scientists worked out how it has diversified into different strains and looked for signs that it was adapting to its human host.

In an unpublished study that has yet to be peer reviewed, the researchers identified two broad groups of coronavirus that have now spread globally. Of the two spike mutations, one was found in 788 viruses around the world, with the other present in only 32.

The study shows that, until January, one group of coronaviruses in China escaped detection because they had a mutation in the genetic region that early tests relied on. More recent tests detect all of the known types of the virus.

Last month, an international team of scientists used genetic analyses to show that the coronavirus likely originated in bats and was not made in a lab as some conspiracy theorists have claimed.

Follow this link:

Scientists concerned that coronavirus is adapting to humans - The Guardian

As the virus that causes COVID-19 traveled out of China and proliferated across the globe, it developed small mutations that accumulated into distinct versions of the virus. Scientists can now tell these versions apart by peering into the viral genome.

For example, here in the United States, there is the "West Coast" version of the virus that came directly from Asia, and a slightly different "East Coast" version which traveled through Europe.

But is one version of coronavirus more dangerous than the other? And should we be afraid of these new mutations?

The short answer according to virologists, is no.

Viruses are constantly copying themselves, so it's rather frequent that some of those copies will have mistakes, or mutations. These mutations are neither inherently good nor bad and are random.

So far, the novel coronavirus responsible for the global pandemic is mutating normally as virologists expected to see based on their experience with other similar viruses.

"Viruses mutate," said Dr. Nels Elde, Ph.D., associate professor of human genetics at the University of Utah. "That's one of the things that makes them such a successful entity."

"The word 'mutation' to people means something bad because it's got that connotation to it," said Dr. Vincent Racaniello, Ph.D., Higgins professor of microbiology and immunology at Mt. Sinai School of Medicine of CUNY.

This handout illustration image taken with a scanning electron microscope shows SARS-CoV-2 (yellow)also known as 2019-nCoV, the virus that causes COVID-19 isolated emerging from the surface of cells (blue/pink) cultured in the lab.

"It simply means a change in the genome sequence. It doesn't mean that it's necessarily bad for you at all," Racaniello said. "Plants grow in the spring. Viruses mutate. It's no big deal."

Tune into ABC at 1 p.m. ET and ABC News Live at 4 p.m. ET every weekday for special coverage of the novel coronavirus with the full ABC News team, including the latest news, context and analysis.

But as scientists across the globe learn more about these mutations, many have been eager to use these discoveries to decipher whether the virus is becoming more or less dangerous.

For example, in early March a group of scientists in China identified two different types of the virus, the L-type and the S-type. The L-type was found to be more widespread, leading to early speculation that the virus had evolved into a more infectious version of itself.

More recently, similar research out of Los Alamos National Laboratory in the United States which has not been peer reviewed identified a common mutation in the virus that began spreading in Europe in early February. The scientists suggested this mutation may have helped the virus spread faster and farther because it is inherently more infectious, generating breathless news coverage about a dangerous "mutant" virus.

But another group of scientists from Arizona State University arrived at a nearly opposite interpretation of the mutations they discovered. Their research led them to believe the virus might become weaker and die off, just like the 2003 SARS outbreak.

So far, the speculation about the virus' infectiousness are guesses, said Racaniello. He said there is no iron-clad evidence that these mutations have made any one version of the virus more contagious, deadlier or more resistant to potential therapies.

That's probably good news for humankind, because it means the vaccines and therapies being tested right now are likely to work against all known versions of the virus.

Scientists are actively monitoring the virus to see if it develops potentially dangerous mutations -- or even if it dramatically transforms into a new "strain" -- a word that has a very specific meaning to virologists but has also been used colloquially to describe the different versions of the virus that exist so far.

A new strain would signal a dramatic event, meaning the virus has mutated so much that it is "functionally different" than its predecessor, Elde said. According to Elde, virologists generally agree there is only one "strain" of novel coronavirus, although there are several versions of the virus in different parts of the world.

In fact, what scientists are observing, in terms of the differences between these viruses, is a phenomenon called viral "isolates," said Racaniello. That's when the genetic material develops slight variations that are not significant enough to make the virus behave in a totally different way.

These small changes happen frequently -- sometimes developing within the same person as the virus spreads throughout the human body.

"You can have different isolates from a single patient, by taking different samples from the respiratory tract and in the lung, for example," said Racaniello. "It does not mean the differences have any significance whatsoever."

"I think the bottom line is we don't really know right now whether mutation signals good news or bad news. It is somewhere in between," said Dr. Jay Bhatt, former medical chief at the American Hospital Association and an ABC News contributor.

"I think we will understand this better in the coming months."

Angela N. Baldwin, M.D., M.P.H., is a pathology resident at Montefiore Health System in the Bronx and is a contributor to the ABC News Medical Unit. Sony Salzman is the unit's coordinating producer.

Read the original:

Yes, COVID-19 is mutating, here's what you need to know - ABC News

The Research Brief is a short take about interesting academic work.

When some people become infected with the coronavirus, they only develop mild or undetectable cases of COVID-19. Others suffer severe symptoms, fighting to breathe on a ventilator for weeks, if they survive at all.

Despite a concerted global scientific effort, doctors still lack a clear picture of why this is.

Could genetic differences explain the differences we see in symptoms and severity of COVID-19?

To test this, we used computer models to analyze known genetic variation within the human immune system. The results of our modeling suggest that there are in fact differences in peoples DNA that could influence their ability to respond to a SARS-CoV-2 infection.

When a virus infects human cells, the body reacts by turning on what are essentially anti-virus alarm systems. These alarms identify viral invaders and tell the immune system to send cytotoxic T cells a type of white blood cell to destroy the infected cells and hopefully slow the infection.

But not all alarm systems are created equal. People have different versions of the same genes called alleles and some of these alleles are more sensitive to certain viruses or pathogens than others.

To test whether different alleles of this alarm system could explain some of the range in immune responses to SARS-CoV-2, we first retrieved a list of all the proteins that make up the coronavirus from an online database.

We then took that list and used existing computer algorithms to predict how well different versions of the anti-viral alarm system detected these coronavirus proteins.

The part of the alarm system that we tested is called the human leukocyte antigen system, or HLA. Each person has multiple alleles of the genes that make up their HLA type. Each allele codes for a different HLA protein. These proteins are the sensors of the alarm system and find intruders by binding to various peptides chains of amino acids that make up parts of the coronavirus that are foreign to the body.

Once an HLA protein binds to a virus or piece of a virus, it transports the intruder to the cell surface. This marks the cell as infected and from there the immune system will kill the cell.

In general, the more peptides of a virus that a persons HLAs can detect, the stronger the immune response. Think of it like a more sensitive sensor of the alarm system.

The results of our modeling predict that some HLA types bind to a large number of the SARS-CoV-2 peptides while others bind to very few. That is to say, some sensors may be better tailored to SARS-CoV-2 than others. If true, the specific HLA alleles a person has would likely be a factor in how effective their immune response is to COVID-19.

Because our study only used a computer model to make these predictions, we decided to test the results using clinical information from the 2002-2004 SARS outbreak.

We found similarities in how effective alleles were at identifying SARS and SARS-CoV-2. If an HLA allele appeared to be bad at recognizing SARS-CoV-2, it was also bad at recognizing SARS. Our analysis predicted that one allele, called B46:01, is particularly bad with regards to both SARS-CoV-2 and SARS-CoV. Sure enough, previous studies showed that people with this allele tended to have more severe SARS infections and higher viral loads than people with other versions of the HLA gene.

Based on our study, we think variation in HLA genes is part of the explanation for the huge differences in infection severity in many COVID-19 patients. These differences in the HLA genes are probably not the only genetic factor that affects severity of COVID-19, but they may be a significant piece of the puzzle. It is important to further study how HLA types can clinically affect COVID-19 severity and to test these predictions using real cases. Understanding how variation in HLA types may affect the clinical course of COVID-19 could help identify individuals at higher risk from the disease.

To the best of our knowledge, this is the first study to evaluate the relationship between viral proteins across a wide range of HLA alleles. Currently, we know very little about the relationship between many other viruses and HLA type. In theory, we could repeat this analysis to better understand the genetic risks of many viruses that currently or could potentially infect humans.

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Your genes could determine whether the coronavirus puts you in the hospital and we're starting to unravel which ones matter - The Conversation US

this and countless other scientific findings led the President of the American Sociologicalin his 2005 presidential addressto call upon members to, Prepare to defend against the genomic data juggernaut heading their way down the pike.'

Introduction

The 2020 presidential campaign, particularly on the Democratic side, has thus far placed the concept of facts and the science at center stage. When former president Barack Obama endorsed his former Vice President, Joe Biden, for President of the United States on April 14th, former President Obama asserted that Vice President Biden wouldunlike conservativesadhere to the facts and the science in running his administration. Then, on April 28th, former Secretary of State Hillary Clinton added her endorsement of Vice President Biden. Secretary Clinton indicated her view that it was necessary to have a president, who listened to the science, put facts over fiction. As such, she suggested that Vice President Bidenunlike President Donald Trumpwould be that person.

