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

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.

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

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

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

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

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 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.


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

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

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 -...

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

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.

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

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


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.

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

MET 2020 Slot booking to commence on July 15, Examination dates available at – Jagran Josh

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 - 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

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

From blood clots to ‘Covid toe’: Experts confounded by series of medical mysteries – The Straits Times

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.


"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.


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

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

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 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 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



Headquartered in San Francisco, California, Vitagene Incorporated and its platform division 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


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


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

Original post:

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

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

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.

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

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

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

Coronavirus may have spread to humans as early as October 2019 – study – The Jerusalem Post

A genetic study of samples from more than 7,500 people infected with COVID-19 suggests the new coronavirus spread quickly around the world after it emerged in China sometime between October and December last year, scientists said on Wednesday.

Scientists at University College London's Genetics Institute found almost 200 recurrent genetic mutations of the new coronavirus - SARS-CoV-2 - which the UCL researchers said showed how it is adapting to its human hosts as it spreads.

"Phylogenetic estimates support that the COVID-2 pandemic started sometime around Oct. 6, 2019 to Dec. 11, 2019, which corresponds to the time of the host jump into humans," the research team, co-led by Francois Balloux, wrote in a study published in the journal Infection, Genetics and Evolution.

Balloux said the analysis also found that the virus was and is mutating, as normally happens with viruses, and that a large proportion of the global genetic diversity of the virus causing COVID-19 was found in all of the hardest-hit countries.

That suggests SARS-CoV-2 was being transmitted extensively around the world from early on in the epidemic, he said.

"All viruses naturally mutate. Mutations in themselves are not a bad thing and there is nothing to suggest SARS-CoV-2 is mutating faster or slower than expected," he said. "So far, we cannot say whether SARS-CoV-2 is becoming more or less lethal and contagious."

In a second study also published on Wednesday, scientists at Britain's University of Glasgow who also analyzed SARS-CoV-2 virus samples said their findings showed that previous work suggesting there were two different strains was inaccurate.


A preliminary study by Chinese scientists in March had suggested there may have been two strains of the new coronavirus causing infections there, with more of them more "aggressive" than the other.

But, publishing their analysis in the journal Virus Evolution, the Glasgow team said only one type of the virus was circulating.

More than 3.71 million people have been reported to be infected by the novel coronavirus globally and 258,186 have died, according to a Reuters tally.

Cases have been reported in more than 210 countries and territories since they were first identified in China in December 2019.

The genetic studies offer "fascinating" insights into the evolution of the virus, and emphasize that it is "a moving target with an unknown evolutionary destination," said Jonathan Stoye, head of the division of virology at Britain's Francis Crick Institute.

"All the evidence is entirely consistent with an origin towards the end of last year, and there's no reason to question that in any way," Stoye said.

The World Health Organization said the French case was "not surprising" and urged countries to investigate any other early suspicious cases.

Balloux's team screened the genomes of more than 7,500 viruses from infected patients around the world. Their results add to a growing body of evidence that SARS-CoV-2 viruses share a common ancestor from late 2019, suggesting this was when the virus jumped from a previous animal host into people.


Coronavirus may have spread to humans as early as October 2019 - study - The Jerusalem Post

Team reveals genomic history of ancient civilizations in the Andes – UC Santa Cruz

An international research team has conducted the first in-depth, wide-scale study of the genomic history of ancient civilizations in the central Andes mountains and coast before European contact.

The findings, published online May 7 in Cell, reveal early genetic distinctions between groups in nearby regions, population mixing within and beyond the Andes, surprising genetic continuity amid cultural upheaval, and ancestral cosmopolitanism among some of the region's most well-known ancient civilizations.

Led by researchers at Harvard Medical School and the University of California, Santa Cruz, the team analyzed genome-wide data from 89 individuals who lived between 500 and 9,000 years ago. Of these, 64 genomes, ranging from 500 to 4,500 years old, were newly sequencedmore than doubling the number of ancient individuals with genome-wide data from South America.

The analysis included representatives of iconic civilizations in the Andes from whom no genome-wide data had been reported before, including the Moche, Nasca, Wari, Tiwanaku and Inca.

"This was a fascinating and unique project," said Nathan Nakatsuka, first author of the paper and an MD/PhD student in the lab of David Reich in the Blavatnik Institute at HMS.

"It represents the first detailed study of Andean population history informed by pre-Colonial genomes with wide-ranging temporal and geographic coverage," said Lars Fehren-Schmitz, associate professor at UC Santa Cruz and co-senior author of the paper with Reich.

"This study also takes a major step toward redressing the global imbalance in ancient DNA data," said Reich, professor of genetics at HMS and associate member of the Broad Institute of MIT and Harvard.

"The great majority of published ancient DNA studies to date have focused on western Eurasia," he said. "This study in South America allows us to begin to discern at high resolution the detailed history of human movements in this extraordinarily important part of the world."

Attention on the Andes

The central Andes, surrounding present-day Peru, is one of the few places in the world where farming was invented rather than being adopted from elsewhere and where the earliest presence of complex civilizations in South America has been documented so far. While the region has been a major focus of archaeological research, there had been no systematic characterization with genome-wide ancient DNA until now, the authors said.

