Category Archives: Transhuman News

A patient in Italy receives intensive care for COVID-19. Human geneticists are coming together to look for genes that make some people more vulnerable to the disease.

By Jocelyn KaiserMar. 27, 2020 , 3:25 PM

Sciences COVID-19 reporting is supported by the Pulitzer Center.

COVID-19, caused by the new pandemic coronavirus, is strangelyand tragicallyselective. Only some infected people get sick, and although most of the critically ill are elderly or have complicating problems such as heart disease, some killed by the disease are previously healthy and even relatively young. Researchers are now gearing up to scour the patients genomes for DNA variations that explain this mystery. The findings could be used to identify those most at risk of serious illness and those who might be protected, and they might also guide the search for new treatments.

The projects range from ongoing studies with DNA for many thousands of participants, some now getting infected with the coronavirus, to new efforts that are collecting DNA from COVID-19 patients in hard-hit places such as Italy. The goal is to compare the DNA of people who have serious cases of COVID-19 (which stands for coronavirus disease 2019)but no underlying disease like diabetes, heart or lung diseasewith those with mild or no disease. We see huge differences in clinical outcomes and across countries. How much of that is explained by genetic susceptibility is a very open question, says geneticist Andrea Ganna of the University of Helsinkis Institute for Molecular Medicine Finland (FIMM).

Its hard to predict what will pop out from these gene hunts, some researchers say. But there are obvious suspects, such as the gene coding for the cell surface protein angiotensin-converting enzyme 2 (ACE2), which the coronavirus uses to enter airway cells. Variations in the ACE2 gene that alter the receptor could make it easier or harder for the virus to get into cells, says immunologist Philip Murphy of the National Institute of Allergy and Infectious Diseases, whose lab identified a relatively common mutation in another human cell surface protein, CCR5, that makes some people highly resistant to HIV.

Ganna heads up a major effort to pool COVID-19 patients genetic data from around the world. The idea came quite spontaneously about 2 weeks ago when everyone was sitting at their computers watching this crisis, says Ganna, who is also affiliated with the Broad Institute, a U.S. genomic powerhouse.

He and FIMM Director Mark Daly quickly created a website for their project, the COVID-19 Host Genetics Initiative, and reached out to colleagues who run large biobank studies that follow thousands of volunteers for years to look for links between their DNA and health. At least a dozen biobanks, mostly in Europe and the United States, have expressed interest in contributing COVID-19 data from participants who agreed to this. Among them are FinnGen, which has DNA samples and health data for 5% of the 5 millionperson Finnish population, and the 50,000-participant biobank at the Icahn School of Medicine at Mount Sinai.

The UK Biobank, one of worlds largest with DNA data for 500,000 participants, also plans to add COVID-19 health data from participants to its data set, the project tweeted this month. And the Icelandic company deCODE Genetics, which is helping test much of the nations population to see who is infected with the new coronavirus, has received government permission to add these data and any subsequent COVID-19 symptoms to its database, which contains genome and health data on half of Icelands 364,000 inhabitants, says its CEO Kri Stefnsson. We will do our best to contribute to figuring this out, Stefnsson says.

Another effort to identify protective or susceptibility DNA variants is the Personal Genome Project led by Harvard Universitys George Church, which recruits people willing to share their full genome, tissue samples, and health data for research. Earlier this month, it sent questionnaires to its thousands of participants, asking about their COVID-19 status. More than 600 in the United States responded within 48 hours. It seems that most people want to do their part, says Church, whose group isnt yet part of Gannas collaboration.

Other researchers working with Gannas initiative are recruiting COVID-19 patients directly within hospitals for such genomics studies. Italian geneticist Alessandra Renieri of the University of Siena expects at least 11 hospitals in the nation to give ethics approval for her team to collect DNA samples from willing patients. It is my opinion that [host] genetic differences are a key factor for susceptibility to severe acute pneumonia, Renieri says.

Pediatrics researcher Jean-Laurent Casanova at the Rockefeller University, who specializes in identifying rare genes that can make healthy young people susceptible to certain serious diseases, is drawing on a network of pediatricians around the world to look for the relatively few young people who develop COVID-19 serious enough to get admitted to intensive care. We study exclusively patients who were previously healthy and under 50, as their serious COVID-19 illness is more likely to have a genetic basis, he explains.