Secretary Clintons endorsement of the former Vice President was followed almost immediately by The New York Times podcast When Science Is Partisan in which Frank Bruni stated: From the very start of his administration President Trump has shrugged off expertise, he has outright mocked experts, and he has shown special disregard for science. Even more dangerous he has frequently presented fiction as fact. So, again and again, Democrats have asserted that their Republican counterparts flagrantly ignore the research findings of experts, thereby regularly running afoul of reality. As I will argue, this Democratic line of argument is simply not correct, and I will trace each groups actual willingness to follow the facts and the science, wherever they might lead.

Failings When It Comes to Science

Conservatives, admittedly, either ignore or reject the well-demonstrated theory of evolution. Simply stated our planet (and all of its many species) were not created in six days. Our Universe is at least 14 billion years old, and the sphere on which we live congealed about 4.5 billion years in the past. But, in 2013, roughly 48% of conservative voters believed that creation according to The Book of Genesis is factual. This is as compared to the 67% of Democrats and 65% of Independents who believe humans evolved over time. As such, rather than alienate this large segment of the Republican electoral base, if a reporter asks a conservative candidate if he or she believes in evolution, the candidate will frequently duck the question. This position is a violation of both the facts and the science, and these Republican politicians should be ashamed of themselves for not endorsing the truth. This is a well-known example of conservatives choosing to ignore the evidence.

Turning to progressivesand the subject of abortionwe find that those on the Left either ignore or reject the scientific facts. In an October, 2019 Quillette article I Asked Thousands of Biologists When Life Begins. The Answer Was Not Popular, Steve Jacobs reported that he had polled 5,337 biologists asking each of them when life begins and 96% answered, at conception. Only 240 (4%) disagreed. Interestingly, 89% of these biologists self-identified as liberal; 85% said they were pro-choice; 63% were secular, and 92% were Democrats. The bottom line is that the scientific consensus does not materially influence their position on the question of life.

Many on the Left also deny the facts and the data regarding the allegation that rising inequality is occurring in the United States. The statistics that rebut this claim can be found in my article published in Merion West entitled In Reply to McManus: Harping on Income Inequality Ignores the Data.

Now we move on to the hard part. Ever since the polymath Francis Galton coined the term Nature Versus Nurture in the second half of the 19th century, the nature-nurture debate has raged on. As Nstor de Buen wrote in Merion West (When We Debate Biological Differences) this past July, All of these cases have one common thread: the Right will argue that differences between human groups (i.e. men and women, or Caucasians and African-Americans) are explained by biology, while the Left will argue that they are largely the result of socialization and historic circumstances. de Buens essay approaches the genes versus environment question from the Left, while my following arguments all spring from the biological side of this basic disagreement.

The first rejection of the idea of genes and human development (often called scientific racism) came from anthropologist Franz Boas. In his 1938 article entitled An Anthropologists Credo, he wrote,It is my conviction that the fundamental ethical point of view is that of the in-group, which must be expanded to include all humanity. This egalitarian bent was formalized in 1942 by one of Boass students, Ashley Montagu, in his book Mans Most Dangerous Myth: The Fallacy of Race. About this book, Aldous Huxley wrote that where most assume that facts speak for themselves, [Montagu] makes it clear that the facts are mere ventriloquists dummies, and can be made to justify a course of action that appeals to the socially conditioned passions of the individuals concerned.

Both men and much of the world were shocked and horrified by the countless travesties of Nazi Germany; as such, this social scientific idea spread far and wide. In his famous and extremely influential 1970 book, The Struggle of the Scientific Revolution, Thomas Kuhn reported:

Spending a year in a community composed predominantly of social scientists confronted me with unanticipated problems about the differences between such communities and those of the natural scientists among whom I had been trained. Particularly, I was struck by the number and extent of the overt disagreements between social scientists about the nature of legitimate scientific problems and methods [] Somehow, the practice of astronomy, physics, chemistry, or biology normally fails to evoke the controversies over fundamentals that today often seem endemic among say, psychologists or sociologists.

In short, the social sciences were rejecting on ethical grounds the findings of the hard sciences.

Then, in 1972, the Left altered course by asserting that the genetic findings of the hard sciences were simply wrong. Richard Lewontins paper The Apportionment of Human Diversity concluded that 80-85% of the variation within human populations is found within local geographic groups and the differences attributable to traditional race groups are a minor part of human genetic variability and thus race had to be a social construct. This idea that there exists no scientific basis for human races spread quickly through the academy and through much of the media.

Next, in their 1984 book Not in Our Genes, Richard Lewontin, Steven Rose, and Leon Kamin added a purely political goal: equal economic outcomes. In their own words, We share a commitment to the project of the creation of a more socially justsocialistsociety. And we recognize that a critical science is an integral part of the struggle to create that society. Their egalitarian goal was now obvious. Diminishing their stature was the recollection of Robert Trivers, a top-notch evolutionary biologist in his own right, who remembered in Vignettes of Famous Evolutionary Biologists Large and Small that Lewontin would lie openly and admit doing so. Lewontin would sometimes admit [] that some of his assertions were indeed fabrications, but he says the fight was ideological and politicalthey lied and so would he. Further deflating Lewontins image was his 1985 book, The Dialectical Biologist, which he co-authored with Richard Levins. In The Dialectical Biologist,they asserted that there was nothing in Marxist or Leninism that could be contradicted by objective reality.

In 1994, Richard Herrnstein & Charles Murray published The Bell Curve, and the battle was truly joined. A number of books written by social scientists were rushed into print all criticizing The Bell Curve, and a rebuttal to this onslaught was signed by over 50 experts regarding the science of intelligence and published in The Wall Street Journal in December of 1994, as an op-ed entitled Mainstream Science on Intelligence. This article stated in part that Intelligence can be measured, and intelligence tests measure it well. (These IQ tests) are among the most accurate (in technical terms, reliable and valid) of all psychological tests and assessments.

Among the books that attacked The Bell Curve was an effort by Russell Jacoby and Naomi Glauberman, who published in 1995 The Bell Curve Debate. Their book contained two essays by Leon Kamin. In one of these essays, he engaged in some initial backpedaling. In The Pioneers of IQ Testing Kamin offered that, There is, of course, the theoretical possibility that the genetic theorists are correct. IQ is highly heritable and perhaps differences between races [] are in large measure due to heredity. There are serious scholars who have assumed this, and who have labored to adduce supporting evidence. Their data ought not to be ignored, and they deserve careful scrutiny.

Things remained relatively quiet until 2000 when the project to synthesize the human genome was completed (after which genetic research took off). Also, in 2003, A.W.F. Edwards struck an important blow against the nurture side of the genes/environment debate by publishing a scholarly paper entitled Human Genetic Diversity: Lewontins Fallacy. In this paper, he found that:

It is therefore been proposed that the division of Homo Sapiens into (ethnic or racial) groups is unjustified by genetic data. This conclusion, due to R.C. Lewontin in 1972, is unwarranted because the argument ignores the fact that most of the information that distinguishes populations is hidden in the correlation structure of the data and not simply in the variation of the individual factors.

This was followed in 2005 by Richard Dawkins writing in The Ancestors Tale that However small the racial partition of the total variation may be, if such racial characteristics, as there are, highly correlate with other racial characteristics, they are by definition informative, and therefore of taxonomic significance. And, thus, any vitality remaining in Lewontins 1972 paper was dissipated.

Then, in 2004, the highly regarded scientific journal, Nature Genetics, devoted an entire special edition (Genetics for the Human Race) to the question of whether human races exist, and the journal found that they did. Next, in a March, 2005 op-ed in The New York Times A Family Tree in Every Gene, Armand Marie Leroi asserted that the consensus regarding social constructs was unraveling and that the new genetic data show that races exist. (Note: Lerois book Mutants: On Human Variety and the Human Body, isby farthe very best book that I have read regarding the role of genes in human development. It is readable, short and persuasive.) One of the 2004 papers that appeared in the Nature Genetics special edition was by Lynn B. Jorde and Stephen P. Wooding entitled Genetic Variation, Classification and Race.' It found that Genetic variation is geographically structured, as expected from the partial isolation of human populations during much of their history. Because traditional concepts of race are in turn correlated with geography, it is inaccurate to state that race is biologically meaningless.

As quoted in Philosophy of Race Versus Population Genetics Round, this and countless other scientific findings led the President of the American Sociologicalin his 2005 presidential addressto call upon members to, Prepare to defend against the genomic data juggernaut heading their way down the pike.

The scientific evidence supporting nature over nurture continued to roll in. For example, in a 2007 article by Tarmo Strenze entitled Intelligence and Socioeconomic Success: A Meta-Analytic Review of Longitudinal Research, it was found that, The relationship between intelligence and socioeconomic success has been the source of numerous controversies. These results demonstrate that intelligence is a powerful predictor of success This sent the progressive lefts claim that economic success is due to privilege down in flames. Even African-American academics joined the fray. In the Winter 2008/2009 edition of The Journal of Blacks in Higher Education, the article Why Family Income Differences Dont Explain the Racial Gap in SAT Scores appeared, and it reported that, For Black and White students from families with incomes of more than $200,000 in 2008, there still remains a huge 149-point gap in SAT scores. Even more startling is the fact that in 2008 Black students from families with incomes of more than $200,000 scored LOWER (emphasis in the original) on the SAT test than did students from White families with incomes between $20,000 and $40,000.

