"Novel coronavirus" is the proper term for this brand-new virus wreaking havoc on our unprepared world.

But you can also call this nasty villain by its scientific name: severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2 for short.

Covid-19 seems to strike the elderly and immunocompromised the hardest, along with any of us with underlying health conditions such as diabetes, heart and lung disease. But the young shouldn't take anything for granted -- there have been numerous deaths among people aged 20 to 50, as well as a very few among children.

Covid-19 can also present with mild symptoms very similar to a typical cold or flu -- or no symptoms at all, which makes controlling the spread of the virus causing Covid-19 very difficult.

What is a coronavirus?

There they set up shop, producing millions of copies of themselves and causing those cells to rupture. Like the famous scene from the movie "Alien," the viral offspring shoot out into the bloodstream, with the goal of invading more and more cells.

As they multiply, humans began to spit them out into the universe with each exhalation, making us contagious days before we begin to cough, sneeze or have diarrhea -- all symptoms the virus creates to ensure it can leap from human to human, thus ensuring its survival.

This "virus zombie invasion" comes in all sort of shapes, sizes and genetic strategies. All coronaviruses are covered with pointy spires of protein, giving them the appearance of having a crown or "corona" -- hence the name. Coronaviruses use these spikes to latch onto and pierce our cells.

Coronaviruses are part of the RNA brigade of viruses, which are much less stable than their DNA-based comrades. Why is that important? Because instability leads to mistakes in copying genetic code.

That leads to mutations -- thousands, millions, billions of mutations. Sooner or later, one mutation hits pay dirt and allows the virus to cross the great divide between different species. A few million/billion/trillion more mistakes creates another mutation that allows that virus to spread easily. Now the virus is both in its new host and it is contagious.

It's that type of mutation which gives humanity viruses like SARS-CoV-2.

Where did the novel coronavirus come from?

Some of those coronviruses can cross species, such as between pigs, cats and dogs, but for the most part coronaviruses stay loyal to their original hosts. Until, of course, they become that lucky mutation.

"Usually viruses from one animal really don't effectively transmit to other animal species or even to people," said Dr. John Williams, chief of the division of pediatric infectious diseases at the University of Pittsburgh Medical Center Children's Hospital of Pittsburgh.

"So usually if a virus goes from an animal to a human, it's sort of dead end. That person gets sick but it doesn't spread further," said Williams, who has studied coronaviruses for decades.

"MERS is extremely deadly, about 30% of people who are infected with MERS will die," Williams said. "So the virus got over one of the barriers -- it's able to infect humans, grow in them and cause disease -- but thankfully it really doesn't spread well person to person, other than very, very close contacts."

SARS has been more difficult to pin down.

"SARS caused death in about 10% of people that became infected and it did spread person to person but not super effectively," Williams said. "There weren't many people walking around without symptoms or with mild symptoms, who could be spreading it.

"This new virus, SARS-CoV-2, has overcome more barriers," Williams added. "It spreads easily person to person and a lot of people can have either mild disease or they might not even have symptoms, yet they can have the virus and spread it."

At this time, scientists don't know where the novel coronavirus began.

"These things are more difficult than [identifying] dinosaurs, because there's no fossil record of a virus," Williams said. "For example, the main virus I study, human metapneumovirus, is clearly a virus that has circulated in humans for decades if not a few centuries.

"However, when you look at the genetics of the virus, its closest genetic relative is a bird virus," he added. "So, did that virus jump to humans way back and become established? That's what we think. But it isn't impossible that a human virus jumped to birds and became established there."

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What is coronavirus and Covid-19? An explainer - CNN

WHAT'S HAPPENING IN SACases update:

The latest number of confirmed cases is 1 353.

The number of coronavirus-related deaths has risen to five.

Gauteng, the Western Cape and KwaZulu-Natal still account for the majority of cases in the country.

READ MORE |All the confirmed cases of coronavirus in SA

About 1 471 South African citizens stranded abroad have appealed to the government to return home amid the global outbreak of Covid-19, government revealed in a briefing on Tuesday.

"We empathise with their plight and are doing whatever is within our means to assist them to be safe, as comfortable as possible, and to travel back to South Africa," Minister of International Relations and Cooperation (Dirco) Naledi Pandor.

The minister further revealed that, of the total stranded citizens, 723 are students, 204 are workers, 224 are tourists and 320 have not disclosed.

"I cannot say that these numbers are 100 percent accurate as it is based on people who have approached us for assistance through our missions and consular services. There may be more people in need of assistance that we do not know about yet," she added.

READ MORE | Govt working hard to bring home almost 1 500 stranded South Africans - Pandor

Gauteng has recorded its first coronavirus casualty.

The province revealed that a 79-year-old male patient, who had tested positive for Covid-19, died on Monday.

The deceased was earlier admitted to a private hospital in Mogale City, west of Johannesburg, on Saturday.

The man is the first Covid-19 casualty in the province, while the number of deaths in the country has risen to five.

Gauteng premier David Makhura said in a statement on Tuesday that he was saddened by the man's death.

"I wish to convey our heartfelt condolences and express our collective grief to the family and friends of the deceased," Makhura said.

READ MORE | Coronavirus: 79-year-old man is Gauteng's first Covid-19 death

Another confirmed Covid-19 death in South Africa is an elderly pastor who was at a church gathering in Bloemfontein which was attended by five international guests who later tested positive for the coronavirus, Health Minister Zweli Mkhize revealed in a briefing on Tuesday.

The Free State Department of Health's spokesperson, Mondli Mvambi, confirmed, after consultation with his family, his identity.

John Hlangeni, 85, died at Pelonomi Hospital in Bloemfontein on Monday.

"Hlangeni succumbed while being treated at our health facility. As it is, as has been explained before, the effects of Covid-19 are more severe in older persons and also to those who have underlying health issues," said Mvambi.

Health MEC Montseng Tsiu has sent her condolences to the Hlangeni family, relatives and the Global Reconciliation Church in which Hlangeni served.

READ MORE | Elderly pastor dies after contracting coronavirus at Bloem church gathering

The government has conceded the first round of social grant collections during the lockdown had teething problems as there was no enforcement of social distancing in the long queues.

Long queues, a lack of queue management, issues of social distancing not being adhered to, and cash running out at certain collection points were just some of the issues faced by the South African Social Security Agency on Monday as people came out in their droves to collect their grants.

News24 reported that at the Denlyn shopping complex in Mamelodi, there was no police presence or queue management as hundreds of people with disabilities and the elderly lined up to collect their grants.

READ MORE | Govt addresses physical distancing, long Sassa queues

Fifty people, who previously tested positive for Covid-19 in Cape Town, have recovered and their period of self-isolation lifted.

According to the premier of the Western Cape, Alan Winde, the 50 completed 14 days of self-isolation and can now, in accordance with the guidelines set out by the National Institute for Communicable Diseases, come out of isolation.

However, they still have to obey the 21-day lockdown laws, like other members of the public, and so can only leave their homes for essentials like medical care, food, cash and to collect grants.

Currently, 13 people are being treated for Covid-19 in hospitals in the province, with three patients in intensive care.

READ MORE | From isolation to lockdown: 50 people in Cape Town recover from coronavirus

For the latest global data, follow this interactive map from Johns Hopkins University & Medicine.

Positive cases worldwide are now more than 860 000, while deaths are more than 42 000.

The United States, Italy and Spain all have more than 90 000 cases.

Italy and Spain both have more than 8 000 deaths.

Strict containment measures might have already saved up to 59 000 lives across 11 European countries battling the spread of the new coronavirus, experts in Britain say.

Basing their modelling on the numbers of recorded deaths from Covid-19, researchers from Imperial College London said most countries it looked at had likely dramatically reduced the rate at which the virus spreads.

Using the experiences of countries with the most advanced epidemics like Italy and Spain, the study compared actual fatality rates with an estimate of what would have happened with no measures such as school closures, event cancellations and lockdowns.

"With current interventions remaining in place to at least the end of March, we estimate that interventions across all 11 countries will have averted 59 000 deaths up to 31 March," said the report, which was released Monday.

READ MORE | Lockdowns may have saved 59 000 lives in Europe, study says

Faced with a looming shortage of lifesaving ventilators, US hospitals are scrambling for solutions and planning for the worst with the coronavirus pandemic.

Intensive care units at besieged hospitals in New York and other cities are taking an "all hands on deck" approach recruiting doctors from various specialties to help handle the influx of severely ill Covid-19 patients.

They are also finding ways to fill another crucial gap: A limited supply of ventilators, machines that provide breathing support to patients in respiratory distress.

Last week, the US Food and Drug Administration officially approved one alternative to standard ventilators: anaesthesia machines. The equipment, normally used to put surgery patients under, can be adjusted to provide oxygen to ICU patients.

READ MORE | Too many patients, too few ventilators: How US hospitals try to cope with coronavirus

From medical workers struggling to care for the rising tide of Covid-19 patients to the billions of people told to stay home to slow the pandemic, everyone is waiting for one thing: a vaccine.

There is no known treatment for the new coronavirus that emerged in China late last year and has since proliferated across the planet, infecting more than half a million people and claiming more than 30 000 lives.

In mid-January, researchers from China published the genetic sequence of the virus, firing the starting gun for dozens of research labs across the world in the race to find effective drugs.

The approaches have varied dramatically. Some teams are looking at the effects of existing medicines as potential treatments, some are experimenting with repurposing common drugs. Others are using cutting-edge technologies to fashion radically new types of vaccines.

Just over 60 days after the genetic sequence of Covid-19 was shared, the first potential vaccine began human trials.

READ MORE | Race for vaccine tests limits of drug innovation

According to a new alert released this week by the American Academy of Ophthalmology (AAO), conjunctivitis, also known as pink eye, may be a symptom of the new coronavirus, with experts estimating it could be present in 13% of Covid-19 cases.

The Covid-19 virus, officially named SARS-CoV-2, primarily causes respiratory infection. Common symptoms include a dry cough, fever, and shortness of breath.

Recent research has revealed that some patients may also experience digestive symptoms such as diarrhoea, nausea, vomiting and abdominal discomfort. Sudden loss of smell also seems be an indicator of the virus - especially in people who may not be exhibiting other symptoms or meeting the vital criteria for testing, a previous article by Health24 reported. And now, most recently, pink eye has been included as a rare symptom of the virus.

READ MORE | Pink eye could be a less common symptom of the new coronavirus

Genetic mutations that put some younger people at high risk for severe illness from the new coronavirus will be investigated in an international study.

Plans call for enrolling 500 patients worldwide who are under age 50, have been diagnosed with Covid-19 and admitted to an intensive care unit, and have no underlying health problems such as diabetes, heart disease or lung disease.

Studying these patients' DNA may identify genetic mutations that make some people more susceptible to infection, according to study leader Jean-Laurent Casanova. That could eventually help doctors identify people most at risk of developing severe coronavirus disease.

"We're going to try to find the genetic basis of severe coronavirus infection in young people," he said. Casanova is an investigator at Howard Hughes Medical Institute in Chevy Chase, Maryland.

READ MORE | Could gene mutations explain coronavirus cases in the young?

HEALTH TIPS(as recommended by the NICD and WHO)

Avoid contact with people who have respiratory infections

Maintain physical distancing stay at least one metre away from somebody who is coughing or sneezing

Practise frequent hand-washing, especially after direct contact with ill people or their environment

Avoid touching your eyes, nose and mouth, as your hands touch many surfaces and could potentially transfer the virus

Practise respiratory hygiene cover your mouth with your bent elbow or tissue when you cough or sneeze. Remember to dispose the tissue immediately after use.

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Coronavirus morning update: SA deaths now 5, but 50 recoveries in CT, and lifesaving lockdown - Health24

Since humans havent previously been exposed to the SARS-CoV-2 coronavirus, our bodies arent well equipped to deal with being infected by it. A vaccine would allow the body to safely develop an immune response to COVID-19 that could prevent or control infection. But it takes time to develop safe and effective vaccines usually five to ten years on average. Despite promising reports about potential coronavirus vaccines being developed worldwide, it could still take an estimated 12-18 months to develop one.

A vaccine must go through six crucial steps. Image credit: Gerd Altmann.

Its becoming quicker to develop new vaccines than it was in the past as we can build on research from vaccines used for other diseases.

During outbreaks, more resources and funding may also become available, which can speed up the process

Products might also be considered for use even before being formally granted licenses to control the disease in severely affected areas during emergencies.

The development of a potential novel coronavirus vaccine is being partly led by experts who were already developing vaccines for other coronaviruses.

This type of virus was identified as a possible cause of the next big pandemic as the other coronaviruses SARS and MERS have been responsible for two global outbreaks in the last 20 years.

Research on vaccines for these coronaviruses was already undergoing clinical trials.

The first new vaccine to enter human trials for COVID-19 was developed by the U.S. firm Moderna Therapeutics.

About 35 other companies and academic institutions are also working on COVID-19 vaccines.

Most are currently in pre-clinical testing, including one being developed by a team of researchers at the University of Oxford. The vaccine candidate was identified in January and is nearing the clinical testing phase.

During development, a vaccine needs to go through the following steps:

Basic understanding of the virus

In the past, most studies of human viruses looked at how the virus altered or affected human or animal cells in the lab.

Scientists first identify the proteins and sugars on the surface of the viruses or infected cells, then study whether these proteins can be used to produce an immune response.

In the present case, this stage was made easier for researchers after Chinese scientists found and published the genetic sequence of novel coronavirus in January.

Researchers worldwide have been able to identify the structure of proteins that make up the virus, create a genetic history of the family of viruses, and determine when the first human was infected.

It also enabled diagnostic testing kits to be developed, and lets researchers identify potential treatment options.

Vaccine candidates

This may involve isolating the live virus before inactivating or weakening it and then determining whether this modified virus, which is known as a vaccine candidate, might produce immunity in people.

Sometimes the live virus is not part of the process. Instead, its genetic sequence is used to make the vaccine.

The genetic sequence can also be used to make recombinant proteins, a vaccine production method that has been used before for vaccines like hepatitis B.