In addition to genetic variants of the ACE2 receptor, scientists want to see whether differences in the human leukocyte antigen genes, which influence the immune systems response to viruses and bacteria, affect disease severity. And some investigators want to follow up a finding, which a Chinese team reported in a preprint: that people with type O blood may be protected from the virus. Were trying to figure out if those findings are robust, says Stanford University human geneticist Manuel Rivas, who is contributing to Gannas initiative.

The catastrophic spread of the coronavirus should soon increase the number of COVID-19 patients available to these gene hunts. And that could speed findings. Ganna expects the first susceptibility genes could be identified within a couple of months.

With reporting by Elizabeth Pennisi.

Here is the original post:
How sick will the coronavirus make you? The answer may be in your genes - Science Magazine

The Department of Molecular & Human Genetics has claimed that it has discovered a new technology to test COVID-19 virus and give accurate results within 5-6 hours.

Sangeeta NairMar 31, 2020 14:04 IST

The Department of Molecular & Human Genetics at the Banaras Hindu University has claimed that it has discovered a new technology to test the COVID-19 virus and give accurate results within 5-6 hours.

The departments Associate Professor Dr. Geeta Rai stated that the department had tried to target a protein sequence present only in the COVID-19 virus. We've tried to target a protein sequence present only in COVID19 & not present in any other viral strain, she said.

Dr. Rai added saying, We're hopeful when testing is done it will only detect COVID19 presence, so there'll be less chance of false detection.

The new technology has been developed by an all-women team of BHUs Department of Molecular & Human Genetics. The team includes four researchers- Dr. Geeta Rai, Dolly Das, Khushbupriya and Hiral Thakar.

The research team had filed a patent on March 27, 2020. However, it needs to be validated by the Indian virology research institute- The National Institute of Virology in Pune and after that it would require approval from the Indian Council of Medical Research.

Download our Current Affairs & GK app For exam preparation

See the article here:
BHU department claims to have discovered new technology to test COVID-19 - Jagran Josh

The genetic quest to understand COVID-19 will help us prevent other diseases.

How the novel coronavirus that causes COVID-19 made the leap from animals to humans is a puzzle that scientists are trying to solve as humanity comes to grip with the deadly pandemic sweeping the globe.

At the frontline of this scientific work isProfessor Edward Holmes, an evolutionary virologist who holds a joint position with the School of Life and Environmental Sciences and the School of Medical Sciences at the University of Sydney.

It is clear that wildlife contains many coronaviruses that could potentially emerge in humans in the future. A crucial lesson from this pandemic to help prevent the next one is that humans must reduce their exposure to wildlife, for example by banning wet markets and the trade in wildlife. Professor Edward Holmes

He has been working closely with scientists in China and around the world to unlock the genetic code of SARS-CoV-2, which is the virus that causes COVID-19, to understand its origins and assist in the race other scientists are engaged in to find an effective vaccine.

Their work will also help in the monitoring and prevention of other viruses that could potentially transfer from wildlife into humans, causing what are known as zoonotic diseases.

Already this year, Professor Holmes has co-authored four papers on the novel coronavirus, including two of the earliest descriptions of the virus (published in Nature[1] and The Lancet[2]).

This week he publishes two more.

Brought forward for early publication on Thursday byNature[3]after peer review, the first paper identifies a similar coronavirus to the one now infecting humans in the Malayan pangolin population of southern China. Professor Holmes, a co-author, is the only non-China based academic on the paper.

The role that pangolins play in the emergence of SARS-CoV-2 (the cause of COVID-19) is still unclear. However, it is striking that the pangolin viruses contain some genomic regions that are very closely related to the human virus, said Professor Holmes.

Understanding the evolutionary pathway by which this novel coronavirus has transferred to humans will help us not only combat the current pandemic but assist in identifying future threats from other coronaviruses in other species.

This paper is an important part of solving that puzzle.

Professor Holmes said: The role that pangolins play in the emergence of SARS-CoV-2 (the cause of COVID-19) is still unclear. However, it is striking that the pangolin viruses contain some genomic regions that are very closely related to the human virus. The most important of these is the receptor binding domain that dictates how the virus is able to attach and infect human cells.