In the interim, neuroscientists had joined the debate. Using functional MRI (fMRI), they were confirming what the geneticists had been discovering. In 2010, Ian J. Deary, Lars Penke, and Wendy Johnson published a paper entitled The Neuroscience of Human Intelligence Differences in the journal Nature Reviews: Neuroscience. They found that, Neuroscience is contributing to the understanding of the biological bases of human intelligence differences [] Quantitative genetic studies have established that there are additive genetic contributions to different aspects of cognitive abilityespecially general intelligenceand how they change through the lifespan. They continued, The brains of some people are more efficient than those of others. The biological foundations of these differences are of great interest to basic and applied neuroscience. There are already some well-replicated general findings. Thus, the differential neuroscience of human intelligence, therefore, has a strong mandate and a firm foundation from which to proceed. Later the authors added, The first adequately powered genome-wide studies of intelligence are in progress.

In 2014, a study by Mark Horowitz entitled Whither the Blank Slate? A Report on the Reception of Evolutionary Biological Ideas Among Sociological Theorists was published in the journal Sociological Spectrum. His paper caused quite a storm in the community of social scientists. Horowitz found that, Sociology is a house divided. Just over half of the (sociological) theorists in our sample deny the role of natural selection in shaping a range of human tendencies. Many more are unwilling to acknowledge the plausibility of evolutionary argument applied to sex differences. (Does this not sound at least a little bit like the beliefs held by Evangelical Christians who also deny evolution?) Progressive social scientists lashed out at this study, but both Jonathan Haidt and Steven Pinker rushed to Horowitzs defense. As Jonathan Haidt wrote in his article Political Diversity Will Improve Social Psychological Studies:

When facts conflict withsacred values, almost everyone finds a way to stick with their values and reject the evidence. On the Left, including the academic Left, the most sacred issues involve race and gender. So thats where you find most direct and I would say flagrant denial of evidence. I think the results of this study do clearly show that political concerns influence the willingness of sociologists to consider a major class of causal factors in human behavior.

To this point, Steven Pinker, in an op-ed in The Washington Post entitled Liberals Deny Science, Too, added that Im not surprised by the findings of this study. Sociology itself is a divided discipline, with radically diverging views on the role of science in general and of course evolution and genetics in particular. Nor am I surprised that gender is the bloodiest shirt. Together with race, gender has always been the biggest impetus for believing in the blank slate, and since the Larry Summers affair almost a decade ago, that has only intensified.

Another uproar came in 2014 with the publication of Nicholas Wades bookTroublesome Inheritances: Genes, Race, and Human History, which asserted that, race has a biological basis, one that is found in the subtle quality of allele frequency. This claim is far more likely than the alternative, that evolution has played no role whatever in shaping present-day societies. (Note: Wade clearly pointed out in the preface of his book that the first half was factual, and the second half was speculation. However, this did not stop 139 geneticists from signing a letter to the editor in The New York Times insisting that the latter portion of Wades book had not yet been demonstrated conclusively.)

A year later, science took a sharp turn away from nurture and toward an almost totally deterministic impact of genes. In an article entitled Meta-analysis of the heritability of human traits based on fifty years of twin studies, J.C. Polderman examined all of the twin studies from 1958 through 2012 (numbering 2,748 separate research projects that looked at 14,558,903 twin pairs, as well as 17,804 human traits). Poldermans meta-analysis was published in the journal Nature Genetics. These scientific researchers found that the observed pattern of twin correlations is consistent with a simple and parsimonious underlying model of the absence of environmental effects shared by twin pairs and the presence of genetic effects that are entirely due to additive genetic variation.

Richard Haier, former editor-in-chief of the scientific journal Intelligence, published a book entitled The Neuroscience of Intelligence in 2017, which found that researchers using functional MRI (fMRI) have concluded that:

Everyone has a notion about defining intelligence and an opinion about how differences among individuals may contribute to academic success and life achievement. Conflicting and controversial ideas are common about how intelligence develops. You may be surprised to learn that the scientific findings about these topics are more definite than you think. The weight intelligence from neuroscience research is rapidly correcting outdated and erroneous beliefs.

He continued, if you already believe that intelligence is due mostly to the environment, new neuroscience facts might be difficult to accept. Denial is a common response when new information conflicts with your prior beliefs. The older you are, the more impervious your beliefs may be. Santiago Casal, the father of neuroscience, once wrote: Nothing inspires more reverence and awe in me than the old man who knows how to change his mind.'

In 2018, Harvard geneticist David Reich published the book Who We Are and How We Got Here, bringing with it the following thoughts: Reich allows readers to discover how the human genome provides not only all the information a human embryo needs to develop but also the hidden story of our species. Reich delves into how the genetic revolution is transforming our understanding of modern humans and how DNA studies reveal deep inequalities among different populations, between the sexes, and among individuals. Even more compelling was the op-ed How Genetics is Changing Our Understanding of Race that Reich wrote for The New York Times in March of 2018. According to Reich, it was found that with Groundbreaking advances in DNA sequencing [we now know that] differences in genetic ancestry that happens to correlate to many of todays racial constructs are real. Later, Reich followed by writing, I have deep sympathy for the concern that genetic discoveries could be misused to justify racism. But as a geneticist, I also know that it is simply no longer possible to ignore average genetic differences among races.' He concluded: I am worried that well-meaning people who deny the possibility of substantial biological differences among human populations (races) are digging themselves into an indefensible position, one that will not survive the onslaught of science.

In 2018, a group of sociologists decided to confront head-on this question, and they published the book Reconsidering Race: Social Science Perspectives on Racial Categories in the Age of Genomics. The forward to this tome was penned by Henry Louis Gates, Jr., and it offered:

For decades most [social science] scholars and even the general publicat least in the United Statesgenerally accepted the story that races are socially constructed [but] after the initial completion of the genome [project] around the year 2000, some in the scientific community began unearthing vestiges of debates and questions around the science-race linkage. Even prominent scientific journals such as Science and Nature published articles that seemed to reassert the existence of categories that match the traditional understanding of racial groups. These developments have forced social scientists to reconsider race: To ask whether there is any credence to the natural science arguments that there might be a biological and genomic foundation to racial categories.

On January 28, 2020, Charles Murrays latest effort Human Diversity: The Biology of Gender, Race, and Class hit bookstore shelves, and another blow was struck against the soft sciences orthodoxy of social construction. According to Murray, All people are equal [but] all groups of people are not the same. Murray also writes:

advances in genetics and neuroscience are overthrowing an intellectual orthodoxy that has ruled the social sciences for decades. The core of the orthodoxy consists of three dogmas: gender is a social construct; race is a social construct and class is a function of privilege. The problem is that all three dogmas are half-truths. They have stifled progress in understanding the rich texture that biology adds to our understanding of the social, political, and economic worlds we live inWhy the resistance? Because social scientists have been in the grip of an orthodoxy (gender, race & class) that is sacred stiff of biologyThe core doctrine of the (gender, race & class) orthodoxy in the social sciences is a particular understanding of human equality.

It is not, for Murray, equality in the sense of Americas traditional idealall are equal in the eyes of God, have inherent dignity, and should be treated equally under the lawbut equality in the sense of sameness. in a properly run society, people of all human groupings will have similar life outcomes. (Emphasis in the original) Individuals might have differences in abilities but groups do not have inborn differences in the distribution of abilities. Inside the cranium, all groups are the same.

I firmly believe that all of the aforementioned scientific evidence, findings, and data lead to the conclusion that many members of the progressive left are failing to accept the clear cut truth on a number of issues, thereby doing precisely what they accuse their conservative counterparts of.

Climate Change

But what about climate change? I now turn to that topic, and readers will quickly see why I saved global warming until the end. First, here is an overview of the alleged scientific consensus regarding Anthropogenic Global Warming (AGW). Three surveys of climatologists have determined that 97% of these scientists believe in AGW. This finding has been repeatedly reported in the media. However, what many media outlets never mention is that a nationwide poll taken of meteorologists in 2016 found that Nearly half of weathercasters (46%) are convinced that the climate change over the past 50 years has been primarily or entirely due to human activity, and nearly one quarter (22%) think it is more or less equally caused by human activity and natural events. About one quarter (24%) think the change has been primarily or entirely due to natural events. But 46% is nowhere near 97%. And, far too frequently, media outlets fail to tell the complete story of scientific findings on climate change. As such, I have included below a non-exhaustive list of findings from climate science that might appear very surprising to those who have exclusively followed certain popular treatments of the issue.

Scafetta et al (2017) concluded that The severe discrepancy between observations and modeled predictions found during the 1922-1941 and 2000-2016 periods further confirms, according to the criteria proposed by the AGW theory advocates themselves, that the current climate models have significantly exaggerated the anthropogenic greenhouse warming effect. According to AGW theory advocates own criteria, a divergence between observations and climate models occurring at a bi-decadal scale would provide strong convincing evidence that the global climate models used to support the AGW theory are severely flawed. Thus the models are not able to reproduce the natural variability observed in the climate system and should not be trusted for future planning.

Cerrone & Fusco (2018) the results herein indicate that a progressive cooling has affected the year-to-year climate of the sub-Antarctic since the 1990s.

Kim et al (2018) the Yellow and East China Seas are widely believed to have experienced robust, basin-scale warming over the last few decades. However, this warming reached a peak in the late 1990s, followed by a significant cooling trend.