Researchers now know how to manufacture and test the relevant vaccine and check it has been made properly.

They even know about likely doses, including how many doses will be needed to build immunity.

This background knowledge speeds up the development of each new vaccine made using the same technology.

Pre-clinical testing

Initial safety testing is usually carried out in animals to give an idea of responses in humans.

These are also used to see how effective the vaccine is at preventing the disease, and allows researchers to adapt the vaccine.

During an outbreak, different research groups often work together to speed up this process.

Clinical trials testing in humans

This step is where many promising potential vaccines fail.

There are three phases of a clinical trial:

(i) testing on a few dozen healthy volunteers, looking at how safe the vaccine is, and if it has any adverse effects;

(ii) testing on several hundred people for efficacy (a target population who are ideally those most at risk of the disease);

(iii) testing on several thousand people for efficacy and safety.

Through these phases the vaccine needs to show its safe, leads to a strong immune response, and provides effective protection against the virus.

During an outbreak, experimental vaccines may be used in severely affected populations if theyre at high risk of disease, before progressing to regulatory approval.

Regulatory approvals

If regulators have approved similar products before, approval can be accelerated although this is not likely for COVID-19.

Use of a vaccine before full licensure can be considered in a public health emergency.

Production

Once a vaccine has been produced at a small scale and passed safety tests, it can be used in clinical trials.

However, significant manufacturing capacity, such as infrastructure, personnel and equipment, will be needed to produce large quantities of a vaccine for use.

Quality control is also needed. All of these processes are very carefully monitored.

Once licensed, policy must be developed to decide how to prioritize those who should be vaccinated, such as those in the most high-risk groups and locations.Along the way, if any of these vaccine candidates are shown to be unsafe or ineffective, researchers must return to the laboratory to develop a new candidate. This is why vaccine development can be a long and uncertain process.

Authors: Samantha Vanderslott, postdoctoral researcher in social sciences at the University of Oxford, Andrew Pollard, professor of pediatric infection and immunity at the University of Oxford, & Tonia Thomas, vaccine knowledge project manager at the University of Oxford.This article was originally published on The Conversation.

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COVID-19 Vaccine: Here Are Steps It Will Need to Go Through During Development | Medicine - Sci-News.com

The coronavirus disease (Covid-19) first appeared in the Wuhan district of Hubei province of China in early December 2019. The first case was reported by China on January 7, 2020, and this aroused variable interest worldwide, with most countries initially ignoring the novel infection. Fortunately, Indian health authorities sensed the danger, largely because the country has always been alert to new infections. The scientific think-tank at the Indian council of Medical Research (ICMR) became active immediately and the first laboratory confirmed case was identified at ICMRs National Institute of Virology (NIV), Pune, sometime towards the end of January.

A look at the world Covid meter shows that there is striking variation in mortality rates across countries, ranging from 0.2% to 15% depending on age, the smoking habit and pre-existing co-morbidities. It may be too early to tell, but in general, countries in the Northern hemisphere have faced the maximum brunt, and those in the Southern hemisphere (and those located proximate to the Equator) have so far escaped high infection numbers.

Three factors seem to be playing a role in the observed lower numbers in India with almost zero occurrence of severe Covid-19 cases (until now). First, broad-based immunity in the population due to the extensive microbial load. The Indian population has been exposed to a vast variety of pathogens, including bacteria, parasites and viruses leading to the generation of broad specific memory T-cells in the system, ready to attack additional foreign invaders.

For example, the three main killers of Tuberculosis, HIV and Malaria have plagued India, Africa and several countries in the Southern hemisphere much more than the European and North American nations. In the context of CoV-2 coronavirus, the beneficial role of chloroquine and hydroxychloroquine has been much talked about and debated, while there has already been an extensive usage of this drug at the community level in India -- this too may ultimately prove beneficial.

Second, epigenetic factors that include environment and food habits may also play a beneficial role for countries such as India; much literature is already available in Ayurveda and other Indian systems of medicine on the definitive beneficial effects of Indian spices in augmenting immunity.

Third, and most important, is the possible role of immune response genes in the Indian population. These genes are collectively referred to as comprising the human leucocyte antigen system or simply, the HLA genes. Their main biological function is to present invading foreign antigens to the immune systems, since T-cells, which act as the bodys soldiers come into play only when pathogens are presented to them in a more formal manner in association with HLA genes. In other words, the pathogen must first attach to compounds created by HLA genes before T-Cells attack it. If no such compounds are produced by the body, then the T-Cells are ineffective. As a consequence of the microbial load, the Indian population possesses a high genetic diversity of HLA, much more extensive than Caucasian populations. Indeed, studies by the author at the All India Institute of Medical Sciences, New Delhi, over several decades revealed the presence of several novel HLA genes and their alleles in the Indian population, most of which do not occur in other ethnic groups. Such genetic diversity of HLA could affect viral fitness.

The question then is:Why should genetic variation in HLA genes play a role in the Covid-19 progression? One hint comes from earlier studies in related viral diseases: Certain genetic variants of the HLA system provide protection against such viruses, while others increase genetic susceptibility to them. Another source of indirect evidence comes from recent clinical Covid-19 studies which showed that rapid T-cell response appears to be crucial for recovery from Covid-19, and reduced functional diversity of T cells in peripheral blood could predict progression of Covid-19.

The big question is:Does this give Indians a better chance at fighting the virus effectively? From the epidemiological data so far, it seems so (although much more extensive research is required). However, it is important for us to keep viral loads in check and below the threshold levels. In this context, the complete lockdown announced by the government is highly timely and most desirable. It is imperative that the virus replication cycle gets disrupted as early as possible before it gains numbers that may become difficult for us to counter.

To this end, the images of crowds gathering in several places whether for panic buying or interstate movements are disturbing. They could jeopardise all efforts and mitigate whatever natural advantages we enjoy.

The State must act fast to enforce the lockdown, even forcibly if necessary. India may be the outlier in fighting the coronavirus infection and succeed in keeping the overall numbers lower than the rest of the world with minimal deaths.

Narinder Kumar Mehra is the ICMR National chair and former Dean of the All India Institute of Medical Sciences, New Delhi

The views expressed are personal

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Can India be an outlier in the spread of Covid-19? | Opinion - Hindustan Times

The McKusick-Nathans Institute of Genetic Medicine | Department of Genetic Medicineseeks to further the understanding of human heredity and genetic medicine and use that knowledge to treat and prevent disease.

The Department of Genetic Medicineis working to consolidate all relevant teaching, patient care and research in human and medical genetics at Johns Hopkins to provide national and international leadership in genetic medicine. The Department of Genetic Medicineserves as a focal point for interactions between diverse investigators to promote the application of genetic discoveries to human disease and genetics education to the public. It builds upon past strengths and further develops expertise in the areas of genomics, developmental genetics and complex disease genetics. The Department of Genetic Medicineworks to catalyze the spread of human genetic perspectives to other related disciplines by collaboration with other departments within Johns Hopkins.

There are more than 300 dedicated employees in the Department of Genetic Medicine, fulfilling the Johns Hopkins tripartite mission of research, teaching and patient care. They include 45 full-time faculty, 15 residents, more than 70 graduate students and 200 staff.

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Institute of Genetic Medicine | Johns Hopkins Medicine

Scientists and doctors have been studying genes and hereditary conditions (those handed down from parent to child) for many years. These days, it's possible for someone to have a genetic test for a number of illnesses. A blood sample is taken and closely examined for abnormal chromosomes, but because so much information is stored on the DNA, scientists only tend to look for particular disorders.

Genomic medicine is the field of study that looks into genes (our DNA) and their interaction with our health. Genomics investigates the complex biological details of an individual and the use of these for effective diagnosis and tailor-made treatment.

While genetics looks at specific genes or groups of 'letters' along the DNA strand, genomics refers to the study of someone's entire genetic makeup. It's about how they relate and react with each other and is associated with conditions that have a broader range of triggers such as diabetes, heart disease, cancer and asthma.

Genomic medicine can help in many ways:

This greater understanding of the links between biology and disease brings benefits on several levels.

There are a number of types of service provider. In the U.K., for example, the National Health Service employs 90 consultant clinical geneticists at 25 centres. They're supported by hundreds of specifically trained staff.5 Referral is usually through a general practitioner (GP or family doctor) and is available to those who are worried about a serious genetic family condition or a family tendency towards developing cancer, or to parents of a child with learning difficulties and other developmental problems looking for an expert assessment.

In places where a public service isn't available, or for those who choose to seek private health care treatment, check to make sure that the clinic you're using has the necessary registration (for example, in the UK this is through the Care Quality Commission, also known as the CQC6) and the lab is also correctly accredited.

Whatever the setting, the appointment might take some time and you may need to bring other members of your family with you. Your family and medical history will be mapped and explored, and it's likely you'll have a medical examination too. Finding out that there may be a life-changing or life-limiting condition in your future is a serious and, for some, traumatic experience. Alongside counselling, you may be offered tests (including blood tests)with the option of having these done on the day or, if you need time to think about the possible implications, to come back at a later date.

Results can take weeks or even months to return (depending on the rarity of the genetic abnormality and how easy it is to find) but pre-natal test results will be returned much sooner.

Aftercare then depends on the results and the nature of what you're being tested for. Some people will be referred back to their family doctor along with full details, or they may go on to receive treatment at a specialist unit. Those who are aren't showing symptoms will be given support and advice about lifestyle changes, in order to minimise their risk, and advice about managing their potential condition in the future.

There are also a number of private companies who offer genetic testing by mail. It involves having a cheek swab or a blood sample taken at a local clinic. It's then sent off to the laboratory. The kinds of things tested for include genetic risk for diabetes and heart conditions, as well as ancestry information. Some companies deliver more of a service than others, with counsellors or other health professionals on hand to help. Convenient (but not necessarily cheap), it must be remembered that this is genetic testing without the usual level of holistic support found in established clinics.

The broad area known as genomic medicine is evolving the study of genetic mutation pathways and their variations is particularly exciting. But what does this mean for people on a practical level? As discussed earlier, there are some hereditary diseases that are difficult to diagnose simply because of the wide range of genes involved.

Scientists are working towards finding a chemical or genetic bottleneck for conditions like these. The ability to switch off a vital reaction along the pathway from genetic trigger to hay fever, dust allergy, or asthma, for example, would aid diagnosis and treatment, and possibly whether or not these traits need cause misery for the next generation.7

The emerging field of epigenetics takes this idea one step further. It's based on the concept that each gene has its own chemical tag that tells the gene how to act. It is possible to turn the gene off (make it dormant) or turn it on (make it active) according to its chemical tag. In this way, the genetic code remains the same but the way in which it is expressed changes.8

This is a very exciting development. If things such as what we eat and drink and how much we sleep affect the way our genetic code manifests itself, what are the implications for disease and ageing? The times when genes are switched from a healthy, normal state into one that causes disease and the end of life?

These chemical modifications can also be passed on to the next generation, creating a more variable level to genetic inheritance. In other words, your lifestyle choices can affect your childs health in a negative or positive way on a basic, biological level.

Advances in genomic medicine mean that more diseases, both rare and more common, can be diagnosed and treated than ever before. But there are a few things to consider:

By understanding that which is already written down in our genetic code, we can predict and manage what happens in the future. New advances in genomic medicine create an environment where we can make sound health care plans, seek advice, and get treatment in the vital early stages of disease.

On a personal level, this doesn't stop at us the principles behind epigenetics suggest that our everyday habits what we eat and whether we smoke can have a positive or negative effect on our grandchildren's biology, meaning that our genetic legacy is also well worth taking care of. At Aetna International, we may cover gene testing on a case by case basis, for example if an oncologist needs to determine the most suitable treatment for a member with cancer.

Read our article: How genetic information can support your familys health: a guide.

For more information on international private medical insurance and accessing the best health care for you and your family, contact one of Aetna International's expert sales consultants today.

Are you looking for expat insurance? Click here to get a quote.

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What is genomic medicine? An introduction to genetics in ...

Another component of more regular monitoring is using sensors for continuous, remote evaluation of blood pressure, breathing, body temperature and other signs, whichideallycould allow providers to intervene when health starts to deteriorate, as opposed to after a patient starts reporting symptoms.

Its not a new idea. But Dr. Steve Xu, medical director at Northwestern Universitys Center for Bio-Integrated Electronics, said he envisions a world where patients could one day have implanted sensors that not only monitor vital signs but also provide automated health insightstransforming healthcare into a system where patients are constantly provided feedback on their health status.

He said he could see that proliferating in the next 20 years, and doesnt think an implantable sensor would be an insurmountable privacy concern for patients. Implantable devices are already being used in healthcare, including birth-control implants and nerve stimulators. However, it would be on companies to provide evidence that these sensors are actually helpful for patient health and transparency into how the data is being used.

Xus research at Northwestern involves working on wearable sensors for pediatric care, such as to better monitor newborns who are born prematurely. Already, one-third of consumers report owning a wearable device to help track their health, according to a 2019 report from the Stanford Medicine Center for Digital Health and early-stage digital health venture fund Rock Health. While most of those devices track more general exercise, sleep and heart rate, and arent used for medical care, they could point to patient interest and comfort with monitoring health data.

And health systems have been looking at the space more closely too. To lay the groundwork for better remote monitoring of patients, such as after discharge, UCHealth in Colorado partnered with startup BioIntelliSense to help develop its health-monitoring patch, as well as to support the company as it sought regulatory clearance. About the size of a Band-Aid, the patch continuously tracks metrics like heart rate, skin temperature and respiratory rate and sends the data back to a provider.

BioIntelliSense earned U.S. Food and Drug Administration clearance for the device earlier this year.

Xu said he expects to see a tipping point within the next decade when almost everyone will collect data with wearable devices, sensors or patches, which can be linked with medical records.

He points to how in the 1980s, it was difficult to imagine everyone would have a cellphone. Flip phones in the mid-2000s provided a shift in perspectiveMotorola came out with the Razr flip phone, and that was a turning point, where things were really coolbut it wasnt until the BlackBerry and Apples iPhone that adoption really took off.