Geneticists, including several of the current team members, previously studied the deep genetic history of South America as a whole, including analysis of several individuals from the Andean highlands from many thousands of years ago. There have also been analyses of present-day residents of the Andes and a limited number of mitochondrial or Y-chromosome DNA analyses from individual ancient Andean sites.

The new study, however, expands on these findings to provide a far more comprehensive portrait. Now, Nakatsuka said, researchers are "finally able to see how the genetic structure of the Andes evolved over time."

By focusing on what is often called pre-Columbian history, the study demonstrates how large ancient DNA studies can reveal more about ancient cultures than studying present-day groups alone, said Reich.

"In the Andes, reconstruction of population history based on DNA analysis of present-day people has been challenging because there has so been much demographic change since contact with Europeans," Reich explained. "With ancient DNA data, we can carry out a detailed reconstruction of movements of people and how those relate to changes known from the archaeological record."

'Extraordinary' ancient population structure

The analyses revealed that by 9,000 years ago, groups living in the Andean highlands became genetically distinct from those that eventually came to live along the Pacific coast. The effects of this early differentiation are still seen today.

The genetic fingerprints distinguishing people living in the highlands from those in nearby regions are "remarkably ancient," said Nakatsuka, who will receive his PhD in systems, synthetic and quantitative biology in May.

"It is extraordinary, given the small geographic distance," added Reich.

By 5,800 years ago, the population of the north also developed distinct genetic signatures from populations that became prevalent in the south, the team found. Again, these differences can be observed today.

After that time, gene flow occurred among all regions in the Andes, although it dramatically slowed after 2,000 years ago, the team found.

"It is exciting that we were actually able to determine relatively fine-grained population structure in the Andes, allowing us to differentiate between coastal, northern, southern and highland groups as well as individuals living in the Titicaca Basin," said Fehren-Schmitz.

"This is significant for the archaeology of the Andes and will now allow us to ask more specific questions with regards to local demographies and cultural networks," said study co-author Jose Capriles of Pennsylvania State University.

Genetic intermingling

The team discovered genetic exchanges both within the Andes and between Andean and non-Andean populations.

Ancient people moved between south Peru and the Argentine plains and between the north Peru coast and the Amazon, largely bypassing the highlands, the researchers found.

Fehren-Schmitz was especially interested to uncover signs of long-range mobility in the Inca period. Specifically, he was surprised to detect ancient North Coast ancestry not only around Cusco, Peru, but also in a child sacrifice from the Argentinian southern Andes.

"This could be seen as genetic evidence for relocations of individuals under Inca rule, a practice we know of from ethnohistorical, historical and archaeological sources," he said.

Although the findings of genetic intermingling throughout the Andes correlate with known archaeological connections, they will likely prompt additional archaeological research to understand the cultural contexts underlying the migrations, said Nakatsuka.

"Now we have more evidence demonstrating important migrations and some constraints on when they happened, but further work needs to be done to know why exactly these migrations occurred," he said.

Long-term continuity

The analyses revealed that multiple regions maintained genetic continuity over the past 2,000 years despite clear cultural transformations.

The finding contrasts with many other world regions, where ancient DNA studies often document substantial genetic turnover during this period, said Reich.

The population structures that arose early on persisted through major social changes and on into modern societies, the authors said. The discoveries offer new evidence that can be incorporated alongside archaeological and other records to inform theories on the ancient history of different groups in the region.

"To our surprise, we observed strong genetic continuity during the rise and fall of many of the large-scale Andean cultures, such as the Moche, Wari and Nasca," said Nakatsuka. "Our results suggest that the fall of these cultures was not due to massive migration into the region, e.g., from an invading military force, a scenario which had been documented in some other regions of the world."

Two exceptions to the continuity trend were the vast urban centers that the Tiwanaku and Inca cultures called home. Rather than being fairly genetically homogeneous, the capital regions of these civilizations were cosmopolitan, hosting people from many genetic backgrounds, the team found.

"It was interesting to start to see these glimpses of ancestral heterogeneity," said Nakatsuka. "These regions have some similarity to what we see now in places like New York City and other major cities where people of very different ancestries are living side by side."

Cooperative authorship

The study included authors from many disciplines and many countries, including Argentina, Australia, Bolivia, Chile, Germany, Peru, the United Kingdom and the United States.

"This is an impressive interdisciplinary but, just as importantly, international collaboration," said study co-author Bastien Llamas of the University of Adelaide. "All worked very closely to draft this manuscript under the leadership of Fehren-Schmitz and Reich."

It was important to team up with local scientists who belong to communities that descend from the individuals analyzed in the study, Fehren-Schmitz said, and to obtain permission from and continually engage with indigenous and other local groups as well as local governments.

The analysis of DNA from ancient individuals can have significant implications for present-day communities. One concerns the physical handling of the skeletal materials, which might be sensitive to the groups involved.

The work provided opportunities to heal past wounds. In one case, a sample from Cusco, previously housed in the U.S., was repatriated to Peru. Other remains that had long ago been taken improperly from burial sites were able to be carbon-dated and reburied.

In the absence of pre-Columbian written histories, archaeology has been the main source of information available to reconstruct the complex history of the continent, said study co-author Chiara Barbieri of the University of Zurich.