Morner (2018) The concept of an anthropogenic global warming (AGW) driven by the increase in atmospheric CO2 is compared to the concept of a natural global warming (NGW) driven by solar variability. The application of the AGW concept only rests on models, whilst the NGW concept rests on multiple observational and evidence-based facts. Even more so, the long-term solar variability predicts a new Grand Solar Minimum with severe climatic conditions (type Little Ice Age) to occur in 2030-2050. This violates all talk about an increasing, even accelerating, global warming. Similarly, there is no true treat of a future sea level rise flooding lowlands and islands.

Shen et al (2018) The results showed both future climate change (precipitation and temperature) and hydrologic response predicted by 20 global climate models were highly uncertain, and the uncertainty increased significantly over time.

Abbott & Marohasy (2018) While general circulation models are used by meteorological agencies around the world for rainfall forecasting, they do not generally perform well at forecasting medium-term rainfall, despite substantial efforts to enhance performance over many years. These are the same models used by the IPCC to forecast climate change over decades.

Scafetta et al (2018) Herein, the authors show that such a temperature peak is unrelated to anthropogenic forcing: it simply emerged from the natural fast fluctuations of the climate associated to the El Nio-Southern Oscillation (ENSO) phenomenon. By removing the ENSO signature, the authors show that the temperature trend from 2000 to 2016 clearly diverges from the general circulation model (GCM) simulations. Thus, the GCMs models used to support the AGWT are very likely flawed.

Lean (2018) Climate change detection and attribution have proven unexpectedly challenging during the 21st century. Earths global surface temperature rose less rapidly from 2000 to 2015 than during the last half of the 20th century, even though greenhouse gas concentrations continued to increase.

Scafetta & Wilson (2019) The climate warming hiatus observed since 2000 is inconsistent with CO2 AGW climate models [citations omitted].CO2 anthropogenic global warming (CAGW) climate models [citations omitted]. This points to a significant percentage of the observed 19802000 warming being driven by TSI variation [citations omitted]. A number of other studies have pointed out that climate change and TSI variability are strongly correlated throughout the Holocene including the recent decades [citations omitted].

Pei et al (2019) During the period of 0-10,000 years before present, Chinas temperature has closely followed the solar forcing. The correlation is as high as 0.800 (p less than 0.01) for Empirical Orthogonal Function-based reconstruction.

Paudel et al (2019) On a global scale changes in cloud cover were found to be significantly related to changes in solar activity through its effect on the flux of cosmic rays reaching the lower atmosphere [citations omitted] suggesting changes in solar emissions could be related to those in cloud cover and global radiation at the Earths surfaceAnalysis by stepwise regression indicated that since 1970 changes in cloud cover accounted for 61% of the changes in Egwhile the major increase in local fossil fuel consumption, serving as a proxy for anthropogenic aerosol emissions, only accounted for an additional 2% of the changes.

Varotsos & Efstathiou (2019) Based on these results and bearing in mind that climate systems are complicated and complex with existing uncertainties in the climate predictions, it is not possible to reliably support the view of the presence of global warming in the sense of an enhanced greenhouse effect due to human activities.

Kauppinen & Malmi (2019) The IPCC climate sensitivity is about one order of magnitude too high because the strong negative feedback of clouds is missing in climate models. If we pay attention to the fact that only a small part of the increased CO2 concentration is anthropogenic, we have to recognize that anthropogenic climate change does not exist in practice. The major part of the extra CO2 is emitted from oceans (cite omitted), according to Henrys Law. The low clouds practically control the global average temperature. The last 100 years the temperature was increased by about 0.1 degrees C because of CO2. The human contribution was about 0.01 degrees C.

Mao et al (2019) In science, when there are two or more ideas to be employed to explain the recent global warming, we always trust which can fit perfectly all the observed monthly anomaly of GLST from 1880 to now. Until now, no one claims that he can fit perfectly the observed monthly anomaly of GLST from 1880 to now as we do The function with best verification result has also been employed to predict the future behavior of the monthly anomaly of GLST; we can see that the downward trend for the monthly anomaly of GLST had already begun; it will reach the lowest point at 0.6051C in 2111.

Conclusion

Given all of this, it appears that both progressives and conservatives ignore or reject the facts and the science when it suits their ideological need to do so. That said, as I have argued, it appears that the Left is actually more guilty of these transgressions against the truth than the Right. Given this reality, perhaps certain Democratic politicians and media outlets should cease and desist slandering their political adversaries with the mostly false allegation that conservatives regularly reject or at least ignore the facts and the science. Regardless of what the Left decides on that matter, one should always remember what Neil DeGrasse Tyson said on Real Time with Bill Maher in April of 2011: The good thing about science is that it is the truth whether or not you believe it..

Richard W. Burcik is a retired economist and attorney.

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Conservatives Are Not the Only Ones Who Ignore Facts and the Science - Merion West

CAMPAIGNERS have called on NHS Scotland to ban an exercise treatment which encourages patients with chronic fatigue to "push through" their symptoms, saying it has left some in a wheelchair.

Charity, ME Action Scotland, is pushing for the change ahead of what it fears will be a surge in cases of post-viral illness in the wake of the coronavirus pandemic.

More than 21,000 Scots already suffer from Myalgic Encephalomyelitis (ME), also known a chronic fatigue syndrome.

Onset typically follows a bout of viral or bacterial infections such as glandular fever or pneumonia, with evidence also suggesting that ME is more likely to arise if the patient felt fearful or anxious during their illness - something which is more likely in a pandemic scenario.

READ MORE: Belle & Sebastian frontman says more must be done for 'urban leper' ME patients

Symptoms include debilitating muscle and joint pain, extreme exhaustion, nausea, dizziness and insomnia.

Most patients will have periods where their condition improves but then relapses, sometimes leaving them bedridden.

Professor Chris Ponting, chair of medical bioinformatics at Edinburgh University and group leader in the MRC Human Genetics Unit, said: "Unfortunately, it is possible that Covid-19 will lead to an increase in the number of people with ME.

"Of those people who have Covid-19 symptoms quite severely, I would expect about 10 per cent to have fatigue-like syndromes after six months.

Currently, many patients with ME in Scotland are prescribed a treatment called Graded Exercise Therapy (GET) which asks patients to continually increase their levels of activity and push through symptoms.

A survey of 2,274 ME patients carried out by research Oxford Brookes University found that 67 per cent of those who underwent GET experienced a deterioration in their physical health.

ME Action Scotland said it has heard from patients who are now housebound or confined to a wheelchair having previously been mobile and able to work.

In 2017, the American Centres for Disease Control removed GET from its recommended therapies for ME following an outcry over a controversial clinical trial.

ME Action Scotland has written to Scotland's Chief Medical Officer and Health Secretary Jeane Freeman asking them to do the same.

READ MORE: ME battle of Scottish rocker - 'I just disappeared'

The PACE study, a randomised control trial with 641 participants from Scotland and England, concluded in 2011 that psychotherapy and exercise could significantly improve and sometimes cure ME.

Patients who claimed GET was actually making them worse were dismissed and accused of hijacking the debate with a "very damaging" agenda.

Unpublished data from the trial was eventually released in 2018 following a lengthy legal battle brought by an Australian patient, resulting in other scientists criticising PACE as fundamentally flawed with "grossly inflated" recovery rates.

A 2019 review of the PACE trial by the UK's Health Research Authority did not find fault with the investigators, however.

Janet Sylvester, of ME Action Scotland, said: We have been campaigning to have GET removed as treatment in Scotland since 2017.

"We are urgently renewing our appeal to have GET removed as treatment in Scotland in the light of the evidence that this harmful treatment not only continues to harm ME patients, but is likely to be recommended to post Covid-19 patients suffering from fatigue related illnesses.

Louise McAllan, from Stirling, was prescribed GET after an acute onset of ME aged 30.

She said: "It would be a six month wait for treatment and during this time I began to recover, but once the treatment began however, I rapidly declined. As my body failed I was told to keep pushing through, that it was just a mindset and that exercising would make me better.

"I trusted them and desperately wanted to be better, so I did what they said and tried to ignore the pain. After treatment I couldnt even lift a fork to my mouth to eat and I remained house bound and unable to walk for many years. I had to give up my job as a teacher and struggled to see friends or do any activity at all.

"Despite how unwell it had made me, I was offered GET several times more by different GPs, who didnt believe that it had made me worse. GET should not be offered to anyone else, it needs to stop immediately."

A spokeswoman for the Scottish Government said it is working with Action for ME to fund research into the biomedical understanding of the illness.

She said: Graded Exercise Therapy (GET) will not be suitable for everyone with ME/Chronic Fatigue Syndrome (CFS). While some studies report people feel worse after GET, these studies also reflect some people with moderate to mild symptoms of ME/CFS have found GET to be beneficial in treating their condition.

"The risks of treatment must always be explained and discussed before individuals decide to proceed with treatment delivered by a suitably trained GET therapist with experience in ME-CFS.

The findings from two projects we are currently undertaking, to understand the needs of people living with ME/CFS and what practices and provision are available, coupled with the forthcoming update of the National Institute for Health and Care Excellences guideline on ME/CFS that will take account of latest evidence, including patients experiences about GET, will inform developments in care and support for ME/CFS in Scotland.