The paper identifies pangolins as possible intermediate hosts for the novel human virus that has emerged. The authors call for these animals and others to be removed from wet markets in order to prevent zoonotic transmission to humans.

There is simply no evidence that SARS-CoV-2 the cause of COVID-19 came out of a lab. In reality, this is the sort of natural disease emergence event that researchers in the field like myself have been warning about for many years. Professor Edward Holmes

Professor Holmes said: It is clear that wildlife contains many coronaviruses that could potentially emerge in humans in the future. A crucial lesson from this pandemic to help prevent the next one is that humans must reduce their exposure to wildlife, for example by banning wet markets and the trade in wildlife.

Just last weekNature Medicine[4] published research co-authored by Professor Holmes with scientists from Scripps Research Institute in La Jolla California, the University of Edinburgh, Columbia University in New York and Tulane University, New Orleans.

That paper has dispelled the fanciful idea that the novel coronavirus was a manufactured biological agent.

Using comparative analysis of genomic data, the scientists show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus.

Professor Holmes said: There is simply no evidence that SARS-CoV-2 the cause of COVID-19 came out of a lab. In reality, this is the sort of natural disease emergence event that researchers in the field like myself have been warning about for many years.

That paper has quickly become the highest ranked academic study of all time as measured by Altmetric, a company that monitors media coverage of research papers.

The high Altmetric is a strong indication of the remarkable global interest in this topic, Professor Holmes said.

Professor Edward Holmes is an evolutionary virologist at the University of Sydney. Credit: University of Sydney

And today, Professor Holmes publishes acommentary in the journalCell[5] with his colleagueProfessor Yong-Zhen Zhangfrom the Shanghai Public Health Clinical Centre and the School of Life Science at Fudan University, Shanghai.

In that article they outline our current knowledge of what the genomic data reveals about the emergence of SARS-CoV-2 virus and discuss the gaps in our knowledge.

This includes taking samples from the Wuhan wet market where it is believed the virus originated. The paper says that genome sequences of environmental samples likely surfaces from the market have now been obtained and phylogenetic analysis reveals that they are very closely related to viruses sampled from the earliest Wuhan patients.

However, Professor Holmes and Professor Zhang are quick to point out that as not all of the early [COVID-19] cases were market associated, it is possible that the emergence story is more complicated than first suspected.

The paper says that the SARS-CoV-2 virus is likely to become the fifth endemic coronavirus in the human population. It concludes that coronaviruses clearly have the capacity to jump species boundaries and adapt to new hosts, making it straightforward to predict that more will emerge in the future.

How we respond to that will require more research to assist develop public health policy.

They point to policy and other measures to help prevent other coronaviruses becoming a health danger to humans. These include:

References:

Read more here:
Unlocking the Genetic Code of the Novel Coronavirus: How COVID-19 Made the Leap From Animals to Humans - SciTechDaily

Q2 Solutions, a leading clinical trial laboratory services organization resulting from an IQVIA and Quest Diagnostics joint venture, today announced its collaboration with the University of Texas Medical Branch (UTMB) to develop a novel assay for COVID-19 (SARS-CoV-2) tests, an essential tool for rapid development of a Coronavirus vaccine. Once a viable assay is developed, Q2 Solutions labs will produce it for use in clinical trials to determine the effectiveness of a COVID-19 vaccine.

An assay is an analysis done to determine the biological or pharmacological potency of a drug. Compared with the conventional plaque-based neutralizing assay, UTMBs novel reporter COVID-19-based test may provide several potential advantages, including increased sensitivity and dramatic increase in assay throughput because the assay time is shifted from multiple days to a single day.

"We have successfully produced a reporter virus system engineered with either luciferase or fluorescent tags to enable quantitative determination of vaccine effectiveness," said Pei-Yong Shi, professor of Human Genetics at UTMB. "This test will enable Q2 Solutions to test sera from individuals participating in vaccine clinical trials to see whether the vaccine has induced antibodies that block infection of the virus and thereby answer critical questions in the vaccine development process."

Current COVID-19 diagnostic tests available through governments and commercial laboratories determine whether a person is infected by the virus. The UTMB research focuses on prevention through vaccine development by creating technology that helps determine the effectiveness of a vaccine candidate protecting a person from COVID-19. The planned approach is to develop a high-throughput method to measure neutralizing antibody concentrations, the gold standard method for determining vaccine effectiveness.