With the study of ancient DNA, we can read the demographic history of ancient groups and understand how ancient and present-day groups are related, she said. The link with the genetic study of living populations opens a direct dialogue with the past and an occasion to involve local communities.

The researchers sought to deeply involve communities with the help of archaeologists from each area, said Nakatsuka. Their efforts included giving public talks about the study and translating materials into Spanish.

"We were really happy to have the summary and key findings of our paper translated and included as part of the Cell paper itself, to increase accessibility of our work," said Nakatsuka. "We hope future studies will do similar translations, including versions suitable for lay audiences for schools, museum exhibits and cultural organizations, which we are in the process of doing as well."

Original post:

Team reveals genomic history of ancient civilizations in the Andes - UC Santa Cruz

Regeneron Reports First Quarter 2020 Financial and Operating Results – BioSpace

TARRYTOWN, N.Y., May 5, 2020 /PRNewswire/ --

Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) today announced financial results for the first quarter of 2020 and provided a business update.

"Over 30 years, the Regeneron team has built a science and technology engine uniquely suited to address the COVID-19 pandemic and we are applying our signature passion, innovation, and drive to advance solutions. Our novel antibody cocktail, REGN-COV2, which is specifically-designed for both prevention and treatment, is expected to begin human studies in June and we are working in parallel to have large-scale quantities available by late summer," said Leonard S. Schleifer, M.D., Ph.D., President and Chief Executive Officer of Regeneron. "Beyond our COVID-19 efforts, we maintain our commitment to the many other patients with serious diseases who are counting on us. In the first quarter, we saw continued growth with EYLEA, Dupixent, and Libtayo in the U.S. driven by underlying demand despite the impact of the pandemic. Moreover, we continue to advance our broad immuno-oncology platform, including the PD-1 inhibitor Libtayo, for which we plan regulatory submissions this year in both non-small cell lung cancer and basal cell carcinoma, based on recent promising late-stage results."

"We believe our recent revision to the accounting presentation better reflects the nature of revenues earned and costs incurred and simplifies our financial reporting," said Robert E. Landry, Executive Vice President, Finance and Chief Financial Officer of Regeneron. "We were also pleased to close the Praluent restructuring transaction with Sanofi, which we expect to be accretive beginning in the second quarter of 2020."

Financial Highlights

($ in millions, except per share data)

Q1 2020

Q1 2019

% Change

Total revenues(4)







GAAP net income







GAAP net income per share - diluted







Non-GAAP net income(1)







Non-GAAP net income per share - diluted(1)







Business Highlights

Key Pipeline Progress

Regeneron has more than 20 product candidates in clinical development, including five marketed products for which it is investigating additional indications. Updates from the clinical pipeline include:

EYLEA (aflibercept) Injection

Dupixent (dupilumab)

Oncology Program

Praluent (alirocumab)

Evinacumab, an antibody to ANGPTL3

Pozelimab, an antibody to C5

REGN-EB3, a multi-antibody therapy to Ebola virus infection

COVID-19 Update

Business Development Update

In December 2019, the Company and Sanofi also announced their intent to restructure their antibody collaboration for Kevzara. The companies continue to assess potential terms of this restructuring in light of the recently launched clinical programs evaluating Kevzara in patients hospitalized with COVID-19.

First Quarter 2020 Financial Results

Effective January 1, 2020, Regeneron has implemented changes in the presentation of its financial statements related to certain reimbursements and other payments for products developed and commercialized with collaborators. The Company made these changes in presentation to better reflect the nature of the Company's costs incurred and revenues earned pursuant to arrangements with collaborators and to enhance the comparability of Regeneron's financial statements with industry peers. The change in presentation has been applied retrospectively. See Note (4) below for further information.


Total revenues increased by 33% to $1.828 billion in the first quarter of 2020, compared to $1.373 billion in the first quarter of 2019.

EYLEA net product sales in the United States were $1.172 billion in the first quarter of 2020, compared to $1.074 billion in the first quarter of 2019. Overall distributor inventory levels for EYLEA in the United States remained within the Company's one-to-two-week targeted range.

Total revenues also include Sanofi and Bayer collaboration revenues(2) of $528 million in the first quarter of 2020, compared to $246 million in the first quarter of 2019. Sanofi collaboration revenue in the first quarter of 2020 included the Company's share of profits from collaboration antibodies (Dupixent, Praluent, and Kevzara) of $171 million, while Sanofi collaboration revenue in the first quarter of 2019 included the Company's share of losses from collaboration antibodies of ($28) million. The change in the Company's share of profits (losses) from collaboration antibodies was primarily driven by higher Dupixent profits.

Refer to Table 4 for a summary of collaboration revenue.