While wearables available today have shown promise for fitness tracking and some limited medical functions like conducting electrocardiograms, theres still opportunities for what the future is, Xu said, which developers will continue to build on. I think these wearables are probably at the flip-phone stage, he added.

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Biotech innovations to spur next phase of personalized care - ModernHealthcare.com

A new international project aims to enroll 500 COVID-19 patients to search for genetic mutations that make some people more vulnerable to severe infection.

HHMI scientists are joining many of their colleagues worldwide in working to combat the new coronavirus.Theyre developing diagnostic testing, understanding the viruss basic biology, modeling the epidemiology, and developing potential therapies or vaccines. Over the next several weeks, we will be sharing stories of some of this work.

Hundreds of clinicians worldwide are banding together in an effort to study some types ofseverecases of the new coronavirus disease.

The project, led by Howard Hughes Medical Institute (HHMI) Investigator Jean-Laurent Casanova at The Rockefeller University, seeks to identify genetic errors that make some younger patients especially vulnerable to the virus that causes COVID-19, the infectious respiratory illness also known as coronavirus disease 2019.

Casanova aims to enroll 500 patients internationally who meet three broad criteria: theyre less than 50 years old, have been diagnosed with COVID-19 and admitted to an intensive care unit, and have no serious underlying illnesses, such as diabetes, heart disease, or lung disease.

By studying these patients' DNA, scientists may pinpoint genetic mutations that make some people more susceptible to infection. Such information could one day help doctors identify people who are most at risk of developing severe coronavirus disease, says Casanova, a pediatrician at Rockefeller. It could also offer clues for scientists searching for new therapeutics. For example, if patients cells arent making enough of a particular molecule, doctors may be able to offer a supplement as treatment.

Were going to try to find the genetic basis of severe coronavirus infection in young people.

Jean-Laurent Casanova, HHMI Investigator at The Rockefeller University

That day may still be years away. This is not a short-term effort, Casanova says. Some scientists have hypothesized that COVID-19 might be a seasonal illness, with infections ebbing in the spring and summer, and then returning in the fall. But Casanovas team is optimistic. They have already begun enrolling patients and have started sequencing their exomes spelling out all of the DNA letters in every gene in a persons genome. Were going to try to find the genetic basis of severe coronavirus infection in young people.

Late last year, when the first coronavirus infections began cropping up in China, Casanova started reaching out to his colleagues there. Though the most severe cases seemed to concentrate among older adults and those with other conditions, Casanova was interested in the outliers kids and young adults hit hard by the illness who didnt have any of the usual risk factors, such as age or underlying illness.

His team kicked off a new project to study these mysterious cases, and in January just weeks after the Wuhan outbreak began enrolling patients. Clinicians mailed patient blood and DNA to his lab, and researchers there and elsewhere began processing samples the first steps needed for scientists to peer into patients genomes. Now, the project is global, and Casanova is collaborating with scientists and healthcare workers from Europe to Africa, Asia, and Oceania.

We will recruit children and adults <50 yo without risk factor admitted to ICU for idiopathic #COVID19. We will test the hypothesis that they carry inborn errors of immunity to this virus. Please refer patients to @casanova_lab and please RT. pic.twitter.com/DXPoFKieEy

Hunting for the genetic underpinnings of severe infectious diseases is nothing new for Casanovas team. What were doing with coronavirus is what my lab has been doing for 25 years with other infections, he says.

They look for weak spots in peoples immune systems small genetic changes that make people more vulnerable to disease. His group has previously searched the genomes of patients infected with viruses, bacteria, fungi, and even parasites. The infection closest to COVID-19 his team has studied is severe influenza pneumonitis, for which theyve discovered three genetic links. Theyve also identified specific genetic errors that can predispose patients with herpes to viral encephalitis. And theyve found that children with mutations in an immunity gene called IFN-gamma are vulnerable to the bacteria that cause tuberculosis. These children make low levels of the IFN-gamma protein, which is critical for fighting off bacterial infections.

Casanovas team has put these findings to use clinically. For example, the researchers have shown that tuberculosis patients with these genetic errors can benefit from treatment with IFN-gamma. Hes hoping to identify problematic genes in patients with severe coronavirus infection that can bring similar clinical gains. These genes could tell scientists which cellular defenses are crucial for warding off COVID-19 and pave the way for understanding whether such defenses are derailed in older adults or patients with an underlying medical condition.

In the US and around the world, severe coronavirus disease seems to hit older patients hardest, though scientists have reported some country-to-country variation. As of March 24, more than 44,000 confirmed and presumptive positive cases have been reported in the US. Fatality has been highest in people over 85 years old, according to a recent report from the Centers for Disease Control and Prevention (CDC). Though young people may be more susceptible than scientists once suspected,the older you are, the higher the likelihood you have a severe form of the disease, Casanova says.

Last week, Rockefeller closed all labs except those working on the coronavirus, and Casanova whittled his team to a skeleton crew of about eight people down from 35 who rotate so there is only one person per room at a time. He and his lab members are following CDC recommendations, and taking protective measures to keep themselves and others safe, including social distancing, washing hands, and disinfecting surfaces. Theyve also taken to Twitter to get the word out about their work. A tweet posted from Casanovas lab last week about recruiting new patients to their study has since been retweeted more than 400 times.

Soon, theyll be testing their genetic theory on a pandemic thats occurring in real time. Im grateful weve been able to start this new project so quickly, he says. God willing, it will be of clinical usein two or three years.

Follow the Casanova lab on Twitter (@casanova_lab) to learn the latest about their work. Doctors interested in enrolling patients in the study can contact Jean-Laurent Casanova at jean-laurent.casanova@rockefeller.edu.

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Patients with Severe Forms of Coronavirus Disease Could Offer Clues to Treatment - Howard Hughes Medical Institute

Battelle and The Ohio State University Wexner Medical Center have jointly developed a new rapid, sensitive diagnostic test for COVID-19. The Ohio State Wexner Medical Center will administer the new test under its existing FDA certification permits. This will increase and improve test processing in Ohio according to existing state clinical guidelines.

The new rapid test will allow for faster turnaround time on test results, which will help flatten the curve.

Battelle researchers spent several weeks working in the companys West Jefferson labs to develop a diagnostic assay and complete a validation process, with early results suggesting exceptionally high sensitivity.

Since March 14, more than 100 Ohio State Wexner Medical Center researchers and clinicians have worked with Battelle researchers nights and weekends to stand up the lab that will support COVID-19 testing. After enough data was gathered by researchers at both institutions, Ohio State processed its first 91 tests for diagnosis Wednesday using cutting-edge Battelle and Ohio State equipment in a Centers for Medicare & Medicaid Services (CMS)-certified pathology lab at Ohio State.

Battelle is now working to bring a second lab online in West Jefferson, with the intent of making more test processing available. Battelle is in the process of receiving a Clinical Laboratory Improvement Amendment (CLIA) from CMS to begin its own clinical testing.

Ohio State and Battelle teams have shown incredible leadership and ingenuity in moving this project forward so rapidly, said Ohio Gov. Mike DeWine. With this collaboration, we will increase testing right here in Ohio to better help health care professionals and public health officials understand, treat and prevent the spread of the virus.

Results of the test can be available in as few as five hours. Initially, the system can process approximately 200 tests per day, but when the infrastructure is fully built over the coming weeks, the goal is to process more than 1,000 test swabs per day.

Battelle has decades of experience in infectious disease research and has worked with virtually all federal health and national security agencies to respond to emerging health threats, said Lou Von Thaer, Battelles president and CEO. I am incredibly proud of the Battelle team, the speed at which it was able to work around the clock to quickly get this operational, and our collaboration with The Ohio State University.

Battelles infectious disease, genetic and virology experts teamed up with researchers and scientists across Ohio States College of Medicine, including immunologists, microbiologists, pathologists, epidemiologists and data analytics researchers for this project.

Were proud of the partnership of our dedicated scientists with Battelle researchers to help find innovative solutions for the coronavirus pandemic sweeping the world, said Dr. Hal Paz, executive vice president and chancellor for health affairs at Ohio State and CEO of the Ohio State Wexner Medical Center. Our physicians and nurses are eager to start administering these tests that will greatly increase our capacity to diagnose more people and assist us in finding solutions for this disease. Testing is just one of more than 50 new research areas aimed at combatting COVID-19 underway at the Wexner Medical Center. We are working hand in hand with Battelle on many of these critical projects.

Battelle is contributing its expertise and using its specialty facilities, including the largest, private BSL-3 laboratory in the United States, and is actively working on several other solutions related to the COVID-19 pandemic.

COVID-19 testing requires an order from a physician or other advanced practice provider. Based on feedback from the Ohio Department of Health, testing is prioritized for inpatients in hospitals and other facilities, outpatients who are moderately ill but who are at high risk for serious illness (e.g, elderly, immune compromised, underlying lung disease, etc.), health care providers and first responders. Asymptomatic patients do not need to be tested.

People who believe they need to be tested should contact their primary care provider, local hospital or your local health department for further direction.

Here is the original post:

Battelle and Wexner Medical Center create new diagnostic test for COVID-19 - The Ohio State University News

An epidemiologist answers the biggest questions she's getting about coronavirus. Wochit

SAN FRANCISCO At least eight strains of the coronavirusare making their way around the globe, creating a trail of death and disease that scientistsare tracking by their genetic footprints.

While much is unknown, hidden in the virus's unique microscopic fragments are clues to the origins of its original strain, how it behaves as it mutates and which strains are turning into conflagrations while others are dying out thanksto quarantine measures.

Huddled in once bustling and now almost empty labs, researchers who oversaw dozens of projects are instead focused on one goal:tracking the currentstrains of the SARS-CoV-2 virus that cause the illness COVID-19.

We're sending daily coronavirus updates: Get USA TODAY's Daily Briefing in your inbox

Labs around the world are turning their sequencing machines, most about the size of a desktop printer, to the task ofrapidly sequencing the genomes of virus samples taken frompeople sick with COVID-19.The information is uploaded to a website called NextStrain.org that shows how the virus is migrating and splitting into similarbut new subtypes.

While researcherscaution they'reonly seeing the tip of the iceberg, the tiny differences between the virus strains suggest shelter-in-place orders are working in some areas and thatno one strain of the virus ismore deadly than another. They also say it does not appear the strains will grow more lethal as theyevolve.

The virus mutates so slowly that the virus strains are fundamentally very similar to each other, said Charles Chiu, a professor of medicine and infectious disease at the University of California, San Francisco School of Medicine.

A map of the main known genetic variants of the SARS-CoV-2 virus that causes COVID-19 disease. The map is being kept on the nextstrain.org website, which tracks pathogen evolution.(Photo: nextstrain.org)

Investigation:How federal health officials mislead states and derailed the best chance at containment.

The SARS-CoV-2 virusfirst began causing illness in China sometimebetween mid-November and mid-December. Its genome is made up of about 30,000 base pairs. Humans, by comparison, have more than 3 billion. So fareven in the virus's most divergent strainsscientists have found only 11 base pair changes.

That makes iteasy to spot new lineages as they evolve, said Chiu.

The outbreaks are trackable. We have the ability to do genomic sequencing almost in real-time to see what strains or lineages are circulating, he said.

So far, mostcases on the U.S. West Coast are linked to a strainfirst identified in Washington state. It may have come from a man who had been in Wuhan, China, the virus epicenter, and returned home on Jan. 15. It is only three mutations away from the original Wuhan strain, according to work done early in the outbreakby Trevor Bedford, a computational biologist at Fred Hutch, a medical research center in Seattle.

On the East Coast there are several strains, including the one from Washington and others that appear to have made their way from China to Europe and then to New York and beyond, Chiu said.

Death rate soars in New Orleans coronavirus 'disaster' that could define city for generations

Charles Chiu, MD, PhD, director of the UCSF-Abbott Viral Diagnostics and Discovery Center, inserts a tray of Universal Transport Medium (UTM) or vials for the collection, transport, maintenance and long term freeze storage of viruses into a Biomatrix sorter that the Chiu Lab will be using, starting Monday to study the genes of the Coronavirus.(Photo: Susan Merrell/UCSF)

This isnt the first time scientists have scrambled to do genetic analysis of a virus in the midst of an epidemic. They did it with Ebola, Zika and West Nile, but nobodyoutside the scientific community paid much attention.

This is the first time phylogenetic trees have been all over Twitter, said Kristian Andersen, a professor at Scripps Research, a nonprofit biomedical science research facility in La Jolla, California, speaking of the diagrams that show the evolutionary relationships between different strains of an organism.

The maps are available on NextStrain, an online resource for scientists that uses data from academic, independent and government laboratories all over the world to visually track the genomics of the SARS-CoV-2 virus. It currently represents genetic sequences of strains from 36 countries on six continents.

While the maps are fun, they can also be a little dangerous said Andersen. The trees showing the evolution of the virus are complex and its difficult even for experts to draw conclusions from them.

Remember, were seeing a very small glimpse into the much larger pandemic. We have half a million described cases right now but maybe 1,000 genomes sequenced. So there are a lot of lineages were missing, hesaid.

The basics on the coronavirus: What you need to know as the US becomes the new epicenter of COVID-19

COVID-19 hitspeople differently, with some feeling only slightly under the weather for a day, others flat on their backs sick for two weeks and about 15% hospitalized. Currently, an estimated1% of those infected die. The rate varies greatly by country and experts say it is likely tied to testing rates rather than actual mortality.

Chiu says it appears unlikely the differences are related to people being infected withdifferent strains of the virus.

The current virus strains are still fundamentally very similar to each other, he said.

The COVID-19 virus does not mutate very fast. It does so eightto 10 times more slowly than the influenza virus, said Anderson, making its evolution rate similar to other coronaviruses such asSevere Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS).

Its also not expected tospontaneously evolve into a form more deadly than it already is to humans. The SARS-CoV-2 is so good at transmitting itself between human hosts,said Andersen,it is under no evolutionary pressure to evolve.