"We are pleased to support UTMB in this important research to develop the COVID-19 assay that, once available, may help accelerate vaccine development," said Kevin Jones, vice president and general manager, Bioanalytical, ADME, and Vaccine Laboratories for Q2 Solutions. "We are excited to take the assay developed from this research collaboration to production in our labs and enable vaccine developers to use it for large-scale human clinical trial testing to drive toward an effective COVID-19 vaccine."

About Q2 Solutions

Q2 Solutions is a leading clinical trial laboratory services organization with end-to-end laboratory services and secure, enterprise-wide biospecimen and consent management solutions. With a relentless focus on quality and innovation, Q2 Solutions uses its global experience and scientific expertise to transform science and data into actionable medical insights that help customers improve human health. With a constant focus on innovation, Q2 Solutions works with clients, using a wide array of technology platforms, to ensure maximum efficiency and quality delivery for every study. A joint venture of IQVIA (formerly QuintilesIMS) and Quest Diagnostics, Q2 Solutions combines the best of each parent organizations clinical trials laboratory services capabilities to fulfill its mission of treating each sample as if a life depends on it. To learn more, visit http://www.q2labsolutions.com.

About The University of Texas Medical Branch

Texas' first academic health center opened its doors in 1891 and today has four campuses, four health sciences schools, four institutes for advanced study, a research enterprise that includes one of only two national laboratories dedicated to the safe study of infectious threats to human health, a Level 1 Trauma Center and a health system offering a full range of primary and specialized medical services throughout the Texas Gulf Coast region. UTMB is an institution in the University of Texas System and a member of the Texas Medical Center.

Click here to subscribe to Mobile Alerts for IQVIA.

View source version on businesswire.com: https://www.businesswire.com/news/home/20200324005381/en/

Contacts

Tor Constantino, IQVIA Media Relations (tor.constantino@iqvia.com)+1.484.567.6732

Andrew Markwick, IQVIA Investor Relations (andrew.markwick@iqvia.com)+1.973.257.7144

Read more here:
Q2 Solutions, an IQVIA and Quest Diagnostics Joint Venture, Collaborates with University of Texas Medical Branch to Help Accelerate Development of...

Some 22 years ago, Icelandic scientists were amazed to discover birch tree seedlings growing on the barren Skeiarrsandur sand plain. The budding forest had sprung up naturally, without any human efforts, despite the dry and seemingly inhospitable environment. Now scientists have determined where the seeds came from.

At 1,300 square kilometres (502 square miles), Skeiarrsandur is the largest sand plain in the world. It stretches from the base of Vatnajkull, Icelands largest glacier, all the way to the ocean.

The first birch trees on the plain were spotted around 1998, two years after a glacial outburst flood caused by the Grmsvtn volcano had flooded Skeiarrsandur. The sediment deposited by the flood may have been a crucial factor in the success of the areas new birch trees. The forest is now on course to become the largest natural birch forest in Iceland in a handful of years.

We have compared genetic material from birch on Skeiarrsandur and birch in three birch forests nearby and now have its paternity test results, if you will, Kristinn Ptur Magnsson, Professor of Genetics at the University of Akureyri, explained to RV reporters recently. It was Kristinns job to determine the origin of the seeds that had unexpectedly thrived on the sand plain.

Scientists compared the genetic material of the birch on Skeiarrsandur to that of birch in Bjarstaaskgur, Npstaaskgur, and the forest on Skaftafellsheii heath. Its clear that this birch comes from Bjarstaarskgur, which is not a bad inheritance, because that old birch forest is particularly beautiful, Kristinn stated.

At the time of settlement, somewhere between 25-40% of Icelands land area was covered by birch forest. Today forests cover less than 2% of Iceland, largely due to settlers clearing of land for firewood and livestock grazing. According to Kristinn, the most remarkable thing about this project is that birch can plant itself in this way [] This shows and proves that if we give these forests that are disappearing today a little room to propagate, then they should be able to do so.

Go here to read the rest:
Icelandic Researchers Discover Origin of New Birch Forest - IcelandReview

But this virus infected only bats, not humans. The researchers named it RaTG13 and then promptly forgot about it.

At the same time, other research groups noted these bat coronaviruses regularly seemed to jump from animals to humans, and posed a significant pandemic threat.