Operating Expenses





($ in millions)

Q1 2020

Q1 2019

Q1 2020

Q1 2019

Research and development (R&D)













Selling, general, and administrative (SG&A)













Original post:

Regeneron Reports First Quarter 2020 Financial and Operating Results - BioSpace

Scientists at Ben-Gurion University of the Negev Develop Anti-Coronavirus Surface Coating Based on Nanomate… – The Auto Channel

BEER-SHEVA, Israel, May 5, 2020 -- The coronavirus, SARS-CoV-2, which is responsible for the current COVID-19 pandemic, is transmitted between people mainly via respiratory droplets, but it is known that the virus remains stable on various surfaces for days. One of the first indications for this came from the Diamond Princess cruise ship, where active virus particles were found even 17 days after the ship was evacuated. In light of the possibility that the virus can spread through contaminated surfaces, it is important to be able to sterilize surfaces with high contamination potential, such as doorknobs, elevator buttons or handrails in public areas in general, and in hospitals and clinics in particular. However, current disinfectants are mainly based on chemicals such as poisonous sodium hypochlorite (bleach) or alcohol, both of which provide only a temporary measure until the next exposure to the virus.

Certain metals can be lethal, even in small quantities, for viruses and bacteria and are not poisonous to humans. In proof of concept experiments, in which also PhD students Yariv Greenshpan and Esti Toledo, and postdoc Guillaume Le Saux participated, the researchers assessed the effect of surfaces coated with nanoparticles of various metals on the infectivity of lentiviruses, which belong to the HIV family, in human cells. Findings show that surfaces coated with copper nanoparticles strongly block infection of the cells by the virus. These ongoing experiments show a huge potential for copper ions in preventing surface-mediated infection with SARS-CoV-2.

Based on these findings, the researchers are developing anti-viral coatings that can be painted or sprayed on surfaces. The coatings are based on polymers, which are the starting materials of plastics and paints, and contain nanoparticles of copper and other metals. The nanoparticles embedded in the polymer will enable controlled release of metal ions onto the coated surface. Studies show that these ions have a strong anti-viral effect, which can eradicate virus particles that adhere to the surface. Because the release of ions is extremely slow, the coating can be effective for a long period of time weeks and even months, and it will reduce the infectivity of the virus particles by more than 10-fold.

Josh Peleg, CEO, BGN Technologies, said, "The need to develop anti-viral coatings has greatly increased recently, with the SARS-CoV-2outbreak, and this need will likely remain high even after the pandemic ends, due to increased awareness. In addition, the product will be efficient as a general anti-viral and anti-bacterial coating. It can be applicable for medical settings, as an anti-pathogenic substance in places with increased risk of contamination, such as hospitals, but also for home use, and in public spaces such as schools, airports, public transportation and cinemas. We see a widespread and multidisciplinary academic commitment for finding solutions to currently medical and financial challenges as well as to the challenge of returning to normalcy once the pandemic wanes."

The research activity of Prof. Porgador and Dr. Schvartzman is part of the coronavirus research task force, founded by Prof. Daniel Chamovitz, President of BGU. To support this activity, it was decided to divert research funds in order to find rapid solutions for various challenges associated with the coronavirus pandemic. This invention received the support of the Israel Innovation Authority, in response to a call for proposals for coping with the coronavirus. The project is one of 27 proposals submitted to the Israel Innovation Authority by BGN Technologies, the technology transfer company of BGU, based on innovative and diverse inventions of researchers at BGU and the National InstituteforBiotechnologyin theNegev(NIBN) for the prevention, diagnosis and treatment of COVID-19.

Prof. Angel Porgador said, "The current coronavirus is transmitted not only through droplet spray but also via various surfaces that can convey the virus from one person to another. Furthermore, research shows that the virus remains viable on various surfaces for extended periods of time, of days and even longer. Therefore, there is a clear need for durable anti-viral coatings that can be sprayed or painted on surfaces, just like paint or varnish, and that will prevent viral transmission. These surfaces can include handles, buttons, railways or any other public surface that poses increased danger, in particular in places with a high concentration of potential carriers, such as hospitals or clinics. It is important to remember that we are developing coatings that will be effective not only against the coronavirus but also against other viruses, as indicated in our proof of concept experiments, and also against bacteria, so they will be relevant for a wide range of applications."

Dr. Mark Schvartzman commented, "While current surface disinfection methods rely mostly on substances that are poisonous for people, such as bleach, or on substances that evaporate readily being based on alcohol, the coating that we are developing is based on metals that are toxic for viruses or bacteria, but completely human friendly. It should be noted that until now using such metals for anti-viral applications has encountered significant challenges due to the nature of the metals, such as the tendency to oxidize and corrode. Nanoparticles provide a solution to these obstacles. Another advantage of nanoparticles is the large surface area to volume ratio, which results in an efficient anti-viral surface area using a relatively small amount of metal. Additionally, nanoparticles of anti-viral metal can be easily embedded in a polymer that can coat the relevant surfaces for extended periods of time."

About BGN Technologies

BGN Technologiesis the technology companyof Ben-Gurion University, Israel. The company brings technological innovations from the lab to the market and fosters research collaborations and entrepreneurship among researchersand students. To date, BGNTechnologieshas established over 100 startup companiesin the fields of biotech, hi-tech, and cleantech as well as initiating leading technology hubs,incubators, and accelerators.Over the past decade, it has focused on creating long-term partnerships with multinational corporations such as Deutsche Telekom, Dell-EMC, IBM, PayPal, Cincinnati Children's Medical Center, Merck, Sigma and Bayer, securing value and growth for Ben-Gurion University as well as for the Negev region.For more information, visit the BGN Technologies website.