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Coronavirus in Scotland: Charity warns Covid will cause a spike in ME cases - as it calls for 'harmful' exercise treatment to be banned -...

Wayengera is behind the country's effort to manufacture test kits. Courtesy photo

Testing is key for diagnosing and tracking the magnitude of the disease to know how many people have been infected or could infect others.

While people in Uganda have been asked to stay at home to contain the spread of the new coronavirus disease (COVID-19), a few others must continue working to find answers to the pandemic.

COVID-19 is wreaking havoc across the world. Uganda, just like most countries globally, is relying on aggressive screening and testing as the best approach to determine whether the virus is present in communities, and how far it has spread.

Testing is key for diagnosing and tracking the magnitude of the disease to know how many people have been infected or could infect others.

But, the high global demand for testing kits has strained supply.

Production and delivery of testing kits to meet demand is short. In turn, it has led to a rise in fake kits and a race to develop standardized, rapid, and accurate diagnostic tests.

Currently, Uganda is able to conduct over 2000 tests daily, and over 40, 000 tests have been carried out in total, which is much higher than tests conducted by any other East African country. But in South Korea alone, nearly 20,000 people are tested daily.

But not to worry, the number of tests could soon go much higher as Dr. Misaki Wayengera a Clinical Geneticist, Immunologist, and Virologist along with a team of other Ugandan scientists, are developing a cheaper COVID-19 testing kit that could deliver results in a minute or two. For him, it is about offering a homegrown solution to the testing gap.

Love For Science and Country

The innovation is not the first for Wayengera, he also developed the pan-filovirus rapid diagnostic test, a paper-strip test that can detect the Ebola and Marburg viruses in five minutes.

Wayengera is a towering and vibrant figure among his peers. He does not hesitate to share knowledge when he gives his time and is always happy to talk about science.

When I joined medical school, my friends were reading books to pass, I wanted to bring about change, he told a Ugandan television in an interview.

He is patriotic, and always talks about how his works should benefit the country, and develop Africa for Africans. His patriotism is rare to find among professionals, says Ian Peter Busuulwa a digital communications officer with Science Stories Africa and a biotechnologist who engages in agricultural research and science.

He is also passionate about sharing knowledge. He could be in some leading global pharmaceutical company earning lots of money, but Wanyengera finds it necessary to stay in Uganda, working with Makerere University to pass on knowledge to young scientists, he adds.

Who is Dr. Wanyengera

Wayengera is a medical doctor with graduate training, Masters of Science (MSc), Fellowship, and Doctorate of Philosophy (Ph.D.) in a diverse array of scientific fields including Immunology, Vaccinology, Clinical Microbiology, Genetics, and Filovirology.

It was in 2000 while a medical student, that he picked interest in studying filoviruses that can cause severe hemorrhagic fever in humans and non-human primates.

In 2007 while studying genomes of filoviruses, Wayengera focused his energy on the understanding of Ebola and Marburg viruses with targets for both vaccine and diagnostic development. He successfully developed a rapid testing kit for both viruses.

Wayengera also holds expert skills-training in Bioentrepeneurship and Research and Development.

Serving, Breaking Boundaries

Over the past 10 years, he has served as In-Charge of the Unit of Genetics and Genomics (a super-specialized referral centre for children and adults born with rare, Mendelian disease at the Mulago National Reference and Teaching Hospital Complex, Kampala, Uganda.

He is also In-Charge of the Unit of Genetic and Genomics, Department of Immunology and Molecular Biology at School of Biomedical Sciences, College of Health Sciences at Makerere University.

Wayengera is also a member of the African Society for Human Genetics (AfSHG) and Ex-Chair of the Education and Coordinated Working Group (ECTWG) of the H3Africa Consortium that empowers African Researchers to be competitive in genomic sciences and nurtures effective collaboration.

My research interests center on pathogens (virus, bacterium and other microorganisms that can cause disease) with a focus on identifying new its molecular targets (minute particles) for research and development of diagnostics, therapeutics, and vaccines, he says.

Together with his team, Wayengera has not only built the necessary expertise and experience but also established a network of partners from across the academia, industry, and public-private partnerships.

For this work and its impact on the 2013 to 2016 Ebola outbreak in West Africa, Wayengera was listed as the 57th of the 100 most influential Africans of 2015.

Last year (2019), his team won the 1st Prize for the World Health Organisation (WHO) innovation Challenge (Product Development), and he was nominated as REACH Award Finalist - Reaching the Last Mile (REACH/RLM).

Wayengera is currently (2019-2020) The World Academy of Sciences Sub Saharan Africa Regional Partner (TWAS-SAREP) Young Scientist award winner (Infectious Diseases).

He is also the Chair of the COVID-19 scientific committee in Uganda leading the response to the coronavirus.

Providing Solutions

I am excited Dr. Wayengera and his team are in the process of developing a testing kit for COVID-19. There is a huge challenge globally for testing kits. We look forward to this innovation closing this gap. He did the same for Ebola, says Professor Rhoda Wanyenze a Physician, Public Health Consultant, and Dean Makerere University School of Public Health.

It is always good to see scientists use their knowledge to develop innovations that address the critical aspects of health for our society. We keep getting epidemics. Right now besides COVID-19, neighbours DR Congo also have Ebola in the town of Beni, she says.

Professor Wanyenze says Wayengera is working on critical matters developing diagnostics. The STDS-Agx (swab tube dipstick agglutination) COVID-19 test kit developed by Wayengeras team can produce results in a minute or two, compared to the four-to-six hours it takes to get results from the WHO accredited Reverse transcription-polymerase Chain Reaction (RT-PCR) based tests that quantitate changes in gene expression, now in use.

Each kit will cost an estimated US$1.07 (about sh4,000), making testing affordable. It is intended for use in rural settings, which often lack laboratory capacity or expertise, says Wayengera.

It is a home-based solution to the evident scarcity of resources for the management of this pandemic globally. Everyone is running to the market and the difference in economic prowess means poor countries such as those in sub-Saharan Africa are left with nothing. We must innovate around these shortages to fight the pandemic, he says.

The Makerere University research team expects to have a prototype ready to be put into use next month, pending expert validations.

Three versions of the test kit are being developed. The tests will work by generating solid particles from the reaction of the virus with antibodies or vice versa.

The work has been seed funded by about US$22,000 from the Makerere University Research and Innovation Fund.

Wayengera says an estimated $272,000 will be required to develop a prototype and over $ 0.5million will be needed to mass-produce the kits.

Additional costs will also be incurred for regulatory approval, intellectual property protection, and commercialisation.

Read this article:

Dr. Misaki Wayengera: The Man Behind Uganda's Covid 19 Test Kits - New Vision

KEY POINTS

Health experts have been baffled as to why there are people infected with COVID-19 and yet barely feel the infection while others suffer life-threatening symptoms even if healthy and young. Scientists are looking for answers in the genes of patients, trying to discover mutations that affect the immune response, hoping that it could help in coming up with new treatments.

Profile Of A Severe Case

During the early days of the pandemic, a general profile of a severe case of coronavirus infection started to emerge. They are older adults with pre-existing medical conditions and are likely to be male. As the virus continued to infect more people, a small fraction started to deviate from the general profile.

Health experts are starting to see around 5% of those infected are under the age of 50 and do not have any underlying health conditions. These are the group of patients that interest Dr. Jean-Laurent Casanova, a geneticist and head of the St. Giles Laboratory of Human Genetics of Infectious Diseases.

Dr. Casanova told the AFP it is possible for someone who joined a marathon in October 2019 to find himself in intensive care, ventilated and intubated in April 2020. He revealed his desire to know if these types of patients have rare genetic mutations that have been triggered by the coronavirus infection. The assumption is that these patients have genetic variations that are silent until the virus is encountered, the doctor said. coronavirus silent mutation in human body may be the one exploited by the virus Photo: TPHeinz - Pixabay

A Huge Global Effort

The geneticist co-founded the COVID Human Genetics Effort, a collaborative work that seeks to know more about the genome of severely-ill young patients in several countries worldwide. These include patients in Europe, Japan, Iran, China, and the United States.

Dr. Casanovas group is also studying those who did not get infected despite being exposed many times. He said their main goal is to know why some are sicker than others, a knowledge that the geneticist said might help them in their quest to develop anti-viral therapies.

Gene Mutations Have A Long History

Scientists have long known that gene mutations can make people more susceptible to an array of infectious diseases, ranging from influenza to viral encephalitis. These gene mutations can also offer protection sometimes.

In the 1990s, a group of researchers found out that some rare mutations of a single gene successfully protected people against HIV infection. This discovery led to a betterunderstanding of how the virus worked and eventually paved the way for scientists to develop new treatments.

View post:

Its In The Genes? Scientists Think Coronavirus Exploits Silent Hidden Mutations In The Body - International Business Times

MET 2020 Slot Booking: The Manipal Academy of Higher Education will be conducting the Manipal Entrance Test 2020 from July 24 to 27 and August 4 to 7, 2020. According to a recent announcement made, the Manipal Entrance Test 2020 will be conducted in the online mode. The slot bookings for the entrance tests will be open from July 15, 2020, onwards. Candidates who have applied for the entrance test can visit the official website for more details related to the entrance test.