In 2013, in the province of Yunnan, about 2000 kilometres west of Wuhan, a horseshoe bat was caught in a trap.

And then ... the world moved on. We had bigger things to worry about than Chinese bat coronaviruses.

It is now clear we made a mistake.

The virus that is causing the first pandemic in 100 years it will likely kill millions before this is all over, and mean that life may never be the same again shares 96 per cent of its genetic code with RaTG13.

We have been monitoring these coronaviruses. Theyve been jumping species boundaries, says Professor Edward Holmes. We knew this was going to happen.

Loading

RaTG13, or another very similar bat virus, has managed to pick up two tiny genetic tweaks that turned it from a bat disease into a virus perfectly adapted to make humans sick.

Then it had the unbelievable misfortune to emerge in exactly the wrong place at exactly the wrong time.

Its got this beautifully adapted set of mutations, says Holmes. In his published work, he calls it a perfect epidemiological storm.

Holmes, a researcher based at the University of Sydney, is among the worlds leading experts on the genetics and evolution of SARS-CoV-2, the virus that causes COVID-19.

He was on the team that first sequenced the genes of the virus from one of the first patients in Wuhan. Their article on the possible origins of the virus is now the most-publicised Nature study in the history of that venerable journal.

He has visited the Huanan seafood and wildlife market where the Wuhan outbreak began. He has visited caves in China, searching for bats so he can survey the viruses they contain.

CoV-2 is a coronavirus, just like SARS and MERS. These viruses get their name from how they look under a microscope: a tiny bubble of fat surrounded by a crown of spikes which are used to penetrate cells.

An electron-microscope image of the COVID-19 virus, isolated from the first Australian coronavirus case.Note the bubble in the centre surrounded by spikes.Credit:CSIRO

Animals have many different types of viruses. But coronaviruses seem uniquely able to jump from animal to human. They just have this ability, says Holmes. We dont know why.

The emergence of SARS in 2003, killing 774 people, should have been a warning: these viruses jumped, and when they did lots of humans died.

CSIRO comparative immunologist Michelle Baker. Credit:CSIRO

We should have started building broad-based vaccines and antivirals that target all coronaviruses.

Instead, SARS was defeated largely by enhanced hygiene measures. Several drugs and vaccine candidates for SARS were developed and then largely abandoned.

We have been completely complacent, says Dr Michelle Baker, the CSIROs leading bat virus researcher.

It gets really difficult to get funding when there is not an outbreak. People feel a sense of security. They dont feel its relevant anymore.

The virus pulled from bats in 2013 could not infect humans. SARS-CoV-2 can. Why?

It appears that two tiny tweaks to the virus genetic code have made a huge difference.

CoV-2 wants to do two things: bind to a human cell and then get inside it. The virus binds to a cellular receptor think of them as little antennae that stick off the side of human cells called ACE2.

ACE2 receptors are designed to listen for signals that change our blood pressure. Fine adjustments to blood pressure are really important in our lungs, so our lung cells are covered in ACE2 receptors.

SARS was able to bind to ACE2. But small genetic changes mean CoV-2 binds almost perfectly, at least 10 times more tightly than SARS. Its beautifully adapted to do that, says Holmes.

But thats not enough. Once CoV-2 is stuck on a cell, it needs to get in. Thats where the second tweak comes in.

CoV-2 is covered in spikes. They act like tiny harpoons. The virus needs to stick to the cell and then fire a harpoon. The harpoon pulls the surface of the cell and the virus together, allowing them to fuse. Thats how the virus gets inside.

A 3D map of the virus's spike protein, which it uses to 'harpoon' human cells. Credit:Science

But you dont want the harpoon firing off randomly, says Professor Stephen Turner, head of microbiology at Monash University. You only want it to fire when its ready to infect the cell. If its going off too early or too late, the virus would not be able to infect us.

To trigger the harpoon at just the right time, viruses rely on human enzymes, little proteins in our blood. Some enzymes trigger the harpoon too early, others trigger it too late. Among the best enzyme triggers the one that fires the harpoon at exactly the right time is an enzyme called furin. Our bodies produce heaps of furin.

Basically, you can work out if a virus is going to be highly pathogenic or not if it is activated by furin, says Turner.