About NIBN

The National Institute for Biotechnology in the Negev Ltd. (NIBN), a unique research institute located within Ben-Gurion University of the Negev (BGU), is the first self-organized, independent research entity established under the auspices of a university in Israel.

The NIBN was established as a company in November 2009 through a trilateral agreement between the Israeli Government, Mr. Edgar de Picciotto, and Ben-Gurion University.

The mission of the NIBN is to conduct multi-disciplinary applied research guided by a clear biotechnology vision, to bridge the gap between basic and applied innovative research, and facilitate the commercialization of novel ideas and technologies developed by NIBN researchers.

Research at the NIBN is focused in several key areas: cancer, infectious diseases, autoimmune and metabolic diseases, human genetic disorders, neurodegenerative diseases, and applied biotechnology, including AgBio. The decision to focus on these topics combines existing strengths and resources unique to the NIBN and BGU. For more information, visit theNIBN website

Media Contact:

Tsipi HaitovskyGlobal Media LiaisonBGN TechnologiesTel: +972-52-598-9892E-mail: [emailprotected]

SOURCE BGN Technologies

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Scientists at Ben-Gurion University of the Negev Develop Anti-Coronavirus Surface Coating Based on Nanomate... - The Auto Channel

COVID-19 and food security – Fitzwilliam College, University of Cambridge

This article is a commentary by Fitzwilliam Honorary Fellow ProfessorM S SwaminathanFRS (PhD Botany 1950), as told to his daughter Nitya Rao.

I started my post-graduate work on potato in 1947 at the Indian Agriculture Research Institute (IARI), New Delhi. Growing up in Tamil Nadu, I had witnessed the damage to the potato crop by a disease called late blight (caused by Phytophthora infestans) in the Nilgiri Hills. Potato was a very important crop here, and its destruction led to considerable distress for the local people, as this coincided with World War II, when rice too was in short supply, due to the lack of imports from Burma (Myanmar). While many scientists were already working on wheat and rice, potato was at that time under-researched in India, perhaps because of its geographical concentration in the hills of southern India and the eastern Himalayas.

I continued my research on potato at the University of Wageningen, the Netherlands, in 1949. I learnt that during World War II, potato became the major food crop in Europe, leading to the abandonment of traditional crop rotations, and subsequently to the problem of resistance to the golden nematode in the polder lands. Potato is prone to a range of viruses, bacterial and fungal infections, and my work therefore focused on developing varietal lines resistant to pests and diseases.

I moved to Cambridge in 1950 and continued my PhD work on potato pests and diseases with Dr H WHoward. My work relied on inter-specific hybridisation, a technique that came to be increasingly used after the Irish potato famine of the 1840s. When I studied the question of why the Irish experienced such a serious epidemic pest, the late blight, I found the main reason to be the cultivation of a single variety. With no genetic variability, the potato became vulnerable to the rapid spread of disease. Fortunately, in Cambridge, there was a large collection of tuber-bearing potato (Solanum) species from Latin America, which provided valuable genes for developing lines of resistance to several serious stresses and diseases.

I published a paper in the American Potato Journal in 1951 on the importance of genetic diversity and variability, and this in fact, led to the US Department of Agriculture asking me to help them establish a potato collection at Sturgeon Bay, University of Wisconsin, Michigan. Here, one of the crosses I developed, between S. tuberosum and S. acaule, a species which grows at high altitudes in Peru, resulted in the frost-tolerant variety Alaska Frostless. Through my research, published in Biblographia Genetica, I demonstrated clearly that if we have enough genetic material in hand, we will be able to make new lines, resistant to disease or bearing specific characteristics.

Over a period of thousands of years, there have been mutations or changes to crops through a process of natural selection, that is, certain strains that are resistant to disease, survive. But once a plant becomes a crop, there is a process of human selection too that comes into play. So, potato breeders, for instance, selected strains of potato resistant to the late blight, after the Irish famine. For the coronavirus, part of the process of developing a vaccine is based on mapping the genetic traits of the virus. While nature conserves genes, human selection additionally takes account of quality, be if of food, or of human life itself.

The importance of genetic diversity and biodiversity cannot be emphasised enough in the context of food security. During the Bavarian war of succession in the late 18th century, there was a period called kartoffelkreig or the potato war. The potato crop was damaged by blight, and as the two armies had nothing to eat, while there were only minor skirmishes, thousands of soldiers died of starvation and disease. In Europe, this too emphasised the need for varietal diversity of potato, the main staple food. A single genetic strain, like the present COVID-19 pandemic, can lead to severe distress, in the absence of resistant strains.

Coming to the lessons in todays context, and for the future of food and agriculture in India, I again draw a parallel with the Irish potato famine. As the famine led to hunger and starvation, it also led to epidemics of infectious diseases. When people are starving, they are more prone to disease. On television, we find stories of migrants reporting that they might starve to death due to lack of food even if not due to the coronavirus. A basic problem we are confronting today is of inadequate food intake, especially for the poor and those already malnourished. This can affect immunity, but also longer-term nutrition and health.