Chius analysis shows Californias strict shelter in place efforts appear to beworking.

Over half of the 50 SARS-CoV-2 virus genomes his San Francisco-based lab sequenced in the past two weeks are associated with travel from outside the state. Another 30% are associated with health care workers and families of people who have the virus.

Only 20% are coming from within the community. Its not circulating widely, he said.

Thats fantastic news, he said, indicating the virus has not been able to gain aserious foothold because of social distancing.

It's like a wildfire, Chiu said. A few sparks might fly off the fire and land in the grass and start new fires. But if the main fire is doused and itsembers stomped out, you can kill offan entire strain.In California, Chiu sees a lot of sparks hitting the ground, most coming from Washington,but they're quickly being put out.

Get daily coronavirus updates in your inbox: Sign up for our newsletter now.

An example wasa small cluster of cases in Solano County, northeast of San Francisco. Chius team did a genetic analysis of the virus that infected patients there and found it was most closely related to a strain from China.

At the same time, his lab was sequencing a small cluster of cases in the city of Santa Clara in Silicon Valley. They discovered the patients there had the same strain as those in Solano County. Chiu believes someone in that cluster had contact with a traveler who recently returned from Asia.

This is probably an example of a spark that began in Santa Clara, may have gone to Solano County but then was halted, he said.

The virus, he said, can be stopped.

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China is an unknown

So far researchers dont have a lot of information about the genomics of the virus inside China beyond the fact that it first appeared in the city of Wuhan sometime between mid-November and mid-December.

The viruss initial sequence was published on Jan. 10 by professor Yong-Zhen Zhang at the Shanghai Public Health Clinical Center. But Chiu says scientists dont know if there was justone strain circulating in China or more.

It may be that they havent sequenced many cases or it may be for political reasons they havent been made available, said Chiu. Its difficult to interpret the data because were missing all these early strains.

Researchers in the United Kingdom who sequenced the genomes of viruses found in travelers from Guangdong in south China found those patients strains spanned the gamut of strains circulating worldwide.

That could mean several of the strains were seeing outside of China first evolved there from the original strain, or that there are multiple lines of infection. Its very hard to know, said Chiu.

There's a new symptom of coronavirus, docs say: Sudden loss of smell or taste

While there remain many questions about the trajectory of the COVID-19 disease outbreak, one thing is broadly accepted in the scientific community: Thevirus was not created in a lab but naturally evolved in an animal host.

SARS-CoV-2s genomic molecular structure thinkthe backbone of the virus is closest to a coronavirus found in bats. Parts of its structure also resemble a virus found in scaly anteaters, according to a paper published earlier this month in the journal Nature Medicine.

Someone manufacturing a virus targetingpeople would have started with one that attacked humans, wrote National Institutes of Health Director Francis Collinsin an editorial that accompanied the paper.

Andersen was lead author on the paper. He said it could have been a one-time occurrence.

Its possible it was a single event, from a single animal to a single human, and spread from there.

Read or Share this story: https://www.usatoday.com/story/news/nation/2020/03/27/scientists-track-coronavirus-strains-mutation/5080571002/

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8 strains of the coronavirus are circling the globe. Here's what clues they're giving scientists. - USA TODAY

Hidden in the virus's unique microscopic fragments are clues to the origins of its original strain. So far, mostcases on the U.S. West Coast are linked to a strainfirst identified in Washington state

SAN FRANCISCO At least eight strains of the coronavirus are making their way around the globe, creating a trail of death and disease that scientistsare tracking by their genetic footprints.

While much is unknown, hidden in the virus's unique microscopic fragments are clues to the origins of its original strain, how it behaves as it mutates and which strains are turning into conflagrations while others are dying out thanksto quarantine measures.

Huddled in once bustling and now almost empty labs, researchers who oversaw dozens of projects are instead focused on one goal:tracking the currentstrains of the SARS-CoV-2 virus that cause the illness COVID-19.

This story is provided free to the community to keep readers informed about coronavirus. | If local news is important to you, please consider a digital subscription.

Labs around the world are turning their sequencing machines, most about the size of a desktop printer, to the task ofrapidly sequencing the genomes of virus samples taken frompeople sick with COVID-19.The information is uploaded to a website called NextStrain.org that shows how the virus is migrating and splitting into similarbut new subtypes.

While researcherscaution they'reonly seeing the tip of the iceberg, the tiny differences between the virus strains suggest shelter-in-place orders are working in some areas and thatno one strain of the virus ismore deadly than another. They also say it does not appear the strains will grow more lethal as theyevolve.

"The virus mutates so slowly that the virus strains are fundamentally very similar to each other," said Charles Chiu, a professor of medicine and infectious disease at the University of California, San Francisco School of Medicine.

The SARS-CoV-2 virusfirst began causing illness in China sometimebetween mid-November and mid-December. Its genome is made up of about 30,000 base pairs. Humans, by comparison, have more than 3 billion. So fareven in the virus's most divergent strainsscientists have found only 11 base pair changes.

That makes iteasy to spot new lineages as they evolve, said Chiu.

"The outbreaks are trackable. We have the ability to do genomic sequencing almost in real-time to see what strains or lineages are circulating," he said.

So far, mostcases on the U.S. West Coast are linked to a strainfirst identified in Washington state. It may have come from a man who had been in Wuhan, China, the virus epicenter, and returned home on Jan. 15. It is only three mutations away from the original Wuhan strain, according to work done early in the outbreakby Trevor Bedford, a computational biologist at Fred Hutch, a medical research center in Seattle.

On the East Coast there are several strains, including the one from Washington and others that appear to have made their way from China to Europe and then to New York and beyond, Chiu said.

Beware pretty phylogenetictrees

This isnt the first time scientists have scrambled to do genetic analysis of a virus in the midst of an epidemic. They did it with Ebola, Zika and West Nile, but nobodyoutside the scientific community paid much attention.

"This is the first time phylogenetic trees have been all over Twitter," said Kristian Andersen, a professor at Scripps Research, a nonprofit biomedical science research facility in La Jolla, California, speaking of the diagrams that show the evolutionary relationships between different strains of an organism.

The maps are available on NextStrain, an online resource for scientists that uses data from academic, independent and government laboratories all over the world to visually track the genomics of the SARS-CoV-2 virus. It currently represents genetic sequences of strains from 36 countries on six continents.

While the maps are fun, they can also be "little dangerous" said Andersen. The trees showing the evolution of the virus are complex and its difficult even for experts to draw conclusions from them.

"Remember, were seeing a very small glimpse into the much larger pandemic. We have half a million described cases right now but maybe 1,000 genomes sequenced. So there are a lot of lineages were missing," hesaid.

Different symptoms, same strains

COVID-19 hitspeople differently, with some feeling only slightly under the weather for a day, others flat on their backs sick for two weeks and about 15% hospitalized. Currently, an estimated1% of those infected die. The rate varies greatly by country and experts say it is likely tied to testing rates rather than actual mortality.

Chiu says it appears unlikely the differences are related to people being infected withdifferent strains of the virus.

"The current virus strains are still fundamentally very similar to each other," he said.

The COVID-19 virus does not mutate very fast. It does so eightto 10 times more slowly than the influenza virus, said Anderson, making its evolution rate similar to other coronaviruses such asSevere Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS).

Its also not expected tospontaneously evolve into a form more deadly than it already is to humans. The SARS-CoV-2 is so good at transmitting itself between human hosts,said Andersen,it is under no evolutionary pressure to evolve.

Shelter in place working in California

Chius analysis shows Californias strict shelter in place efforts appear to beworking.

Over half of the 50 SARS-CoV-2 virus genomes his San Francisco-based lab sequenced in the past two weeks are associated with travel from outside the state. Another 30% are associated with health care workers and families of people who have the virus.

"Only 20% are coming from within the community. Its not circulating widely," he said.

Thats fantastic news, he said, indicating the virus has not been able to gain aserious foothold because of social distancing.

It's like a wildfire, Chiu said. A few sparks might fly off the fire and land in the grass and start new fires. But if the main fire is doused and itsembers stomped out, you can kill offan entire strain.In California, Chiu sees a lot of sparks hitting the ground, most coming from Washington,but they're quickly being put out.

An example wasa small cluster of cases in Solano County, northeast of San Francisco. Chius team did a genetic analysis of the virus that infected patients there and found it was most closely related to a strain from China.

At the same time, his lab was sequencing a small cluster of cases in the city of Santa Clara in Silicon Valley. They discovered the patients there had the same strain as those in Solano County. Chiu believes someone in that cluster had contact with a traveler who recently returned from Asia.

"This is probably an example of a spark that began in Santa Clara, may have gone to Solano County but then was halted," he said.

The virus, he said, can be stopped.

China is an unknown

So far researchers dont have a lot of information about the genomics of the virus inside China beyond the fact that it first appeared in the city of Wuhan sometime between mid-November and mid-December.

The viruss initial sequence was published on Jan. 10 by professor Yong-Zhen Zhang at the Shanghai Public Health Clinical Center. But Chiu says scientists dont know if there was justone strain circulating in China or more.

"It may be that they havent sequenced many cases or it may be for political reasons they havent been made available," said Chiu. "Its difficult to interpret the data because were missing all these early strains."

Researchers in the United Kingdom who sequenced the genomes of viruses found in travelers from Guangdong in south China found those patients strains spanned the gamut of strains circulating worldwide.

"That could mean several of the strains were seeing outside of China first evolved there from the original strain, or that there are multiple lines of infection. Its very hard to know," said Chiu.

The virus did not come from a lab

While there remain many questions about the trajectory of the COVID-19 disease outbreak, one thing is broadly accepted in the scientific community: Thevirus was not created in a lab but naturally evolved in an animal host.

SARS-CoV-2s genomic molecular structure thinkthe backbone of the virus is closest to a coronavirus found in bats. Parts of its structure also resemble a virus found in scaly anteaters, according to a paper published earlier this month in the journal Nature Medicine.

Someone manufacturing a virus targetingpeople would have started with one that attacked humans, wrote National Institutes of Health Director Francis Collinsin an editorial that accompanied the paper.

Andersen was lead author on the paper. He said it could have been a one-time occurrence.

"Its possible it was a single event, from a single animal to a single human," and spread from there.

Originally posted here:

8 strains of coronavirus are circling the globe; heres the clues theyre giving scientists - Canton Repository

DetailsCategory: Small MoleculesPublished on Tuesday, 31 March 2020 10:23Hits: 79

MAVERICK-HCM Phase 2 Clinical Trial Results Consistent with Tolerability Observations from Prior Studies of Mavacamten

Improvement in NT-proBNP and Troponin Levels Support Future Development in Non-Obstructive HCM and Heart Failure with Preserved Ejection Fraction (HFpEF)

BRISBANE, CA, USA I March 30, 2020 I MyoKardia, Inc. (Nasdaq: MYOK) today announced results from the dose-ranging MAVERICK-HCM Phase 2 clinical trial of mavacamten for the treatment of non-obstructive hypertrophic cardiomyopathy (HCM). Data were presented during a late-breaker session at the American College of Cardiologys 69th Annual Scientific Session together with the World Congress of Cardiology (ACC.20/WCC Virtual) In the MAVERICK-HCM study, mavacamten was generally well tolerated, and statistically significant improvements in key biomarkers of cardiac injury and wall stress were observed. Further, subgroup analyses of study participants with indicators of more advanced disease demonstrated clinical responses across multiple parameters among patients on active treatment versus placebo.

Non-obstructive HCM is especially challenging to treat as there are no proven or approved pharmacological therapies. Thus, for patients who develop symptoms refractory to medications, cardiac transplantation may be the only option, saidCarolynHo, M.D., Medical Director of the Cardiovascular Genetics Center at Brigham and Womens Hospital and lead author on behalf of the MAVERICK-HCM study investigators. Although the primary objective of MAVERICK was to assess the safety and tolerability of mavacamten in non-obstructive HCM, in exploratory analyses we observed an encouraging result with reductions in serum levels of NT-proBNP, a biomarker of hemodynamic stress, and also cardiac troponin I, a biomarker of myocardial injury. We believe MAVERICK is the first study to show an improvement in important serum biomarkers in this patient population and suggests that there is potential physiological benefit from the drug. We were also intrigued by findings that patients with more severe disease expression, those with elevated serum troponin levels or evidence of diastolic dysfunction by echo, may have achieved functional benefit. These findings, combined with mavacamtens tolerability profile, are encouraging, and they provide direction for further evaluation of mavacamten for patients with non-obstructive HCM.

MAVERICK has succeeded in providing us with the important data we needed to proceed in our planned clinical trials in non-obstructive HCM, as well as a targeted subset of patients with heart failure with preserved ejection fraction, or HFpEF. We gained unique insights into dosing strategies using markers linked to clinical benefit, as well as how to identify patients who may be most likely to benefit from mavacamten, said Jay Edelberg, M.D. Ph.D., MyoKardias Senior Vice President of Development. The MAVERICK results also further our confidence in mavacamtens development in obstructive HCM, as we approach our Phase 3 EXPLORER-HCM readout, which is expected in the second quarter.

MAVERICK-HCM ResultsSafety and Tolerability ObservationsMavacamten was generally well tolerated, consistent with prior clinical studies.

Effect on Exploratory Endpoints of Efficacy: Biomarkers of Cardiac Wall Stress and Injury Among several pre-specified endpoints analyzed, treatment with mavacamten resulted in significant changes in circulating biomarkers associated with heightened risks of cardiac complications.

For the intent-to-treat population, no difference was observed between active and placebo groups in the other exploratory endpoints.

The effect of mavacamten on NT-proBNP and cardiac troponin levels in non-obstructive HCM patients is a first-of-its-kind finding for a product candidate in this patient population, said Michael R.Zile, M.D.,Director of Cardiology, Ralph H. Johnson VA Medical Center. NT-proBNP is a measure of cardiac wall stress, and elevated troponins signal heart muscle injury, both of which have been established in the literature as prognosticators of dire complications in both HCM and HFpEF patients, including the need for hospitalizations, surgical intervention and death. The reductions in biomarkers associated with poor outcomes are encouraging, and I look forward to seeing the potential for mavacamten to impact outcomes in HCM, as well as certain targeted HFpEF populations, over time.