The instructions to be followed by candidates during the slot booking process is available on the official website. Candidates are advised to read through the instructions provided carefully in order to complete the slot booking procedure without any mistakes.

MET 2020 Slot booking Guidelines

Candidates are advised to visit the official website - manipal.edu. To check the demo of the slot booking process for the Manipal Entrance Test 2020 candidates is advised to click on the link provided below.

MET Slot Booking Demo Direct Link

According to the notification available on the official website the MET 2020 examination is scheduled to be conducted in the decided number of cities and all the applications will be able to book their entrance test slots via the Online Test Booking System (OTBS) based on the availability of the seats. It must also be noted that in case a low number of applicants are seen in a particular city, the test centre will be shifted to the nearest city which is available on the OTBS.

The list of cities in each state where the Manipal Entrance Test 2020 will be conducted is available on the official website of MET. Candidates can also check the list of cities through the direct link provided below.

MET 2020 List of cities Direct Link

Manipal Academy of Higher Education conducts the Manipal Entrance Test 2020 for the admissions to the BTech, BTech (Lateral Entry Admissions), BPharm / PharmD, MTech, ME, MPharm / PharmD Post Baccalaureate, MSc Medical Biotechnology, MSc Molecular Biology & Human Genetics, MSc Systems Biology, MSc Genome Engineering, MSc by Research in Life Sciences programmes offered by the university.

Also Read: APSCHE to begin online GATE 2020 sessions for students during COVID-19 lockdown from today onwards

See the original post here:

MET 2020 Slot booking to commence on July 15, Examination dates available at manipal.edu - Jagran Josh

LONDON When the first cases of a new coronavirus started to appear in China last December, the disease seemed to be a particularly aggressive respiratory infection. An "urgent notice" that month from the Wuhan health commission warned of "successive cases of unknown pneumonia".

Respiratory symptoms are still the first signs that doctors look for in suspected Covid-19 cases: cough, shortness of breath and fever.

But, less than five months after it was first identified, this new coronavirus is managing to throw up a series of medical mysteries - from blood clots and strokes to digestive problems - that are confounding the scientific community.

From head to foot, Covid-19 causes a fiendish variety of symptoms. Some are relatively mild, such as loss of smell and taste or chilblain-like sores on toes. But others may be fatal, such as when what doctors call an immune storm destroys vital organs. The more this virus is studied, the more complex it appears to be. "Every day we're learning of new tricks that the virus plays," Imperial College London's professor of experimental medicine Peter Openshaw says. "It is remarkable to see a disease unfolding in front of our eyes with so many twists and turns."

The proliferation of complex symptoms is not just a challenge for doctors treating the disease, but also for health systems trying to adapt to the pandemic. In the early months, the focus was on getting hold of ventilators that could help patients with severe respiratory problems. But now hospitals are also scrambling for more kidney dialysis machines and anticoagulant drugs.

A single individual can suffer the disease in more than one form, Prof Openshaw adds. "There are accounts of people experiencing one symptom, for example coughing, appearing to recover or go into remission and then returning with a more serious systemic disease."

With the worldwide death toll from Covid-19 already nearing 260,000 and confirmed cases close to exceeding 3.7 million, according to Johns Hopkins University, scientists have mobilised at a speed and on a scale unprecedented in the history of medicine, in an effort to understand the myriad ways in which the virus affects the human body. They hope that their research will not only improve clinical care of patients but also help the development of drugs and vaccines.

The initial diagnosis was that it was a respiratory infection, like its sister diseases Sars and Mers which are also caused by coronaviruses.

Respiratory symptoms remain the most common manifestations of Covid-19 in patients who go to hospital, according to a study of almost 17,000 people admitted to 166 UK hospitals carried out by a research consortium from Imperial College and Liverpool and Edinburgh universities. About two-thirds of patients in the study - the largest of Covid-19 hospital patients outside China - were admitted suffering from respiratory symptoms, says Dr Annemarie Docherty of Edinburgh, the lead author of the paper. But that proportion may have been raised by the fact that they reflect the official case definition of Covid-19.

But two other clusters of symptoms also dominate hospital admissions: systemic musculoskeletal symptoms (muscle and joint pain and fatigue) and enteric symptoms (abdominal pain, vomiting and diarrhoea). Many patients suffer from several symptoms simultaneously.

How the immune system reacts to Covid-19 is key to the course of the disease in adults. People who have been suffering with mild to moderate symptoms for a week or so often seem to hit a critical point: usually their immune system gets the virus under full control and sets them on a path to full recovery - but sometimes it goes into overdrive, triggering systemic inflammation and in severe cases a "cytokine storm" that destroys tissues and whole organs.

Inflammation also helps to explain why obesity makes people more susceptible to severe Covid-19. Seventy-three per cent of coronavirus patients in UK intensive care units are overweight or obese, with a body mass index above 25. "Fat cells secrete chemicals that increase the body's inflammatory response," says Liverpool University's professor of child health Calum Semple.

Kidney damage has emerged as another of the most frequent serious consequences of Covid-19, with 23 per cent of patients in intensive care requiring renal support. As with other organs, it is uncertain to what extent the virus is directly attacking the kidneys or whether the harm results more from generalised overactivity of the immune system and consequent changes in the patient's blood circulation.

Cardiovascular disease is the most common pre-existing health condition in people who die of Covid-19, ahead of lung and respiratory disorders such as asthma and chronic obstructive pulmonary disease. And many patients without a previous history of heart trouble develop severe cardiac symptoms while they are in hospital.

"When we first heard about the coronavirus we expected people with lung and breathing problems to be most at risk but that has not been the case," says the British Heart Foundation's medical director Nilesh Samani. "We need to understand why the virus is causing so many problems outside the lungs - and cardiovascular complications in particular."

The exaggerated immune response to the virus sometimes causes abnormal blood clotting. If this thrombosis happens in the brain, it may trigger a stroke. Neurologists at University College London (UCL) studied six Covid-19 patients who suffered acute stroke as a result of a large arterial blockage - in five of the cases more than a week after suffering headache, cough and fever and in one patient before other symptoms appeared.

The UCL researchers found all six patients had markedly raised blood levels of a protein fragment called D-dimer associated with abnormal clotting. The findings suggest that early testing for D-dimer could enable doctors to prescribe blood-thinning drugs to people at risk, reducing the chance of stroke or harmful clotting elsewhere in the body. "Early use of anticoagulant drugs might be helpful but this needs to be balanced against their brain bleeding risk," says study leader David Werring.

STRAITS TIMES GRAPHICS

"This study is consistent with the growing evidence that people hospitalised with Covid-19 are at risk from blood clots in multiple locations: the lungs (causing pulmonary embolus), the brain (causing stroke) and the veins (causing DVT)," says professor of cardiovascular medicine Tim Chico at Sheffield University. "The risk of blood clots with Covid-19 appears to be even greater than the increased risk of blood clots seen in other severe illnesses."

The coronavirus also seems capable of attacking the brain and nervous system directly, as well as indirectly through abnormal blood clotting, though the evidence for acute symptoms of neural infection is limited. The effects may show up in the longer term as post-viral fatigue.

Neurons in the olfactory bulb, which transmits information from the nose to the brain, are apparently infected by the virus. Indeed, anosmia - loss of the sense of smell - is one of the most frequently reported symptoms of mild infection, affecting about half of patients and lasting for several weeks in some cases.

The good news for those who develop anosmia is that they are much less likely to become seriously ill with Covid-19. Dr Carol Yan and colleagues at the University of California San Diego (UCSD) reported last week that patients reporting loss of smell were 10 times less likely to be admitted to hospital for Covid-19 than those without loss of smell.

The UCSD researchers suggest that a relatively small dose of virus delivered to the upper airway, where it causes anosmia, may be less likely to overwhelm the host immune response. "This hypothesis is in essence the concept underlying live vaccinations, where low dosage and a distant site of inoculation generates an immune response without provoking a severe infection," they say.

The declining strength of the immune system with age is a partial explanation for the increasing incidence of Covid-19 in older people. PHOTO: AFP

Besides anosmia, the most frequently seen minor symptoms are rashes, pustules and blisters on the skin - including lesions like chilblains that dermatologists are calling "Covid toe".

The results from the study led by Imperial College, Liverpool and Edinburgh universities echo other findings that the disease is much more common in men - who make up 60 per cent of UK Covid-19 hospital admissions - and its severity rises markedly with advancing years (the median age of patients is 72). The strong associations with the male sex and old age are a particular feature of Covid-19 compared with other infectious illnesses.

Data from the UK Intensive Care National Audit & Research Centre shows that men make up 71.5 per cent of patients whose disease becomes severe enough to require intensive care treatment. A comparable control group of patients critically ill with non-Covid viral pneumonia was just 54.3 per cent male.

"The reason behind this difference in Covid risk is unknown," says Dr James Gill, honorary clinical lecturer at Warwick Medical School. "There are several schools of thought on the matter, from the assumption that simply men don't look after their bodies as well, with higher levels of smoking, alcohol use, obesity and other deleterious health behaviours, through to immunological variations in genders. Women may have a more aggressive immune system, meaning a greater resilience to infections."

University of Oxford's professor of immunology Philip Goulder points out that several critical immune genes are located on the X chromosome - of which women have two copies and men one. "The immune response to coronavirus is therefore amplified in females," he says.