There are two key lessons for food and nutrition security and agriculture more broadly. On the production side, the main moral lesson is to promote genetic heterogeneity. The late blight devastated the entire potato crop, leading to severe famine and loss of many lives. This implies the need to preserve and cultivate a range of varieties, be it of potato or other crops. In India, we are fortunate to have enough diversity of crops, so if one fails, there is always another crop.

However, at the present moment there is an issue of availability of suitable seed varieties, given that many of the standing crops have not been harvested. The government needs to ensure that seeds in adequate quantity and for a diversity of farming systems are made available to the farmer preparing now for the kharif sowing.

In the 1960s, I had started the first seed village in Jaunti in Delhi state. The idea was that the whole village produce seed to meet farmers demand, but also ensure farmers control over the varieties. Later known as participatory breeding, scientists from IARI and farmers worked together to develop characteristics there were desirable, both in terms of production yields, but equally taste and colour preferences. Farmers at that time preferred amber coloured wheat to red varieties such as Sonora, which we had acquired from Mexico, for making chapattis.

We experimented with vegetable seeds production villages in Tamil Nadu, in the early years of the M.S. Swaminathan Research Foundation (MSSRF) and while entire villages have not taken this up, there remain clusters of farmers who produce seeds for pulses, vegetables and so on. It is even more important now to support local production of seeds that ensure genetic variability. We need to specifically identify donor genes that can help develop varietal lines resistant to a range of pests, pathogens and weeds.

The other important lesson is in the field of post-harvest technology. In the present context of corona, and the national lockdown, farmers distress (especially for those producing horticultural crops) is intensified due to lack of post-harvest processing, storage, value addition and marketing mechanisms. The Amul model, supported by the National Dairy Development Board (NDDB), has demonstrated that even during the present COVID-19 crisis, the livelihoods of small farmers, in this case, milk producers, can be secured through collective action that ensures procurement, storage, transportation, value addition and marketing.

It is time that the National Horticultural Board is supported to play a proactive role similar to the NDDB. Even food crops are likely to get infected with fungi, aflatoxins and micro-toxins, in the absence of proper post-harvest storage and processing. In fact, following the Irish potato famine, in addition to potato collections to preserve genetic diversity, measures to protect both seed and food were put in place including modern storage systems.

Finally, during the Irish potato famine, people did not know what had happened, there was no information available till after the event. In India today, we have the advantage of excellent information and communication technology, which needs to be put to full use to reach the unreached with appropriate and timely information. There are several small initiatives towards this end. While the government machinery is providing good information on dealing with COVID-19, at the same time, we need to help our farmers and small producers deal with the threat of pest and disease in their farming systems too. For instance, close to a 100 farmers joined a plant clinic run by MSSRF, online for the first time.

The Green Revolution helped us move from a ship to mouth existence to a commitment to the right to food. Our food stocks need to be used to ensure the food security of the poor and hungry many of them farmers who have contributed to the building of this stock. This crisis is a time to recognise and strengthen our farming community women and men.


Swaminathan, M.S. (1951) Notes on induced polyploids in the tuber-bearing solanum species and their crossability with s.tuberosum. American Potato Journal. 28: 472-482.

Swaminathan, M.S andHoward H.W (1953) The cytology and genetics of the potato (solanum tuberosum) and related species. Bibliographia Genetica. 16: 1-192.

M.S. Swaminathan is an eminent agricultural scientist, the winner of the World Food Prize, and was the Chairman of the National Commission on Farmers. Nitya Rao is Professor of Gender and Development at the School of International Development, University of East Anglia, the UK.

This article originally featured onMongabay-India.

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COVID-19 and food security - Fitzwilliam College, University of Cambridge

Val Sheffield elected to the American Academy of Arts and Sciences – Iowa Now

Val Sheffield, the Roy J. Carver Chair in Molecular Genetics at the University of Iowa Roy J. and Lucille A. Carver College of Medicine, has been elected tothe 2020 class of the American Academy of Arts andSciences.

Sheffield was recognized for playing a key role in constructing human genetic maps and developing efficient disease-gene discovery approaches. This paved the way for the completion of the human genome project and significantly contributed to genetic discoveries in blinding eye diseases, obesity, hypertension, and neurological disorders, potentially leading to noveltherapies.

The American Academy of Arts and Sciences, founded in 1780 by John Adams and John Hancock, is both an honorary society that recognizes and celebrates the excellence of its members and an independent research center convening leaders from across disciplines, professions, and perspectives to address significant challenges. Elected members join with other experts in cross-disciplinary efforts to produce reflective, independent, and pragmatic studies that inform public policy and advance the publicgood.

This year, 276 new members were elected and include notable scientists, artists, scholars, and leaders in the public, nonprofit, and private sectors. Sheffield joins 58 other leaders in the medical sciences specialty. Academy members are nominated and elected by current members and chosen for excellence in their field and a record of continuedaccomplishment.

Sheffield is eager to contribute hisexpertise.

Genetic and genomic data are increasingly being integrated into the practice of medicine. With my expertise in human molecular and clinical genetics and genomics, Im hoping to be a useful resource to the academy, Sheffieldsays.

This is an incredible honor and well-deserved national recognition. We are extremely proud of Dr. Sheffield and his achievements, says Brooks Jackson, UI vice president for medical affairs and the Tyrone D. Artz Dean of the Carver College of Medicine.Given these turbulent times, it is especially gratifying to be able to celebrate hissuccess.