Patient Subgroups with Advanced Diastolic Disease MyoKardia also shared its analyses of the effect of mavacamten treatment on two subgroups of patients with advanced disease: one comprising 19 of the 59 enrolled patients (32%) with elevated cardiac troponin levels of >0.03ng/mL and another including 25 patients (42%) who had elevated filling pressures, defined by E/e >14(4). HCM patients with higher cardiac troponin levels are known to be at greater risk for serious complications, and elevated filling pressures are indicative of impaired diastolic compliance, or the ability of the left ventricle to relax and fill with oxygenated blood.

A trend toward potential benefit was observed across numerous clinical measurements in patients with elevated cardiac troponin I levels and those with higher diastolic filling pressures versus placebo:

Composite Functional Endpoint Analysis A composite functional endpoint(4) analysis was utilized to compare responses among the intent-to-treat population and the subgroups of patients with more advanced disease to those within the placebo population.

Based on our observations that multiple markers responded to mavacamten, we believe we may be able to utilize markers of likely clinical benefit to guide dosing in the non-obstructive HCM patient population moving forward, similar to the way we are utilizing LVOT gradient to guide dosing in obstructive HCM, said Jay Edelberg, M.D., Senior Vice President, Development at MyoKardia. Additionally, we observed in MAVERICK that patients who were most impaired showed the most meaningful trends toward benefit with mavacamten treatment within the 16-week treatment period. We look forward to leveraging these learnings, as well as knowledge gained from the longer exposures to treatment provided by our long-term extension study, as we look to advance mavacamten for the treatment of non-obstructive HCM patients and adjacent HFpEF populations.

Data from the MAVERICK-HCM Phase 2 clinical trial were presented by Carolyn Ho, M.D., Medical Director of the Cardiovascular Genetics Center at Brigham and Women's Hospital and Associate Professor of Medicine at Harvard Medical School, during the American College of Cardiologys Annual Scientific Session together with World Congress of Cardiology virtual meeting this morning during the Featured Clinical Research III Session in a presentation titled Mavacamten Improves Biomarkers Of Myocardial Wall Stress And Injury In Patients With Symptomatic Non-Obstructive Hypertrophic Cardiomyopathy (nHCM): Results From The Phase 2 MAVERICK-HCM Study (#412-16).

About the Phase 2 MAVERICK-HCMClinical TrialThe Phase 2 MAVERICK-HCM trial assessed the safety and tolerability of a range of exposures over 16 weeks of treatment in patients with symptomatic, non-obstructive HCM. All study participants were required to be diagnosed with non-obstructive HCM, with left ventricular wall thickness either 15mm or 13mm with a family history of HCM,New York Heart Association(NYHA) classifications of Class II or III, and NT-proBNP levels of greater than 300 pg/mL at rest.Baseline characteristics, such as age, weight, gender, pathogenic mutation status, background beta blocker use, NYHA classification and exercise capacity were evenly distributed between active and placebo arms.

A total of 59 participants were enrolled in the study and randomized into one of three groups to receive once-daily doses of mavacamten or placebo.The active mavacamten treatment arms were designed to assess a range of drug concentrations around target levels of 200 ng/mL and 500 ng/mL. All participants in the active treatment arms began the study receiving 5mg doses of mavacamten. At Week 4, pharmacokinetic (PK) assessments were conducted and doses were adjusted in a blinded fashion per the protocol based on the participants assigned cohort. Following the 16-week treatment period, participants were monitored for an additional 8 weeks and became eligible to participate in MyoKardias MAVA Long-Term Extension (LTE) study.

Conference Call and WebcastMyoKardia management will also host a virtual event for investors and analyst today to review the data from MAVERICK-HCM and discuss future development plans for mavacamten in targeted groups of patients with diastolic disease. This live webcast event will begin at 4:30 p.m. EDT / 1:30 p.m. PDT and include remarks by Dr. Anjali Owens, Medical Director, Center for Inherited Cardiac Disease at the University of Pennsylvania, and Dr. Michael Zile, Professor of Medicine at the Medical University of South Carolina.

To access the call, please dial (844) 494-0193 (U.S.) or (508) 637-5584 (international), and reference the conference ID 2982709. A live webcast of the event will be available on the Investors section of MyoKardias website at http://investors.myokardia.com. A replay of the webcast, and accompanying slides, will be available on theMyoKardiawebsite for 90 days following the call.

About Non-obstructive HCM and Heart Failure with preserved Ejection FractionHypertrophic cardiomyopathy is the most common genetic form of heart disease, affecting an estimated one in every 500 people worldwide.There are two main forms of HCM, obstructive HCM and non-obstructive HCM, which often share the same underlying genetic defects in the sarcomere that result in hypercontractility.In non-obstructive HCM, the heart contracts excessively and the left ventricle becomes abnormally thick, restricting the ability of the heart to relax and fill or pump to meet the bodys needs, but no physical obstruction is present in the outflow tract of the left ventricle. Non-obstructive HCM affects an estimated one-third of all HCM patients and presents unique treatment challenges.Patients may progress to a more advanced state of disease than those with obstructive disease before being diagnosed, and there are no approved pharmacological treatment options available.As non-obstructive HCM progresses, symptoms begin to resemble those of a congestive heart failure patient and heart transplantation may become the only viable treatment option.

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous clinical syndrome, which in many patients is characterized by impairment of the left ventricles ability to relax and fill during diastole, resulting in insufficient blood flow to meet the bodys needs.HFpEF is estimated to affect approximately three million people in the U.S. and is associated with significant morbidity and mortality. There are currently no approved therapies for HFpEF.

About Mavacamten (MYK-461)Mavacamten is a novel, oral, allosteric inhibitor of cardiac myosin being developed for the treatment of hypertrophic cardiomyopathy (HCM). Mavacamten is intended to reduce cardiac muscle contractility by inhibiting the excessive myosin-actin cross-bridge formation that underlies the excessive contractility, left ventricular hypertrophy and reduced compliance characteristic of HCM.MyoKardiais currently evaluating mavacamten in multiple clinical trials for the treatment of obstructive and non-obstructive HCM. The pivotal Phase 3 clinical trial, known as EXPLORER-HCM, is being conducted in patients with symptomatic, obstructive HCM andMyoKardiaanticipates data from this program in the second quarter of 2020. Two long-term follow-up studies are also ongoing, the PIONEER open-label extension study of obstructive HCM patients from MyoKardias Phase 2 PIONEER trial and the MAVA-LTE, an extension study for patients who have completed either EXPLORER-HCM or MAVERICK-HCM, the companys Phase 2 clinical trial of symptomatic non-obstructive HCM patients. InApril 2016, the U.S.FDAgranted Orphan Drug Designation for mavacamten for the treatment of symptomatic obstructive HCM.

About MyoKardiaMyoKardia is a clinical-stage biopharmaceutical company discovering and developing targeted therapies for the treatment of serious cardiovascular diseases. The company is pioneering a precision medicine approach to its discovery and development efforts by 1) understanding the biomechanical underpinnings of disease; 2) targeting the proteins that modulate a given condition; 3) identifying patient populations with shared disease characteristics; and 4) applying learnings from research and clinical studies to inform and guide pipeline growth and product advancement. MyoKardias initial focus is on small molecule therapeutics aimed at the proteins of the heart that modulate cardiac muscle contraction to address diseases driven by excessive contraction, impaired relaxation, or insufficient contraction. Among its discoveries are three clinical-stage therapeutics: mavacamten (formerly MYK-461); danicamtiv (formerly MYK-491) and MYK-224.

MyoKardias mission is to change the world for people with serious cardiovascular disease through bold and innovative science.

SOURCE: MyoKardia

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MyoKardia Announces Mavacamten Treatment Well Tolerated and Significantly Reduced Biomarkers of Cardiac Injury and Wall Stress in Non-Obstructive...

Three Keck School of Medicine professors created Argus II retinal prosthesis systems, an implant that helps patients who have become blind by retinitis pigmentosa. With the grant, the team looks to create a new device to prevent vision loss. (Daily Trojan file photo)

Inspired by his life research in retinal prosthesis, co-director of the Roski Eye Institute Mark Humayun is in the early stages of developing retinal contacts that could prevent or slow down vision loss. Humayun, along with a team of experts that includes Keck School of Medicine Provost Gianluca Lazzi and assistant professor of translational genomics Bodour Salhia, won an award of nearly $2 million from the National Science Foundation Emerging Frontiers in Research and Innovation to further research on the contacts.

As a Keck professor of ophthalmology and director of the USC Ginsburg Institute for Biomedical Therapeutics, Humayuns idea for retinal contacts came from his prior work in vision restoration. Humayun invented Argus II retinal prosthesis systems, an implant behind the eye that helps restore vision to blind patients with retinitis pigmentosa, a genetic disorder where the retinal cells at the back of the eye start to break down and become damaged.

[The grant] led us to consider this approach to try a controlled electrical stimulation to see if we could slow down or even prevent vision loss from certain types of retinal degeneration and retinal diseases, Humayun said.

The purpose of retinal research and lens device creation is to develop preventative measures for patients who are at risk of becoming blind from these diseases, whereas the Argus II treats patients after theyve already gone blind. The team of experts plans to continue this in their research funded by the grant.

The first step is to really demonstrate whether true utilization of this device through electrical stimulation will in fact result in meaningful slowing of neuron loss, Lazzi said.

The device also induces indirect electrical pulses that activate the remaining neurons in the retina. After working with Lazzi and finishing final tests, Humayun trained numerous surgeons on how to properly install the Argus II implant behind the eye. Approved by the Federal Drug Administration in 2013, the system became the first approved artificial retina system and has been commercially released through Second Sight, a medical prosthetics company for neurostimulation devices.

For more than 20 years, Lazzi has been part of the development team for Argus IIs hardware, ensuring its electronic functionality while implanted behind the eye. Lazzi said Argus II activates similarly to a scoreboard where hundreds of LED lights behind the eye turn on and off to display a partial image the blind patient sees by targeting certain points in the retina.

From his previous work in the bioelectromagnetic field, Humayun was able to develop the idea to use electrical stimulation to restore vision to people who are blind while Lazzi designed electrodes that would be placed on the retina to ensure the electronics used work properly in the eye.

The engineering work for the project has proved challenging because contacts were composed of electronic systems that pose a safety risk and may be damaged when submerged in the salty vitreous humor of the eye, Lazzi said. The issues have since been resolved by having electric currents and wireless transmissions strictly regulated in a casing.

Humayun also reached out to colleague Salhia in 2018 to ask her to collaborate on the project based on her translational genomics labs research with rat retinas that have degenerative diseases. Through this work, the team was able to show that electrical stimulation to the retina caused changes to genes associated with neuroprotection that maintains the structural integrity of neurons, which aids in preventing cell death.

The beauty of the project lies in how three groups from very different backgrounds basically come together to solve a problem, Salhia said. Its been one the funnest and most exciting and most innovative projects that Ive recently engaged in because its just so highly interdisciplinary and people from very different backgrounds are coming together to solve a problem.

Although the team of three has just begun its research for a new vision device with the funds provided from the grant, its members have already seen encouraging results in Salhias research on rat retinas and are looking forward to continuing their work to help patients in the coming years.

We have this grant for three years, so we hope to be in a pretty good position, Humayun said. In three years, we hope to be pretty far along in all these aspects as to whether we would be ready to do human studies.

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Keck professors receive grant to further retinal research - Daily Trojan Online

SALT LAKE CITY, March 30, 2020 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (NASDAQ: MYGN), a leader in molecular diagnostics and precision medicine, announced it has submitted a supplementary application with the Japanese Ministry of Health Labour and Welfare for its BRACAnalysis Diagnostic System (i.e., BRACAnalysis) to be used as a companion diagnostic to help to identify people with metastatic pancreatic or metastatic castration-resistant prostate cancer who have germline BRCA1 and BRCA2 mutations and may be candidates for targeted therapy with the PARP inhibitor, Lynparza (olaparib), subject to regulatory approval.

Todays regulatory filing potentially will expand the approved indications for BRACAnalsyis as companion diagnostic test in Japan, said Gary King, executive vice president of International Operations at Myriad. We look forward to helping people with pancreatic and prostate cancers access precision medicine therapy.

Myriad estimates there are more than 78,000 cases of prostate cancer and 40,000 cases of pancreatic per year in Japan. The BRACAnalysis Diagnostic System previously was approved in Japan to identify patients with ovarian or breast cancer who have a germline BRCA mutation and are eligible for Lynparza therapy. BRACAnalysis is the only germline test for BRCA1 and BRCA2 mutations to receive regulatory approval in Japan.

Myriad has partnered with SRL Inc., a subsidiary of Miraca Group, to commercialize the BRACAnalysis Diagnostic System in Japan.

About the BRACAnalysis Diagnostic SystemBRACAnalysis is a diagnostic system that classifies a patients clinically significant variants (DNA sequence variations) in the germline BRCA1 and BRCA2 genes. Variants are classified into one of the five categories; Deleterious, Suspected Deleterious, Variant of Uncertain Significance, Favor Polymorphism, or Polymorphism. Once the classification is completed, the results are sent to medical personnel in Japan for determining the eligibility of patients for treatment with Lynparza.

Myriad has been collaborating with AstraZeneca (LSE/STO/NYSE: AZN) since 2007 on the development of companion diagnostics for Lynparza. Lynparza is a trademark of AstraZeneca Lynparza is marketed by AstraZeneca and MSD (known as Merck & Co., Inc. in the United States and Canada).