The declining strength of the immune system with age is also a partial explanation for the increasing incidence of the disease in older people, though it is not clear why this trend is more pronounced in Covid-19 than in many other viral infections.

Children are remarkably - but not completely - resistant to the disease. Just 3 per cent of UK hospital patients are under 18. Again no one knows quite why. But one answer may lie in the "keyhole" through which coronavirus enters human cells, known as the ACE2 receptor. In children these receptors have not developed to their full adult stage and therefore may not fit the "spike protein" that the virus uses to enter cells.

It is also possible that ACE2 develops more quickly in children's upper airways than their lower respiratory tract, allowing them to become infected - and thus able to transmit Covid-19 - without showing the same progression to severe symptoms.

The National Health System in London and the UK Paediatric Intensive Care Society recently alerted doctors to a rise in the number of children suffering from "a multi-system inflammatory state" similar to toxic shock, which might result from the immune system overreacting to viral infection. Italian and US paediatricians have noticed a similar body-wide inflammatory syndrome in children.

This paediatric condition is rare but researchers are investigating, says Prof Semple. "Some respiratory viruses are associated with a systemic inflammatory response, typically two weeks after infection. But this could be a phenomenon of heightened awareness."

Research also shows that children are remarkably - but not completely - resistant to the disease. PHOTO: AFP

For Prof Openshaw, the mysteries of Covid-19 recall the early days of the HIV/Aids outbreak in the 1980s - except that this time, they are unfolding much more quickly. "We need the answers also to appear far faster than they did with HIV," he says.

A global research effort is on to discover human genetic factors that would help to explain why Covid-19 infection varies so much in its symptoms.

Although much of the variation results from environmental and lifestyle factors, scientists are convinced that genetics play a significant role too.

"Experience with other viruses shows that genetics can explain some of the different responses to infection," says Dr Mark Daly, director of the Institute for Molecular Medicine Finland in Helsinki, who is coordinating the global response through the Covid-19 Host Genetics Initiative.

For example, genetic mutations on the CCR5 protein, which HIV uses to enter human cells, make rare individuals resistant to Aids. Researchers may find comparable variations in the human ACE2 protein, entry point of the coronavirus, designated as Sars-Cov-2, that causes Covid-19.

The Covid programme has two overlapping components. One uses human genomes already obtained for other research purposes from volunteers through bodies such as UK Biobank and Genomics England - and looks for differences in DNA between participants who become ill with Covid-19 and those who do not.

The other part obtains the fresh genomes from Covid-19 patients, looking for variations that might explain why some experience only mild symptoms while others become severely ill.

Genomics England, a public body owned by the UK Department of Health and Social Care, is involved in both approaches. Dr Mark Caulfield, its chief scientist, says it is too early to have obtained any results. "But I am confident that reading whole genomes will help to identify variation that affects response to Covid-19 and to discover new therapies."

Prof Daly hopes the initiative will have tens of thousands of human genomes to analyse. "We particularly want to identify a subset of younger individuals with no comorbidities who have a severe response to Sars-Cov-2 infection," he says.

FINANCIAL TIMES

Read more:

From blood clots to 'Covid toe': Experts confounded by series of medical mysteries - The Straits Times

SAN FRANCISCO--(BUSINESS WIRE)--Vitagene, the precision health company, announced the immediate availability of 50,000 FDA authorized Zero Contact at home COVID-19 test kits for use during the current public emergency. Vitagene is using the 1Health.io platform to facilitate compliance with FDA requirements for assessment of symptoms, telehealth and electronic tracking of the test kit.

Simple At-Home Testing: Currently, consumers who are showing symptoms of COVID-19 infection are expected to drive or take mass transit to a clinic or stay for hours in a drive-through testing line. With the Zero Contact COVID-19 test, patients will get a kit at home eliminating the need to drive or be at risk going to a clinical setting.

Our mission as a team is to help our customers improve their health and wellness, said Mehdi Maghsoodnia, CEO at Vitagene. Our customers number one need right now is access to COVID-19 testing. That is why our team, alongside our partners, have been working day and night to bring this test to market with physician approval, telehealth supervision and a clear chain of custody tracking.

Protect Healthcare Providers: The current COVID-19 tests require that the healthcare provider be in the same room as the patient with symptoms, creating risk of infection for the healthcare provider. Once the traditional specimen collection is conducted, the provider then needs to disinfect their garments to minimize the risk of cross contamination. With Zero Contact, both patients and healthcare workers need not be in the same place while the test is being administered.

Saliva vs. Nasal Testing: Saliva test kits are readily available today; in fact, Vitagene is committed to providing 50,000 tests in the first month of service and scaling that number to 300,000 tests per month beginning in middle of May 2020. Additionally, Vitagene has partnered with supply chain manufacturers to provide the kits, which are manufactured in the U.S., supporting our economy and providing local employment.

Our new, efficient, and self-contained saliva collection kits using the EUA approved SDNA-1000 device, makes not only sample collection easy but sample transport as well, said Stephen Fanning. CEO of Spectrum Solutions. The proprietary preservation solution inactivates the virus once a biosample is collected to the point that we are able to suspend and stabilize the viral RNA transcripts for sensitive and specific qPCR testing by the lab. Another incredible benefit of our process is that we can help limit undue exposure making the testing for COVID-19 safer for everyone involved.

Convenient Access to Testing: Today, many communities do not have convenient access to hospitals or other testing facilities. This - combined with limited nasal test availability - has led to only ~1 percent of people being tested in the U.S. to date. In order to decrease and manage the health and economic risks of COVID-19, we need access to widespread testing. Now, anyone who thinks that he or she might have been exposed can go to Vitagene.com and start the process of being tested.

Our saliva-based test kit makes it possible for patients across the United States to have access to testing, not just those located near a hospital, clinic or testing facility. said Andrew Brooks, chief operating officer and director of technology development at the university's RUCDR Infinite Biologics lab. Millions of Americans, who until now might have to travel hours to their nearest testing location, can be sent a test by their doctor or clinic.

For more information or to order a Zero Contact COVID-19 test, please visit http://www.vitagene.com.

###

ABOUT VITAGENE

Headquartered in San Francisco, California, Vitagene Incorporated and its platform division 1health.io are focused on helping consumers improve their health and lifestyle. Vitagene leverages the latest science in machine learning and data analytics, as well as genomics, to provide actionable health plans to consumers. Vitagene keeps all data private and secure and does not share or sell data to third parties. Vitagene has a team of accomplished engineers, scientists and physicians dedicated to improving the health of its customers. To learn more, go to https://vitagene.com/.

ABOUT RUCDR

RUCDR Infinite Biologics, which is part of Rutgers' Human Genetics Institute of New Jersey, is the world's largest university-based cell and DNA repository. Its mission is to understand the genetic causes of common, complex diseases and to discover diagnoses, treatments and cures for them. The organization collaborates with researchers in the public and private sectors throughout the world, providing the highest quality bio-banking services and biomaterials, as well as scientific and technical support. For more information, please visit https://www.rucdr.org/.

ABOUT SPECTRUM SOLUTIONS AND SPECTRUM DNA

Headquartered in Salt Lake City, Utah, Spectrum Solutions and its medical device and services division, Spectrum DNA, focus on innovative, end-to-end product development, manufacturing, and global fulfillment solutions. With concentrated industry expertise, Spectrum DNA specializes in engineering innovative molecular diagnostic solutions that simplify the biosample collection process while offering donors complete physical and digital chain-of-custody. With on-site production facilities, we are a single-source provider of full-service medical device manufacturing, custom and private label packaging, kitting, and direct-to-donor global fulfillment. Our new biosample collection devices, patented technology, and services provide measurable process optimization, unprecedented efficiency, and unmatched global scalability. For more information, please visit https://spectrumsolution.com/.

Original post:

Vitagene Launches The First FDA Authorized Saliva based Zero Contact COVID-19 At Home Test - Business Wire

Amid the steady stream of stories on the lives lost to coronavirus are cases that stand out as remarkable. In the past month, at least two pairs of twins have died in Britain and two pairs of brothers, all within hours or days of each other. But do the deaths point to genetic factors that make some more likely than others to succumb to the disease?

Most scientists believe that genes play a role in how people respond to infections. A persons genetic makeup may influence the receptors that the coronavirus uses to invade human cells. How resilient the person is to the infection, their general health, and how the immune system reacts will also have some genetic component.

A team led by Prof Tim Spector, head of twin research and genetic epidemiology at Kings College London, has reported that Covid-19 symptoms appear to be 50% genetic. But Spector said more work is needed to understand which genes are involved and what difference they make to the course of the disease. We dont know if there are genes linked to the receptors or genes linked to how the infection presents, he said.

Identical twins Katy and Emma Davis, aged 37, died at Southampton general hospital last month. The sisters, who lived together, had underlying health problems and had been ill for some time before they contracted the virus. Another pair of twins, Eleanor Andrews and her sister Eileen, aged 66, died earlier this month. They too lived together and had underlying health conditions.

Two brothers from Newport, Ghulam Abbas, 59, and Raza Abbas, 54, died within hours of each other at Royal Gwent hospital. Another pair of brothers from Luton, Olume Ivowi, 46, and Isi Ivowi, 38, died within days of each other.