Sheffield joined the UI in in 1990 to perform research and practice clinical genetics in the Division of Medical Genetics for the UI Stead Family Department of Pediatrics. He has spent his entire career at Iowa, where he served as director of the Division of Medical Genetics for 22 years until stepping down in January 2020. He conducts scientific research related to human genetic diseases, however, he has recently converted a portion of his lab to join researchers across the world fighting the coronaviruspandemic.

Since the COVID-19 shutdown, I have switched some of my laboratory personnel to a COVID-19 project. We are trying to devise a simple method for collecting samples from patients for COVID-19 testing that doesnt require nasal swabs (in short supply) or use medical personnel to collect samples. The person being tested will self-collect the sample, thus saving on personnel and personal protective equipment. I am hoping to get FDA approval soon for this method so that it can be used to expand needed testing throughout Iowa, Sheffieldsays.

At the UI, Sheffield trains doctoral and medical students as a professor of pediatrics and a professor of ophthalmology and visual sciences. He also is an investigator for the UI Institute for Vision Research and practices medicine, caring for patients with human genetic disorders. He has co-authored more than 330 peer-reviewed scientific papers. He previously was an investigator for the Howard Hughes Medical Institute (HHMI), from 1998 to2016.

The members of the class of 2020 have excelled in laboratories and lecture halls, they have amazed on concert stages and in surgical suites, and they have led in board rooms and courtrooms, says academy President David W. Oxtoby. These new members are united by a place in history and by an opportunity to shape the future through the academys work to advance the publicgood.

Sheffield attended Brigham Young University, where he earned a bachelors degree in zoology and a masters degree in developmental biology. He received a doctoral degree in developmental biology and a medical degreewith honors from the University of Chicago. He was a resident in pediatrics and fellow in medical genetics at the University of California, SanFrancisco.

His research has been funded by the National Institutes of Health (NIH) for 29 consecutive years, as well as by the Roy J. Carver Charitable Trust. Sheffields honors include the E. Mead-Johnson Award for Pediatric Research and the Lewis Rudin Prize from the New York Academy of Science, and he is a member of the National Academy of Medicine. Sheffield is board certified by the American Board of Medical Genetics and Genomics in both clinical genetics and clinical moleculargenetics.

Sheffield joins the following UI faculty and administrators who havebeen elected members of the American Academy of Arts andSciences:

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Val Sheffield elected to the American Academy of Arts and Sciences - Iowa Now

DNA gives clues into risk of developing Alzheimer’s disease and other dementias – Alabama NewsCenter

Neurodegenerative diseases such as Alzheimers disease, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia can be devastating for patients and families, particularly in cases when symptoms show up in people younger than 65.

More than 5 million Americans are currently living with Alzheimers disease. Another 20,000-30,000 people have frontotemporal dementia and at least 16,000 have ALS. While scientists have some ideas about what causes these conditions, theres a lot of information they dont have, particularly about how a persons genome the suite of genetic material or DNA that theyre born with might affect disease onset.

Now, scientists at the HudsonAlpha Institute for Biotechnology, the University of California, San Francisco (UCSF) and the University of Alabama at Birmingham (UAB) have uncovered a gene that doubles the risk of becoming ill with one of these diseases.

This work would have been impossible without the grassroots support of local Huntsville donors, said Richard M. Myers, PhD, HudsonAlpha president and science director. Being able to do projects like this that address the underlying causes of multiple different neurodegenerative diseases could make a real difference in finding earlier diagnostics and new treatments.

The researchers gathered DNA samples from more than 1,100 people in an effort led by Jennifer Yokoyama, PhD, an assistant professor of neurology at the University of California, San Francisco. About half of these people were healthy, while the other half had Alzheimers disease, ALS or frontotemporal dementia. Then the scientists used a technique called whole-genome sequencing to learn what each individuals genetic code looks like.

With more than one thousand genetic codes in hand, the researchers used computer programs to comb through the sequences and find genetic variants, or things that were different. They determined that people with neurodegenerative diseases were more likely to have variants in a gene named TET2. They discovered this gene after analyzing both the parts of the genome that serve as a blueprint for making proteins, the molecules that do things in the bodys cells, and the parts of the genome that control when and where those proteins get made.

Then, the research team looked at DNA sequences from more than 32,000 healthy people and people with neurodegenerative diseases. They confirmed that the variants they saw in the first 1,100 genomes they looked at were also present in other people with Alzheimers disease, ALS and frontotemporal dementia more often than in healthy people.

Were excited that we did find a new genetic association here, said Nicholas Cochran, PhD, a senior scientist in the Myers Lab at HudsonAlpha.

You never know what genes might show up in a research project like this, but TET2 is exciting. This gene is the DNA blueprint for a protein called TET2, which has already been shown to have a role in maintaining the brains DNA. The researchers think the variants that they found that lead to a non-functional version of the protein might disrupt how the brain ages and contribute to the development of Alzheimers disease, ALS and frontotemporal dementia.