About SRLSince the establishment in 1970, SRL, Inc., a member of the Miraca Group, Japan-based leading healthcare group, has been providing comprehensive testing services as the largest commercial clinical laboratory in Japan. SRL carries out nearly 400,000,000 tests per year, covering a wide range of testing services including general/emergency testing, esoteric/research testing, companion diagnostics tests, genomic analysis, and etc. For more information, please visit http://www.srl-group.co.jp/

About Myriad GeneticsMyriad Genetics Inc., is a leading personalized medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that: determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on five strategic imperatives: build upon a solid hereditary cancer foundation, growing new product volume, expanding reimbursement coverage for new products, increasing RNA kit revenue internationally and improving profitability with Elevate 2020. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, myPath, myRisk, Myriad myRisk, myRisk Hereditary Cancer, myChoice, myPlan, BRACAnalysis CDx, Tumor BRACAnalysis CDx, myChoice HRD, EndoPredict, Vectra, GeneSight, riskScore, Prolaris, Foresight and Prequel are trademarks or registered trademarks of Myriad Genetics, Inc. or its wholly owned subsidiaries in the United States and foreign countries. MYGN-F, MYGN-G.

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the regulatory filing with the Japanese Ministry of Health, Labour, and Welfare helping to expand the approved indications for BRACAnalsyis as companion diagnostic test in Japan; helping people with prostate and pancreatic cancers access precision medicine therapy; and the Company's strategic directives under the caption "About Myriad Genetics." These "forward-looking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: uncertainties associated with COVID-19, including its possible effects on our operations and the demand for our products and services; our ability to efficiently and flexibly manage our business amid uncertainties related to COVID-19; the risk that sales and profit margins of our molecular diagnostic tests and pharmaceutical and clinical services may decline; risks related to our ability to transition from our existing product portfolio to our new tests, including unexpected costs and delays; risks related to decisions or changes in governmental or private insurers reimbursement levels for our tests or our ability to obtain reimbursement for our new tests at comparable levels to our existing tests; risks related to increased competition and the development of new competing tests and services; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and pharmaceutical and clinical services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and pharmaceutical and clinical services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and pharmaceutical and clinical services and any future tests and services are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities and our healthcare clinic; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to our projections about our business, results of operations and financial condition; risks related to the potential market opportunity for our products and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents or other intellectual property; risks related to changes in intellectual property laws covering our molecular diagnostic tests and pharmaceutical and clinical services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decisions in Mayo Collab. Servs. v. Prometheus Labs., Inc., 566 U.S. 66 (2012), Assn for Molecular Pathology v. Myriad Genetics, Inc., 569 U.S. 576 (2013), and Alice Corp. v. CLS Bank Intl, 573 U.S. 208 (2014); risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that we may be unable to comply with financial operating covenants under our credit or lending agreements; the risk that we will be unable to pay, when due, amounts due under our credit or lending agreements; and other factors discussed under the heading "Risk Factors" contained in Item 1A of our most recent Annual Report on Form 10-K for the fiscal year ended June 30, 2019, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

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Myriad Seeks Japanese Regulatory Approval for its BRACAnalysis Diagnostic System in People with Advanced Pancreatic and Prostate Cancer -...

Covid-19 proliferates freely across the region. The more people with whom you come in contact, the greater likelihood you will contract it. Your age, health and genetics will dictate whether you get sick, end up hospitalized or die.

You also may need to reconsider your Easter plans.

These are the conclusions at this point from Dr. Thomas A. Russo, chief of the Division of Infectious Diseases in the University at Buffalo Jacobs School of Medicine and Biomedical Sciences.

The number of people impacted regionally will grow in the weeks to come, he said.

"Of those who are symptomatic based on data to date, about 80%, maybe 85%, have less serious disease that does not require hospitalization; about 15% require hospital treatment; and about 5% become critically ill, said Russo, who also works at the VA Medical Center in Buffalo, where at least four patients were on ventilators with Covid-19 late last week.

He talked with The Buffalo News about the dangers of the novel coronavirus and the mysteries that cloud saving the sickest of its victims. Below are excerpts.

Dr. Thomas Russo, professor and chief of infectious diseases in the University at Buffalo Jacobs School of Medicine and Biomedical Sciences. (Photo courtesy of UB)

Q: What are the symptoms?

Someone could be minimally symptomatic, which could be some combination of fever, rhinitis (stuffiness and runny nose), sore throat. They could have a mild cough, more of an upper respiratory tract infection. Loss of taste or smell were first anecdotally recognized in England and are being increasingly described. I certainly think those are symptoms that someone could develop early on as well.

Q: Are these symptoms emblematic of other conditions, too?

Flu and other respiratory viruses can mimic them. Right now, we still have circulating Influenza A, Influenza B, and some parainfluenzas (respiratory viruses that differ from the flu) around. In the absence of a diagnostic test, it's very difficult to be absolutely sure. Flu is on the downswing right now. Because coronavirus is starting to become the dominant virus in Western New York, its more likely to be coronavirus.

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Q: Do epidemiologists have a sense about how often people are asymptomatic?

That is part of the problem. Right now, the kits we use to test the RNA of the virus, the genetic footprint, arent being used on people that are asymptomatic. We're saving our tests for the most part for people with symptoms that are critically ill, so the tests are not a good tool to gauge what proportion of the population is asymptomatic.

People can be asymptomatic and be infected and able to spread the virus.

Q: Why does the disease progress in some people and not others?

The biology depends on our genetics and probably how much of the virus we get. If someone gets a huge dose of the virus, it may be such that the hosts defenses which are imperfect because we've never seen this virus before may be overwhelmed. If you get a lower dose, combined with the genetics, you may hopefully have a milder course. Everyone can be a little different.

Greater exposure to the coronavirus almost certainly raises your risk of infection and may boost the chance you will get sicker.

Q: How do you get a small dose versus a big dose?

The people who are going to be at risk for a large dose are those in close contact with someone whos infected with coughing and sneezing for prolonged periods of time. They're constantly going to be shedding virus. If you're in contact with multiple individuals, you may get sort of multiple repeat doses over time. Whether that's better or worse than with one person who is sick, who knows?

Q: What symptoms tend to first appear?

I'm not aware of any pecking order. I can tell you through years of experience in infectious diseases that were all different in terms of how we present which symptoms, what combination of symptoms, how severe. We're obviously seeing that with the new coronavirus as well.

Q: When is it time to get medical help?

Present recommendations are that if you develop an upper respiratory tract infection, even with a fever or cough, you're going to feel a little bit miserable but not critically ill. It's OK to touch base with your primary care physician. You should sort of isolate yourself at that point. The critical tell is always shortness of breath, which suggests you're developing pneumonia. That's the complication that we're concerned about. If pneumonia becomes extensive, you have problems with oxygen exchange and as that difficulty increases, that's when you end up on a ventilator.

Q: Is there anything to beat this back once you start to notice that your taste or sense of smellhas left you and that you're starting to develop other symptoms?

Using Star Trek terminology, our shields are completely down. With the flu, even if we've had a bad match in the vaccine, we've still got 30-40% of our shields. We've also got Tamiflu, which we know can both prevent disease and shorten symptoms. But so far for this new coronavirus, we have no drugs. We have no vaccine. We're all susceptible.

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Q: Who is most at risk in Western New York?

The vulnerable population with underlying cardiac disease, underlying pulmonary disease, underlying immunocompromised states due to certain cancers or drugs they may be on. Diabetes and hypertension have also been associated. It certainly makes sense that if you're a smoker, you're going to be an increased risk.

We think probably people that are older are still at increased risk, even if they don't have any comorbidities, but it seems the comorbidities are a little bit more important. I'd probably rather be a 70-year-old with no comorbidities than a 60-year-old with bad lungs and heart. The relative risk we're still sorting out. And even though younger adults and children are in terms of a bad consequences relatively spared, with significantly less risk, they're not absolutely bulletproof.

Q: Who should limit contact with others right now and what should be the threshold?

The smaller the number, the better. As the number increases, you're increasing your likelihood of getting infected, and that likelihood increases as the prevalence of infection in our community increases, which is happening right now. It's a mathematical thing. If the prevalence is increased tenfold, then it takes tenfold less people to potentially be exposed. We need to button down with our social distancing more than ever to cut the prevalence.

Q: What about big celebrations like Easter?

A common question Im getting is, I want to have a small group gathering for Easter, can I do it safely? The answer is no, you cant do so with 100% certainty. Theres the whole asymptomatic issue, which makes it impossible to be sure that you are not infected.

Both parties need to be quarantined for 14 days, not previously infected. It has to be rigorous. It can't be you running out to work, running out to Wegmans. You really can't have that contact with anyone. And as long asyou follow that and both parties are fine at the end of 14 days, then when you get together you want to really practice modified social distancing. No kissing, hugging, sharing any sort of foods and utensils, anything where there could be sort of transference of saliva or respiratory secretions. Maintain rigorous hand hygiene, especially after contacting high-touch areas such as phones, refrigerator door handles, TV remotes, etc. You're gonna minimize risk, but you can't drive it to zero.

How to celebrate Easter, Passover and Ramadan in the midst of coronavirus

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UB infectious disease doctor breaks down Covid-19 and its potential impact on WNY - Buffalo News

TORONTO , March 31, 2020 /CNW/ - The Gairdner Foundation is pleased to announce the 2020 Canada Gairdner Award laureates, recognizing some of the world's most significant biomedical research and discoveries. During these challenging times, we believe it is important to celebrate scientists and innovators from around the world and commend them for their tireless efforts to conduct research that impacts human health.

2020 Canada Gairdner International AwardThe five 2020 Canada Gairdner International Award laureates are recognized for seminal discoveries or contributions to biomedical science:

Dr. Masatoshi Takeichi Senior Visiting Scientist, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan ; Professor Emeritus, Kyoto University , Kyoto, Japan

Dr. Rolf Kemler Emeritus Member and Director, Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany

Awarded "For their discovery, characterization and biology of cadherins and associated proteins in animal cell adhesion and signalling."

Dr. Takeichi

The Work: The animal body is made up of numerous cells. Dr. Takeichi was investigatinghow animal cells stick together to form tissues and organs, and identified a key protein which he named 'cadherin'.Cadherin is present on the surface of a cell and binds to the same cadherin protein on the surface of another cell through like-like interaction, thereby binding the cells together. Without cadherin, cell to cell adhesion becomes weakened and leads to the disorganization of tissues. Dr. Takeichi found that there are multiple kinds of cadherin within the body, each of which are made by different cell types, such as epithelial and neuronal cells. Cells with the same cadherins tend to cluster together, explaining the mechanism of how different cells are sorted out and organized to form functional organs.

Further studies by Dr. Takeichi's group showed that cadherin function is supported by a number of cytoplasmic proteins, includingcatenins, and their cooperation is essential for shaping of tissues. His studies also revealed that the cadherin-dependent adhesion mechanism is involved in synaptic connections between neurons, which are important for brain wiring.

Dr. Kemler

The Work: Dr. Kemler, using an immunological approach, developed antibodies directed against surface antigens of early mouse embryos. These antibodies were shown to prevent compaction of the mouse embryo and interfered with subsequent development. Both Dr. Kemler and Dr. Takeichi went on to clone and sequence the gene encoding E-cadherin and demonstrate that it was governing homophilic cell adhesion.

Dr. Kemler also discovered the other proteins that interact with the cadherins, especially the catenins, to generate the machinery involved in animal cell-to-cell adhesion. This provided the first evidence of their importance in normal development and diseases such as cancer. It has been discovered that cadherins and catenins are correlated to the formation and growth of some cancers and how tumors continue to grow. Beta catenin is linked to cell adhesion through interaction with cadherins but is also a key component of the Wnt signalling pathway that is involved in normal development and cancer. There are approximately 100 types of cadherins, known as the cadherin superfamily.

Dr. Takeichi

The Impact: The discovery of cadherins, which are found in all multicellular animalspecies, has allowed us to interpret how multicellular systems are generated and regulated. Loss of cadherin function has been implicated as the cause of certain cancers, as well as in invasiveness of many cancers. Mutations in special types of cadherin result in neurological disorders, such as epilepsy and hearing loss. The knowledge of cadherin function is expected to contribute to the development of effective treatments against such diseases.

Dr. Kemler

The Impact: Human tumors are often of epithelial origin. Given the role of E-cadherin for the integrity of an epithelial cell layer, the protein can be considered as a suppressor of tumor growth. The research on the cadherin superfamily has had great impact on fields as diverse as developmental biology, cell biology, oncology, immunology and neuroscience. Mutations in cadherins/catenins are frequently found in tumors. Various screens are being used to identify small molecules that might restore cell adhesion as a potential cancer therapy.

Dr. Roel Nusse Professor & Chair, Department of Developmental Biology; Member, Institute for StemCell Biology andRegenerativeMedicine, Stanford University , School of Medicine. Virginia and Daniel K. Ludwig Professor of Cancer Research. Investigator, Howard Hughes Medical Institute

Awarded"For pioneering work on the Wnt signaling pathway and its importance in development, cancer and stem cells"

The Work: Dr. Nusse's research has elucidated the mechanism and role of Wnt signaling, one of the most important signaling systems in development. There is now abundant evidence that Wnt signaling is active in cancer and in control of proliferation versus differentiation of adult stem cells, making the Wnt pathway one of the paradigms for the fundamental connections between normal development and cancer.

Among Dr. Nusse's contributions is the original discovery of the first Wnt gene (together with Harold Varmus) as an oncogene in mouse breast cancer. Afterwards Dr. Nusse identified the Drosophila Wnt homolog as a key developmental gene, Wingless. This led to the general realization of the remarkable links between normal development and cancer, now one of the main themes in cancer research. Using Drosophila genetics, he established the function of beta-catenin as a mediator of Wnt signaling and the Frizzleds as Wnt receptors (with Jeremy Nathans ), thereby establishing core elements of what is now called the Wnt pathway. A major later accomplishment of his group was the first successful purification of active Wnt proteins, showing that they are lipid-modified and act as stem cell growth factors.

The Impact: Wnt signaling is implicated in the growth of human embryos and the maintenance of tissues. Consequently, elucidating the Wnt pathway is leading to deeper insights into degenerative diseases and the development of new therapeutics. The widespread role of Wnt signaling in cancer is significant for the treatment of the disease as well. Isolating active Wnt proteins has led to the use of Wnts by researchers world-wide as stem cell growth factors and the expansion of stem cells into organ-like structures (organoids).