Bird flu is triggered by furin. We got lucky, though, because it wasnt very good at sticking to our cells. CoV-2 is great at sticking to our cells. And its triggered by furin, among the best triggers a virus can have.

The combination is what makes it so infectious, says Turner.

How does a bat virus pick up these tricks?

Bats live essentially symbiotic relationships with their viruses. The viruses dont want to kill the bats, because then theyd have nowhere to live.

When scientists test bats, they find lots of different viruses but at very low levels. Often its really difficult to find a virus in a bat, says Baker.

And these viruses are, in evolutionary terms, very stable. They dont change much. It is unlikely RaTG13 turned into SARS-CoV-2 within a bat, Baker says.

Loading

But things change when a bat virus jumps to another animal.

Heres one potential scenario.

RaTG13 has the ability to bind to ACE2. But it did not have the furin tweak which makes the virus so infectious.

It is possible RaTG13, or a similar virus, jumped from a bat into a pangolin a small, scaly anteater common to Asia and highly valued in traditional Chinese medicine.

Pangolins also have the ACE2 receptor, as do other animals like ferrets.

Either of these animals, or many others, could have been the middle animal between bats and humans.But in this particular origin story, the pangolin was infected at the same time with another bat coronavirus. This virus possessed the furin tweak.

When two viruses infect the same host, they can recombine swapping their genes.

This may have created a virus that could both stick to ACE2 and use furin to quickly get inside human cells. That could have been how SARS-CoV-2 was born. Then it jumped to humans in the close confines of the Wuhan wet market.

An image of a bamboo rat caged on top of a deer allegedly sold at the Wuhan seafood market has circulated online. Credit:Weibo

And Wuhan is the perfect spot for a virus to jump. The city is home to millions. It is an international travel hub. The virus appeared just before the biggest travel period of the year: the Chinese Spring festival.

That story is neat. But it is no certainty. The first documented COVID-19 patient had no exposure to the wet market.

It is possible, although unlikely, this virus was circulating in humans for years before breaking out into a pandemic.

It could have spread silently, causing only mild cold-like symptoms, before suddenly acquiring a key mutation or two that made it much more contagious - and much more dangerous. You cannot rule that out, says Holmes.

Whether that market was involved or not, its really unclear at the moment. We may never answer that question.

Holmes is shocked at how fast SARS-CoV-2 has spread. But hes not shocked it was a bat coronavirus that caused a worldwide pandemic.

Environmental damage, illegal wildlife trading (pangolins in particular are heavily traded), wet markets and the climate crisis are all combining to push humans and bats closer than ever before.

It is blindingly obvious that we as humans have to change the way we interact with the animal world. There is no doubt about that, he says. And its not the animals' fault.

Bats have been carrying these viruses for millennia. Its not them thats changed, its us the way we interact with them.

The whole world is now set up for a pandemic - we live in megacities, there is transport. Its an accident waiting to happen, and it happened.

Loading

When the world eventually starts to recover from the pandemic, steps need to be put in place to widen the gap between bats and humans so this cannot happen again, Holmes says.

We have to cut our exposure. Those markets have to go, he says. The illegal trade in wildlife has to end. We have to cut our exposure. Thats very very clear.

Liam is The Age and Sydney Morning Herald's science reporter

Continue reading here:
The perfect virus: two gene tweaks that turned COVID-19 into a killer - Sydney Morning Herald

We all know, by now, what it looks like. A sphere, some 120 nanometres in diameter, hedgehogged by what appear to be microscopic Nik Naks, the most famous positive-sense single-stranded RNA virus in history.

We think we know where it came from likely a Wuhan wet market, where live animals of all stripes are stored and slaughtered in close quarters. And we know the likely candidates maybe a bat, possibly a pangolin. We know its zoonotic, which is to say it went from them to us.

And we know, of course, what it does once it gets there: once in the lungs' mucus, those Nik Nak protrusions will get incredibly lucky, because once it bumps into one of the cells that line the lung wall it will find, protruding from the cells surface, a chunk of protein, which normally helps modulate hormones within the body, but whose shape matches the virus protrusions so perfectly they stick together. The cells will fuse and the RNA payload of the virus will be deployed.