In addition to the generous support of local Huntsville donors to the HudsonAlpha Foundation Memory and Mobility Program, the work, which was recently published in The American Journal of Human Genetics, was funded by the Rainwater Charitable Foundation, the Daniel Foundation of Alabama, the Larry L. Hillblom Foundation, and the National Institutes of Health National Institute on Aging.

About HudsonAlpha: HudsonAlpha Institute for Biotechnology is a nonprofit institute dedicated to developing and applying scientific advances to health, agriculture, learning, and commercialization. Opened in 2008, HudsonAlphas vision is to leverage the synergy between discovery, education, medicine, and economic development in genomic sciences to improve the human condition around the globe. The HudsonAlpha biotechnology campus consists of 152 acres nestled within Cummings Research Park, the nations second largest research park. The state-of-the-art facilities co-locate nonprofit scientific researchers with entrepreneurs and educators. HudsonAlpha has become a national and international leader in genetics and genomics research and biotech education and includes more than 30 diverse biotech companies on campus. To learn more about HudsonAlpha, visit

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DNA gives clues into risk of developing Alzheimer's disease and other dementias - Alabama NewsCenter

Rare Gene Discovered That Nearly Doubles Risk of Developing a Neurodegenerative Disease – Clinical OMICs News

A multi-institutional team of researchers from the HudsonAlpha Institute for Biotechnology, the University of California, San Francisco (UCSF), and the University of Alabama at Birmingham (UAB), have identified a rare genetic variant that sigifnicantly incresases the risk of developing diseases like Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD).

Finding evidence for a risk factor that contributes to multiple neurodegenerative diseases is exciting, said Richard M. Myers, Ph.D., president and science director of HudsonAlpha, in a press release. We already know that these diseases share some pathologies. This work shows that the underlying causes of those pathologies may also be shared.

The teams research, Non-Coding and Loss-of-Function Coding Variants in TET2 are Associated with Multiple Neurodegenerative Diseases was published April 23 in The American Journal of Human Genetics. For their study, the investigators sequenced and analyzed whole genomes of more than 1,100 people of European descent 435 cases of early-onset Alzheimers disease (EOAD) and frontotemporal dementia (FTD) and 671 controls. They found that rare variation in the gene TET2 nearly doubled the risk of developing diseases like Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD).

The project wouldnt have been possible without extensive collaboration between institutions, said first author Nicholas Cochran, Ph.D., a senior scientist in the Myers Lab. You end up being able to find things that you cant find working alone.

Jennifer Yokoyama, Ph.D., an assistant professor of neurology at UCSF, collaborated with Cochran on technical details and also managed the projects sample collection, the majority of which were collected over decades at the UCSF Memory and Aging Centerand then sequenced and analyzed at HudsonAlpha.

Once they had the sequencing results, the researchers noticed that many of the patients had early-onset versions of neurodegenerative disease, suggesting there would be a genetic component of their illness. During genome analysis, the researchers looked at both coding and non-coding regions of the genome for DNA sequence variants, a strategy that allowed them to be more confident that any possible genes they discovered would be implicated in these diseases

Upon identifying TET2, the investigators then compared their findings with existing genetic data from more than 32,000 healthy people and people with neurodegenerative diseases. This data confirmed that variants in TET2, in both protein-coding and non-coding regions, were more likely to be present in the genomes of people with AD, ALS, or FTD than in people without these diseases.

Given well-defined changes in DNA methylation that occur during aging, rare variation in TET2 may confer risk for neurodegeneration by altering the homeostasis of key aging-related processes, the researchers wrote. Additionally, our study emphasizes the relevance of non-coding variation in genetic studies of complex disease.

Next steps for this continued research will focus on how changes in TET2 levels or function could contribute to aging and neurodegenerative disease.

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Rare Gene Discovered That Nearly Doubles Risk of Developing a Neurodegenerative Disease - Clinical OMICs News

Progress in understanding the genetic basis of mental health – SFARI News

On May 6, 2020, Benjamin Neale will discuss progress in mapping genetic risk factors for autism, schizophrenia and bipolar disorder.

His talk is part of the Simons Foundation Autism Research lecture series.

The past decade has seen rapid progress in mapping genetic risk factors for autism, schizophrenia and bipolar disorder. In this talk, Benjamin Neale will review this progress, delving into how study designs and genetic variants are teaching us about different aspects of mental health. With that backdrop, he will then introduce the International Common Disease Alliance (ICDA), a nascent effort to bring the community together to tackle the challenge of moving from genetic maps to biological mechanisms and medicine. The ICDA has developed a set of recommendations for realizing the promise of human genetics to transform our understanding of and treatment for common disorders, such as autism.

Registration is required for this free event.Further instructions and access to join the webinar will be sent to all registrants upon sign up.

Benjamin Nealeis an associate professor in the Analytic and Translational Genetics Unit at Massachusetts General Hospital, where he directs the Genomics of Public Health Initiative. He is also an associate professor in medicine at Harvard Medical School and an institute member at the Broad Institute. Neale is strongly committed to gaining insights into the genetics of common, complex human diseases. Neale and Mark Daly, both of whom are associated with the Broad Institute and Massachusetts General Hospital, lead the ADHD Initiative. This collaborative effort focuses on genomic studies of attention deficit hyperactivity disorder (ADHD).

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Progress in understanding the genetic basis of mental health - SFARI News