Dr. Mina J. Bissell Distinguished Senior Scientist, Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory; Faculty; Graduate Groups in Comparative Biochemistry, Endocrinology, Molecular Toxicology and Bioengineering, University of California Berkeley , Berkeley, CA , USA

Awarded "For characterizing "Dynamic Reciprocity" and the significant role that extracellular matrix (ECM) signaling and microenvironment play in gene regulation in normal and malignant cells, revolutionizing the fields of oncology and tissue homeostasis."

The Work: Dr. Mina Bissell's career has been driven by challenging established paradigms in cellular and developmental biology. Through her research, Dr. Bissell showed that tissue architecture plays a dominant role in determining cell and tissue phenotype and proposed the model of 'dynamic reciprocity' (DR) between the extracellular matrix (ECM) and chromatin within the cell nucleus. Dynamic reciprocity refers to the ongoing, bidirectional interaction between cells and their microenvironment. She demonstrated that the ECM could regulate gene expression just as gene expression could regulate ECM, and that these two phenomena could occur concurrently in normal or diseased tissue.

She also developed 3D culture systems to study the interaction of the microenvironment and tissue organization and growth, using the mammary gland as a model.

The Impact:Dr. Bissell's model of dynamic reciprocity has been proven and thoroughly established since its proposal three decades ago and the implications have permeated every area of cell and cancer biology, with significant implications for current and future therapies. Dr. Bissell's work has generated a fundamental and translationally crucial paradigm shift in our understanding of both normal and malignant tissues.

Her findings have had profound implications for cancer therapy by demonstrating that tumor cells can be influenced by their environment and are not just the product of their genetic mutations. For example, cells from the mammary glands grown in two-dimensional tissue cultures rapidly lose their identity, but once placed in proper three-dimensional microenvironments, they regain mammary form and function. This work presages the current excitement about generation of 3D tissue organoids and demonstrates Dr. Bissell's creative and innovative approach to science.

Dr. Elaine Fuchs Howard Hughes Medical Institute Investigator and Rebecca C. Lancefield Professor and Head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Cell Biology; The Rockefeller University , New York, NY , USA

Awarded"For her studies elucidating the role of tissue stem cells in homeostasis, wound repair, inflammation and cancer."

The Work: Dr. Fuchs has used skin to study how the tissues of our body are able to replace dying cells and repair wounds. The skin must replenish itself constantly to protect against dehydration and harmful microbes. In her research, Fuchs showed that this is accomplished by a resident population of adult stem cells that continually generates a shell of indestructible cells that cover our body surface.

In her early research, Fuchs identified the proteins---keratinsthat produce the iron framework of the skin's building blocks, and showed that mutations in keratins are responsible for a group of blistering diseases in humans. In her later work, Fuchs identified the signals that prompt skin stem cells to make tissue and when to stop. In studying these processes, Fuchs learned that cancers hijack the fundamental mechanisms that tissue stem cells use to repair wounds. Her team pursued this parallel and isolated and characterized the malignant stem cells that are responsible for propagating a type of cancer called "squamous cell carcinoma." In her most recent work, she showed that these cells can be resistant to chemotherapies and immunotherapies and lead to tumor relapse.

The Impact: All tissues of our body must be able to replace dying cells and repair local wounds. Skin is particularly adept at performing these tasks. The identification and characterization of the resident skin stem cells that make and replenish the epidermis, sweat glands and hair provide important insights into this fountain of youth process and hold promise for regenerative medicine and aging. In normal tissues, the self-renewing ability of stem cells to proliferate is held in check by local inhibitory signals coming from the stem cells' neighbours. In injury, stimulatory signals mobilize the stem cells to proliferate and repair the wound. In aging, these normal balancing cues are tipped in favour of quiescence. In inflammatory disorders, stem cells become hyperactivated. In cancers, the wound mechanisms to mobilize stem cells are hijacked, leading to uncontrolled tissue growth. Understanding the basic mechanisms controlling stem cells in their native tissue is providing new strategies for searching out refractory tumor cells in cancer and for restoring normalcy in inflammatory conditions.

2020 John Dirks Canada Gairdner Global Health AwardThe 2020 John Dirks Canada Gairdner Global Health Award laureate is recognized for outstanding achievements in global health research:

Professor Salim S. Abdool Karim Director of CAPRISA (Centre for the AIDS Program of Research in South Africa), the CAPRISA Professor in Global Health at Columbia University , New York and Pro Vice-Chancellor (Research) at the University of KwaZulu-Natal, Durban, South Africa

Professor Quarraisha Abdool KarimAssociate Scientific Director of CAPRISA, Professor in Clinical Epidemiology, Columbia University , New York and Professor in Public Health at the Nelson Mandela Medical School and Pro Vice-Chancellor (African Health) at the University of KwaZulu-Natal, Durban, South Africa

Awarded"For their discovery that antiretrovirals prevent sexual transmission of HIV, which laid the foundations for pre-exposure prophylaxis (PrEP), the HIV prevention strategy that is contributing to the reduction of HIV infection in Africa and around the world."

The Work: UNAIDS estimates that 37 million people were living with HIV and 1.8 million people acquired HIV in 2017. In Africa, which has over two thirds of all people with HIV, adolescent girls and young women have the highest rates of new HIV infections. ABC (Abstinence, Be faithful, and use Condoms) prevention messages have had little impact - due to gender power imbalances, young women are often unable to successfully negotiate condom use, insist on mutual monogamy, or convince their male partners to have an HIV test.

In responding to this crisis, Salim and Quarraisha Abdool Karim started investigating new HIV prevention technologies for women about 30 years ago. After two unsuccessful decades, their perseverance paid off when they provided proof-of-concept that antiretrovirals prevent sexually acquired HIV infection in women. Their ground-breaking CAPRISA 004 trial showed that tenofovir gel prevents both HIV infection and genital herpes. The finding was ranked inthe "Top 10 Scientific Breakthroughs of 2010" by the journal, Science. The finding was heralded by UNAIDS and the World Health Organization (WHO) as one of the most significant scientific breakthroughs in AIDS and provided the first evidence for what is today known as HIV pre-exposure prophylaxis (PrEP).

The Abdool Karims have also elucidated the evolving nature of the HIV epidemic in Africa , characterising the key social, behavioural and biological risk factors responsible for the disproportionately high HIV burden in young women. Their identification of the "Cycle of HIV Transmission", where teenage girls acquire HIV from men about 10 years older on average, has shaped UNAIDS policies on HIV prevention in Africa .

The impact: CAPRISA 004 and several clinical trials of oral tenofovir led tothe WHO recommending a daily tenofovir-containing pill for PrEP as a standard HIV prevention tool for all those at high risk a few years later. Several African countries are among the 68 countries across all continents that are currently making PrEP available for HIV prevention. The research undertaken in Africa by this South African couple has played a key role in shaping the local and global response to the HIV epidemic.

2020 Canada Gairdner Wightman AwardThe 2020 Canada Gairdner Wightman Award laureate is a Canadian scientist recognized for outstanding leadership in medicine and medical science throughout their career:

Dr. Guy Rouleau Director of the Montreal Neurological Institute-Hospital (The Neuro); Professor & Chair of the Department of Neurology and Neurosurgery, McGill University ; Director of the Department of Neuroscience, McGill University Health Center

Awarded "For identifying and elucidating the genetic architecture of neurological and psychiatric diseases, including ALS, autism and schizophrenia, and his leadership in the field of Open Science."

The Work: Dr. Rouleau has identified over 20 genetic risk factors predisposing to a range of brain disorders, both neurological and psychiatric, involving either neurodevelopmental processes or degenerative events. He has defined a novel disease mechanism for diseases related to repeat expansions that are at play in some of the most severe neurodegenerative conditions. He has significantly contributed to the understanding of the role of de novo variants in autism and schizophrenia. In addition, he has made important advances for various neuropathies, in particular for amyotrophic lateral sclerosis (ALS) where he was involved in the identification of the most prevalent genetic risk factors -which in turn are now the core of innumerable ALS studies worldwide.

Dr. Rouleau has also played a pioneering role in the practice of Open Science (OS), transforming the Montreal Neurological Institute-Hospital (The Neuro) into the first OS institution in the world. The Neuro now uses OS principles to transform research and careand accelerate the development of new treatments for patients through Open Access, Open Data, Open Biobanking, Open Early Drug Discovery and non-restrictive intellectual property.

The Impact: The identification of genetic risk factors has a number of significant consequences. First, allowing for more accurate genetic counselling, which reduces the burden of disease to affected individuals, parents and society. A revealing case is Andermann syndrome, a severe neurodevelopmental and neurodegenerative condition that was once relatively common in the Saguenay-Lac-St-Jean region of Quebec . Now this disease has almost disappeared from that population. Second, identifying the causative gene allows the development of treatments. For instance, his earlier work on a form of ALS linked to the superoxide dismutase-1 gene (SOD1) opened up studies which are now the focal point of phase 2 clinical studies showing great promise.

Byactingasalivinglabforthelast coupleofyears,TheNeuroisspearheading the practice of OpenScience (OS).TheNeurois alsoengagingstakeholdersacross Canadawiththegoal of formalizinganational OSallianceforthe neurosciences.Dr.Rouleau'sworkinOScontributesfundamentallytothetransformationoftheveryecosystemofsciencebystimulatingnewthinkingandfosteringcommunitiesofsharing.InspiredbyTheNeuro'svision,theglobalsciencecommunityisreflecting oncurrentresearchconventionsandcollaborativeprojects,andthemomentumforOSisgainingafootholdinorganizationsandinstitutionsinallcornersoftheearth.

About the Gairdner Foundation:

The Gairdner Foundation was established in 1957 by Toronto stockbroker, James Gairdner to award annual prizes to scientists whose discoveries have had major impact on scientific progress and on human health. Since 1959 when the first awards were granted, 387scientists have received a Canada Gairdner Award and 92 to date have gone on to receive the Nobel Prize.The Canada Gairdner Awards promote a stronger culture of research and innovation across the country through our Outreach Programs including lectures and research symposia. The programs bring current and past laureates to a minimum of 15 universities across Canada to speak with faculty, trainees and high school students to inspire the next generation of researchers. Annual research symposia and public lectures are organized across Canada to provide Canadians access to leading science through Gairdner's convening power.

http://www.gairdner.org

SOURCE Gairdner Foundation

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2020 Canada Gairdner Awards Recognize World-renowned Scientists for Transformative Contributions to Research That Impact Human Health - Yahoo Finance

Coronavirus, novel coronavirus, COVID-19. Theres a lot of information and misinformation around the new virus thats affecting all corners of the world. Its tricky to understand why its so devastating without understanding how it attacks the human body. So were going to explain it.

First off, why does this affliction have so many names?

Lets start with the term coronavirus. Think of that as a family name. Some members of the coronavirus family are commonly spread among people and can cause more mild illnesses, like the common cold. Other coronaviruses infect animals. And sometimes, though its rare, coronaviruses that infect animals evolve and then infect people. This is what is suspected to have happened with the SARS-CoV-2 coronavirus, according to the Centers for Disease Control and Prevention.

COVID-19 is the name of the disease caused by this new, or novel, coronavirus, which was first identified in Wuhan, China, in December.

Now, back to the family of coronaviruses. They all have one important thing in common: crown-like spikes on their surface.

On HoustonChronicle.com: Does climate change play a role in infectious diseases like COVID-19?

Why should I care that the virus has spikes?

This is key to how it infiltrates the body.

When people infected with the new coronavirus cough, sneeze or simply speak, they send respiratory droplets into the air. People nearby, within roughly six feet (hence the signs in grocery stores), can inhale those droplets and bring the virus into their bodies. This is thought to be the main way the virus spreads, though a person touching an infected surface and then touching his or her eyes, mouth or nose might also get sick.

The virus can infect the upper respiratory tract the nose and throat, for instance or travel down into the lungs, including alveoli air sacs that bring oxygen into the bloodstream and expel carbon dioxide.

The virus then uses its spikes to attach to cells. Once attached, the virus inserts its genetic material, RNA. Thats used to create particles that are assembled to create more of the virus. Those are ejected from the cell and become attached to other cells, replicating the virus in the respiratory tract.

A virus cannot live by itself. It has to have a living cell in order to continue reproducing, said Dr. Laila E. Woc-Colburn, an associate professor and director of medical education for the National School of Tropical Medicine at Baylor College of Medicine. The cell serves as a little factory to produce more of them.

How does the body respond?

Each cell has its own internal defense system. Much like a home alarm would go off, the cell activates its own defenses and then calls for help from the immune system. Cytokine proteins bring in white blood cells to help fight the virus.

The release of cytokine proteins causes inflammation, which prompts symptoms such as fever, body aches and feeling tired. The dry cough associated with COVID-19 could be caused by inflammation or injury in the respiratory tract.

For many people, the bodys response will succeed in killing the virus over time. But for some, the release of cytokines can be too aggressive of a response, leading to acute respiratory distress syndrome and other respiratory issues that require a breathing tube.

It might even lead to shock, when organs dont receive adequate blood supply and oxygen, and organ failure.

Your immune response can overreact and cause more damage than the virus itself is causing, said Vineet D. Menachery, assistant professor in the Department of Microbiology & Immunology at the University of Texas Medical Branch, and this is particularly pronounced in older people and people with health issues.

How long am I contagious for?

Some people can be contagious before showing symptoms. And that contributes to the virus spreading because its hard to identify people who are sick.

By the time you figure out somebody is infectious, they probably have already transferred the disease to other people, said Dr. Howard J. Huang, medical director of lung transplantation at Houston Methodist Hospital.

People are thought to be most contagious when they are the sickest, and they can remain contagious for weeks after their symptoms disappear, with the exact timeframe unknown.

Am I immune to COVID-19 if I survive?

Yes, at least in the short term.