These deaths alert people to the fact that this could be genetic, but when people live together they share an environment as well, Spector said. The upshot is that twins who live together are more likely to have similar lifestyles and behaviours, from diet and exercise habits to how quickly they seek medical care. Twins are not generally less healthy than the wider population.

Twin deaths made headlines long before the coronavirus struck. When Julian and Adrian Riester died on the same day in Florida in 2011, a cousin of the twin Franciscan monks said it was confirmation that God favoured them. But Spector sees the hand of cold statistics at work. When you look formally at this, you see that twins rarely die at the same time, he said. There are billions of people on the planet. One in 70 is a twin and one in 200 is an identical twin.

Marcus Munafo, professor of biological psychiatry at Bristol University, said reports of twin deaths must be interpreted with caution. Twin deaths are unusual, which makes them newsworthy, but coverage can distort our perceptions. Salience bias refers to the fact that we tend to focus on information that stands out more, even if its not particularly relevant. So we need to be careful not to read too much into events that might stand out for reasons that are not actually related to the issue were interested in, he said.

When twins or siblings tragically die with Covid-19 that captures our attention, but that doesnt mean theres any particular reason to think twins or siblings are at greater risk.

View original post here:

Genetics in focus after coronavirus deaths of siblings and twins - The Guardian

There is a clinical list of COVID-19 symptoms that includes a dry cough, a fever and shortness of breath. And then there is how the disease actuallyfeels.It is like a lengthy hangover. An anvil on your chest. An alien takeover. It is like being in a fight with Mike Tyson.

More than 1 million people in the United States have become unwilling hosts to the coronavirus. We spoke with some who were sickened by it in many cases severely and have since recovered. In vivid terms, they described what it was like to endure this scary and disorienting illness.

Kinchen, 39, is a hairstylist in film production in Jersey City, New Jersey.

I woke up with a headache that was Top 5 of my life, like someone inside my head was trying to push my eyes out. I got a 100.6-degree fever.

The fever went away, and then I had nausea and a metallic taste in my mouth. I was hungry, and then the taste of food was unappetizing. I put some onions in the Instant Pot to saut. I put my face in the pot, but I couldnt smell the onions. I had the runs that lasted a couple of days.

My partner had a cough and shortness of breath. I would just start sobbing. I was totally freaked out. We got nasal swabs together, and it felt like they took a piece of our brain.

My partner got his results in 10 days. I got mine in 22.

Henry, 43, owns a public relations firm in Lathrup Village, Michigan.

It happened so fast. On Monday, I am in the parking lot of my allergists office with back pain and a cough that I thought was a sinus infection. On Saturday, I am in an ambulance headed to an emergency room.

Three days later, the doctors placed me in a medically induced coma and put me on a ventilator. I was in the hospital for two weeks.

Everything hurt. Nothing in my body felt like it was working. I felt so beat up, like I had been in a boxing ring with Mike Tyson. I had a fever and chills one minute my teeth are chattering and the next minute I am sweating like I am in a sauna.

And the heavy, hoarse cough, my God. The cough rattled through my whole body. You know how a car sounds when the engine is sputtering? That is what it sounded like.

My sister kept telling me to fight. All I could do was pray because my body had gone kaput.

Theres a list of coronavirus symptoms that many can now recite from memory. And then theres how it actually feels when you have it. (Thoka Maer via The New York Times)

Hammer,45, is an investigative reporter in New Orleans.

On Day 10, I woke up at 2:30 a.m. holding a pillow on my chest. I felt like there was an anvil sitting on my chest. Not a pain, not any kind of jabbing just very heavy.

When I told my wife I had this terrible pressure in my chest, she was like, Sit up. She made me some tea, and told me to cough.

Ive never really had a panic attack before, but Id never felt anything like this. I started to feel tingling in my fingers and my extremities, and Im thinking, This is a heart attack.

What I was experiencing was not extreme difficulty breathing it was panic about whether I had extreme difficulty breathing.

The thing that makes this so scary is that it is not linear, and the recovery is not linear.

Backlund, 72, is a retired French teacher in Anacortes, Washington.

Youre just so paranoid because all these weird symptoms come up that you havent read about. There is such a wide range of symptoms that you just keep waiting for the other shoe to fall. Youre always asking yourself, Is this the virus?

One of my friends started getting better and then she ended up dying. Several people started feeling better, and then took a dive. So, youre never really confident. For at least a couple of weeks, youre just not, because it could go awry.

I dont ever want to get this again. Its a pretty awful feeling. Its just so weird the way you swear that its mutating in your body every day, trying something else.

Backlund,73, is a psychiatrist in Anacortes, Washington.

It was just a loss of all energy and drive. There was no horizontal surface in my house that I didnt want to just lay down on all day long.

I didnt want to do anything. And my brain wasnt working very well. I was calling it the corona fog.

The LA Times actually sent a reporter and a photographer to our house and took a photograph of my wife at the piano and me with her singing. And I looked at the picture the next day, and I looked like Skeletor.

I just looked, and I thought, Ive got to start taking this seriously. I had to slap myself in the face and say, Youve got to start eating, and youve got to start drinking.

Miller,27, lives in Brooklyn, New York, and is a general manager at a food delivery platform.

It felt like a very long hangover. Smelling something, getting nauseous. The headache. The overall weakness that your body feels, but more severe.

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It was chills on a level that Ive never experienced. Intense shivering. It was very hard to move. I had really intense body aches. It felt like I was in a UFC match and beaten up.

Doing anything other than laying in bed and sleeping was difficult. You had to be in the right position in order for your chest to not hurt. Or you had to be in a certain position in order to be able to take a full, comfortable breath.

Its like deep inside your chest. You feel it. Something is definitely inside of me, and Im definitely infected with something.

Chow,38, is an assistant professor of human genetics in Salt Lake City.

Walking made me lose my breath. I was just gasping. It felt like drowning.

I was in the ICU for my whole stay five days. The scariest part was being alone. My wife dropped me off at the ER and then was asked to leave. I didnt see her or my kids until I was discharged.

While in the ICU, I spent nights awake thinking about whether I was going to die. The first night they told me that they might have to intubate me, and I spent that whole night wondering whether I would ever see my family again.

The physical pain was mostly taken care of by drugs and oxygen. But the loneliness was real. The staff, too everyone was in PPE, so the interactions were very impersonal. I still dont know what any of the staff look like.

I did have great staff. They are amazing. Just didnt realize that seeing peoples faces was so important to feeling safe.

Taylor,71, is a geriatric social worker in New York.

My chest was tight, I was feverish, my appetite was going away and I had digestive issues. I lost 7 pounds. I called my doctor, and she said I needed to go to a hospital.

They put me in an isolation room, took my vitals, swabs and did a chest X-ray. It came back showing multifocal pneumonia. An ER doc said to me: You can still breathe on your own. Youre better off going home. If something changes, let me know, but we are about to run out of equipment in six days.

My fever broke two weeks after the emergency room visit. There were a couple of days when I thought, Im not going to make it this is taking over my body.

Im at the beginning of a very long recovery. Yesterday morning, I woke up feeling like I had difficulty breathing. The doctor said it was a scare, not a relapse.

Lat, 44, is a legal journalist and recruiter in New York.

I was barely able to walk or even stand, perhaps from not getting enough oxygen. But luckily, I had enough strength to make it to my nearest emergency room, which is where I belonged.

The intubation itself felt like a scene out of ER or Chicago Hope, one of controlled intensity. Attached to the ventilator, I slept for the next six days or so. I was later told that I woke up at various points, sometimes to try and remove the breathing tube or to write down questions. But I remember nothing of this.

When I woke up, I felt like Rip Van Winkle. It was as if those six days never happened. In my first conversation with my husband after extubation, I returned to the exact same topic we had been discussing right before I was intubated: whether he could bring a duffel bag of clothes and books to the hospital.

Wade, 44, lives in Chandler, Arizona, and works at a security and surveillance company.

Ive never felt so bizarre. My body felt like it was not my own. I had crazy back pain. Sometimes I felt like I couldnt move my shoulders.

I had a raw, dry cough, and the fevers spiked in the night. I have a C-section scar from 10 years ago that hurt again because I was coughing so much.

Everything I did left me feeling a little winded, and just the simple act of getting up and having a shower was tiring.

I had no appetite. I had to force myself to eat. I lost 9 pounds.

The only thing I can tell anyone else, especially people who dont know what they have and who are wondering, is: If you can get up and walk a little bit, walk two steps more. Just do whatever you can to keep moving.

Maer, 35, illustrator who is based in New York.

Its not like a common cold, where you feel a sore throat and sniffles. It just goes straight into your lungs, and you feel other symptoms coming from it.

My stomach pain was so bad, it felt like I had appendicitis. I also had a bad cough, shortness of breath and a heavy feeling in my lungs. I slept 19 hours a day, and it still didnt feel like enough.

When I started to recover, I lost my sense of smell and taste. It happened in one day.

The entire recovery process is two steps forward, one step back. You keep wondering the whole time, Is this it?

When it was over, I woke up feeling like a weight let go of me. It feels like I got a get-out-of-jail-free card now that I can move around outside a little more freely.

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'An anvil on my chest': What it's like to have COVID-19 - LancasterOnline