The body creates antibodies to help ward off future attacks. But since the new coronavirus has only been found in humans since December, its not yet known how long the immune system will remember this virus. Some viruses, like those that cause the flu, require a vaccine every year.

On HoustonChronicle.com: How Texas compares to other states in testing for COVID-19

Is this new coronavirus more prone to mutate?

No. Huang said it is mutating at a slower rate than influenza, with the latest data showing at least eight strains circulating worldwide.

They have proofreading enzymes that keep mutations lower than most RNA viruses, added Menachery. Therefore, they are more stable than other viruses like influenza.

Is there a vaccine?

Not yet, but a variety of research is underway to help treat or prevent COVID-19.

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How the spiky coronavirus attacks your cells and makes them into little virus factories - Houston Chronicle

CRISPR-Cas9, which is short for clustered, regularly interspaced short palindromic repeats and CRISPR-associated protein 9. The technique is faster, cheaper, more accurate, and more efficient than other existing genome editing methods.

For the CRISPR-Cas9 system to work, a bacterial defense protein got Cas9 seeks out an adjacent protospacer motif (PAM) that is present in the viral DNA yet not in the bacterial DNA. CRISPR-Cas9 has been harnessed for editing the human genome because such PAM sequences are also quite common in our DNA; however, genes that are not near a PAM cannot be targeted.

To conquer this problem, a team led by Benjamin P. Kleinstiver, a biochemist at MGHs Center for Genomic Medicine, engineered variations of a Cas9 protein that dont require a particular PAM to bind and cut DNA. The two new Cas9 variations, named SpG and SpRY, allow editing of DNA sequences at efficiencies not achievable with conventional CRISPR-Cas9 enzymes.

As engineered proteins target independently, they enable targeting of previously inaccessible regions of the genome.

Benjamin P. Kleinstiver, a biochemist at MGHs Center for Genomic Medicine, said,By nearly completely relaxing the requirement for the enzymes to recognize a PAM, many genome editing applications are now possible. And since almost the entire genome is targetable, one of the most exciting implications is that that the entire genome is druggable from a DNA-editing perspective.

Scientists are further planning to comprehend the function of these proteins. They also want to explore their unique capabilities for a variety of different applications.

Lead author Russell T. Walton, also of MGHs Center for Genomic Medicine, said,We have demonstrated that these new enzymes will allow researchers to generate biologically and clinically relevant genetic modifications that were previously unfeasible.

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Scientists expanded the Capabilities of CRISPR gene editing technique - Tech Explorist

At least eight strains of the coronavirus are making their way around the globe, creating a trail of death and disease that scientists are tracking by their genetic footprints.

While much is unknown, hidden in the virus'unique microscopic fragments are clues to the origins of its original strain, how it behaves as it mutates and which strains are turning into conflagrations while others are dying out thanks to quarantine measures.

KATHRYN GEORGE/STUFF

Scientists are tracking eight strains of the coronavirus by their genetic footprints.

Huddled in once bustling and now almost empty labs, researchers who oversaw dozens of projects are instead focused on one goal: tracking the current strains of the SARS-CoV-2 virus that cause the illness Covid-19.

Labs around the world are turning their sequencing machines, most about the size of a desktop printer, to the task of rapidly sequencing the genomes of virus samples taken from people sick with Covid-19. The information is uploaded to a website called NextStrain.org that shows how the virus is migrating and splitting into similar but new subtypes.

READ MORE:* Three months into the pandemic, here is what we know about the coronavirus* Coronavirus isn't alive and that's why it's so hard to kill* Coronavirus vaccine hunters: meet the scientists racing to find a cure* Key terms of the coronavirus outbreak, explained: From asymptomatic to zoonotic

While researchers caution they're only seeing the tip of the iceberg, the tiny differences between the virus strains suggest shelter-in-place orders are working in some areas and that no one strain of the virus is more deadly than another. They also say it does not appear the strains will grow more lethal as they evolve.

"The virus mutates so slowly that the virus strains are fundamentally very similar to each other," said Charles Chiu, a professor of medicine and infectious disease at the University of California, San Francisco School of Medicine.

The SARS-CoV-2 virus first began causing illness in China sometime between mid-November and mid-December. Its genome is made up of about 30,000 base pairs. Humans, by comparison, have more than 3 billion. So far even in the virus's most divergent strains scientists have found only 11 base pair changes.

That makes it easy to spot new lineages as they evolve, said Chiu.

"The outbreaks are trackable. We have the ability to do genomic sequencing almost in real-time to see what strains or lineages are circulating," he said.

So far, most cases on the USWest Coast are linked to a strain first identified in Washington state. It may have come from a man who had been in Wuhan, China, the virus' epicentre, and returned home on January 15. It is only three mutations away from the original Wuhan strain, according to work done early in the outbreak by Trevor Bedford, a computational biologist at Fred Hutch, a medical research centrein Seattle.

On the East Coast there are several strains, including the one from Washington and others that appear to have made their way from China to Europe and then to New York and beyond, Chiu said.

BEWARE PRETTY PHYLOGENETIC TREES

This isn't the first time scientists have scrambled to do genetic analysis of a virus in the midst of an epidemic. They did it with Ebola, Zika and West Nile, but nobody outside the scientific community paid much attention.

"This is the first time phylogenetic trees have been all over Twitter," said Kristian Andersen, a professor at Scripps Research, a nonprofit biomedical science research facility in La Jolla, California, speaking of the diagrams that show the evolutionary relationships between different strains of an organism.

The maps are available on NextStrain, an online resource for scientists that uses data from academic, independent and government laboratories all over the world to visually track the genomics of the SARS-CoV-2 virus. It currently represents genetic sequences of strains from 36 countries on six continents.

While the maps are fun, they can also be "little dangerous" said Andersen. The trees showing the evolution of the virus are complex and it's difficult even for experts to draw conclusions from them.

"Remember, we're seeing a very small glimpse into the much larger pandemic. We have half a million described cases right now but maybe 1000 genomes sequenced. So there are a lot of lineages we're missing," he said.

MANU FERNANDEZ/AP

Health workers applaud in support of the medical staff that are working on the Covid-19 virus outbreak in Spain.

DIFFERENT SYMPTOMS, SAME STRAINS

Covid-19 hits people differently, with some feeling only slightly under the weather for a day, others flat on their backs sick for two weeks and about 15 per centhospitalised. Currently, an estimated 1 per centof those infected die. The rate varies greatly by country and experts say it is likely tied to testing rates rather than actual mortality.

Chiu says it appears unlikely the differences are related to people being infected with different strains of the virus.

"The current virus strains are still fundamentally very similar to each other," he said.

The Covid-19 virus does not mutate very fast. It does so eight to 10 times more slowly than the influenza virus, said Anderson, making its evolution rate similar to other coronaviruses such as Ebola, Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS).

It's also not expected to spontaneously evolve into a form more deadly than it already is to humans. The SARS-CoV-2 is so good at transmitting itself between human hosts, said Andersen, it is under no evolutionary pressure to evolve.

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The Covid-19 virus does not mutate very fast. It does so eight to 10 times more slowly than the influenza virus.

SHELTER IN PLACE WORKING IN CALIFORNIA

Chiu's analysis shows California's strict shelter in place efforts appear to be working.

Over half of the 50 SARS-CoV-2 virus genomes his San Francisco-based lab sequenced in the past two weeks are associated with travel from outside the state. Another 30 per centare associated with health care workers and families of people who have the virus.

"Only 20 per centare coming from within the community. It's not circulating widely," he said.

That's fantastic news, he said, indicating the virus has not been able to gain a serious foothold because of social distancing.

It's like a wildfire, Chiu said. A few sparks might fly off the fire and land in the grass and start new fires. But if the main fire is doused and its embers stomped out, you can kill off an entire strain. In California, Chiu sees a lot of sparks hitting the ground, most coming from Washington, but they're quickly being put out.

An example was a small cluster of cases in Solano County, northeast of San Francisco. Chiu's team did a genetic analysis of the virus that infected patients there and found it was most closely related to a strain from China.

At the same time, his lab was sequencing a small cluster of cases in the city of Santa Clara in Silicon Valley. They discovered the patients there had the same strain as those in Solano County. Chiu believes someone in that cluster had contact with a traveller who recently returned from Asia.

"This is probably an example of a spark that began in Santa Clara, may have gone to Solano County but then was halted," he said.

The virus, he said, can be stopped.

CHINA IS AN UNKNOWN

So far researchers don't have a lot of information about the genomics of the virus inside China beyond the fact that it first appeared in the city of Wuhan sometime between mid-November and mid-December.

The virus's initial sequence was published on January 10 by professor Yong-Zhen Zhang at the Shanghai Public Health Clinical Center. But Chiu says scientists don't know if there was just one strain circulating in China or more.

"It may be that they haven't sequenced many cases or it may be for political reasons they haven't been made available," said Chiu. "It's difficult to interpret the data because we're missing all these early strains."

Researchers in the United Kingdom who sequenced the genomes of viruses found in travellers from Guangdong in south China found those patients' strains spanned the gamut of strains circulating worldwide.

"That could mean several of the strains we're seeing outside of China first evolved there from the original strain, or that there are multiple lines of infection. It's very hard to know," said Chiu.

THE VIRUS DID NOT COME FROM A LAB

While there remain many questions about the trajectory of the Covid-19 disease outbreak, one thing is broadly accepted in the scientific community: The virus was not created in a lab but naturally evolved in an animal host.

SARS-CoV-2's genomic molecular structure - think the backbone of the virus - is closest to a coronavirus found in bats. Parts of its structure also resemble a virus found in scaly anteaters, according to a paper published earlier this month in the journal Nature Medicine.

Someone manufacturing a virus targeting people would have started with one that attacked humans, wrote National Institutes of Health Director Francis Collins in an editorial that accompanied the paper.

Andersen was lead author on the paper. He said it could have been a one-time occurrence.

"It's possible it was a single event, from a single animal to a single human," and spread from there.

- USA Today

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Eight strains of the coronavirus are circling the globe. They're giving scientists clues - Stuff.co.nz

To treat babies, young children with spinal muscular atrophy

EMA has recommended granting a conditional marketing authorisation in the European Union for the gene therapy Zolgensma (onasemnogene abeparvovec) to treat babies and young children with spinal muscular atrophy (SMA), a rare and often fatal genetic disease that causes muscle weakness and progressive loss of movement.

There are currently limited treatment options for children with SMA in the EU. Patients also receive physical aids to support muscular functions and help them and their families cope with the symptoms of the disease.

Spinal muscular atrophy is usually diagnosed in the first year of life. Most patients with severe SMA do not survive early childhood. Patients with the disease cannot produce sufficient amounts of a protein called survival motor neuron (SMN), which is essential for the normal functioning and survival of motor neurons (nerves from the brain and spinal cord that control muscle movements). Without this protein, the motor neurons deteriorate and eventually die. This causes the muscles to fall into disuse, leading to muscle wasting (atrophy) and weakness.

The SMN protein is made by two genes, the SMN1 and SMN2 genes. Patients with spinal muscular atrophy lack the SMN1 gene but have the SMN2 gene, which mostly produces a short SMN protein that cannot work properly on its own. A one-time intravenous administration of Zolgensma supplies a fully functioning copy of the human SMN1 geneenabling the body to produce enough SMN protein. This is expected to improve their muscle function, movement and survival of children with the disease.

Treatment with Zolgensma should only be administered once in suitable clinical centres under the supervision of a physician experienced in the management of patients with SMA.

EMAs recommendation for conditional marketing authorisation is based on the preliminary results of one completed clinical trial and three supporting studies in patients with spinal muscular atrophy with different stages of disease severity. These included genetically diagnosed and pre-symptomatic patients.

The clinical trial providing the main body of data for the assessment of Zolgensma was conducted in 22 patients who were less than six months of age at the time of the gene replacement therapy with Zolgensma. The trial assessed the percentage of patients who had improvement in their survival (i.e. without the need to be permanently on a ventilator) and motor milestones, such as head control, crawling, sitting, standing and walking (with or without assistance).

The survival of patients treated with Zolgensma exceeded what can be expected from untreated patients with severe SMA. Out of 22 patients enrolled in the trial, 20 patients (91 per cent) were alive and did not need permanent ventilatory support at 14 months of age. The experience with this disease shows that at 14 months of age only 25 per cent of patients are still alive. These patients also achieved motor milestones, which are usually not achieved in the natural history of the disease. 14 patients (64 per cent) reached the milestone of independent sitting before 18 months of age. One patient (4 per cent) reached the milestone of walking unassisted before reaching 16 months of age. Patients with less motor deterioration appeared to benefit the most from the treatment with Zolgensma.

The most common side effects found in participants in the clinical trials for Zolgensma wereincreases in liver enzymes (transaminases) seen in blood tests. This is an effect of the immune response to the treatment.

Because Zolgensma is an advanced-therapy medicinal product (ATMP), it was assessed by the Committee for Advanced Therapies (CAT), EMAs expert committee for cell- and gene-based medicines.

On the basis of the CATs assessment and positive opinion, EMAs committee for human medicines (CHMP) recommended a conditional approval for this medicine. This is one of the EUs regulatory mechanisms to facilitate early access to medicines that fulfil an unmet medical need. This type of approval allows the Agency to recommend a medicine for marketing authorisation with less complete data than normally expected, in cases where the benefit of a medicines immediate availability to patients outweighs the risk inherent in the fact that not all the data are yet available.

Additional efficacy and safety data are being collected through three ongoing studies, a long-term registry and further investigations on the product, including recommendations for future quality development. All results must be included in post-marketing safety reports, which are continuously reviewed by EMA.

The opinion adopted by the CHMP is an intermediary step on Zolgensmas path to patient access. The opinion will now be sent to the European Commission for the adoption of a decision on an EU-wide marketing authorisation.Once amarketing authorisationhas been granted, decisions about price and reimbursement will take place at the level of each Member State, taking into account the potential role/use of this medicine in the context of the national health system of that country.

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EMA grants conditional marketing authorisation in EU for gene therapy Zolgensma - Express Healthcare