We know that some people wont have symptoms at all, unwitting members of the virus shadow-spreader army. And we know for others that it starts with a persistent cough and then a fever. For most, we know that means a week, maybe two, in bed. But we know that for others, as the virus is copied over and over again by our own ribosomal proteins, that each breath will feel like a battle: we know they may need medical help, they may need a ventilator and we know that for some, no amount of help will be enough.

We know it hardly affects children, though we dont know why. We know it affects the old much more severely, though we dont understand the disparity. We know that if youre relatively young and healthy and dont smoke and exercise regularly your symptoms will be mild. Or, rather, we thought we knew. That was last week. Now we know its far more egalitarian than we ever suspected.

And yet, for a virus currently spreading across the globe at pandemic speed, taking the lives of thousands and threatening the lives of millions, we actually do know an incredible amount.

Just as the Chinese government were looking to quarantine the entire city of Wuhan in mid-January, the country's scientists had already identified the virus one that would officially be named sars-cov-2; Covid-19 is the disease it creates in humans and shared its genetic sequence with scientists all over the world. The race was on.

All vaccines, points out Professor Paul Klenerman, a specialist in virology at Oxford University, essentially do the same thing: They introduce some component of the virus so that the immune system can recognise it, so when it sees the real thing it's already got that memory.

The old-school approach would have seen a weakened version of the virus this involves growing it in culture until its attenuated introduced. Its how we came up with a vaccine for yellow fever. It can produce good protection, but its slow.

And yet, with sars-cov-2, there are problems. Even a weakened novel virus could make a patient significantly sick and weakening it in the first place is difficult.

So, new virus, new rules: the World Health Organization currently lists more than 40 companies and institutions around the world all working on a cure at breakneck speed, with only a couple using anything similar to this method.

But while the advanced techniques are elegant such as a method that essentially gives your body instructions on how to create the perfect antibodies without any version of the virus ever being introduced all vaccines have some old-school bottlenecks, such as animal and human testing, along with mass production.

And while at a meeting of the WHO in mid-February it was agreed that, for the first time, human testing could start before animal testing had ended, the reality is it will take a year to develop, even with the most optimistic estimate, with anything up to two years likely.

One of the quickest ways to get a vaccine to market is to use a vector vaccine that essentially uses another virus to deliver a piece of the problematic virus to the immune system. In the case of theOxford Universityteam, theyre delivering the genetic sequence of the spike protein that latches onto the lung cells.

Its about using a platform that is already quite tried and tested, says Klenerman. You know the vector can accept enough antigen from the viral information. You know it produces a good enough immune response. You basically know its safe, because the safety of the vaccine really depends on the vector.

The Oxford team will be using an adenovirus it originally comes from chimpanzees which has been tested endlessly in studies of infectious diseases and cancers as a suitable genetic smuggler. The team has also already done several trials with Middle East respiratory syndrome (mers) using the same technique and with significant success.

So we already know quite a lot about what sorts of immune responses can be generated against that sort of protein, says Klenerman.

And theyre not the only ones.The German Centre For Infection Researchare looking to use measles as the vector, researchers at theUniversity Of Hong Kongare using a weakened fly virus, whileJohnson & Johnsonin the States are using a virus that causes the common cold.

Animal trials of the Oxford vaccine will start next month on ferrets and macaques, with the team hopeful of the first human trials in the summer.

Yet even with the shortened testing and manufacturing periods that a known vector vaccine would allow, Klenerman says around a year is the most optimistic timeframe for it to arrive.

You cant shortcut this too much, he says. You need the data. Itll take many months of trialling. Everyone is really cautious about introducing a vaccine thats safe, that doesnt cause any harm.

When Stphane Bancel, the chief executive of a small Boston biotech groupModernathat, after almost a decade, had still yet to turn a profit, called a colleague at the National Instututes Of Health last autumn, the idea was for the two organisations to run a test at the companys manufacturing plant to see how swiftly they could respond to a potential pandemic. But before that test was even possible, the real world intervened.

Moderna has moved with breakneck speed. From receiving the virus entire genetic sequence on 10 January, its 40 scientists managed to develop a vaccine in what is a world record from identification to potential cure: just 42 days. And just two weeks ago, on 16 March, Neil Browning a 46-year-old software engineer at Microsoft became the second human test subject, after being injected with a substance Moderna is calling mRNA-1273 as early clinical testing began, making it total of 63 days from sequencing to injection.

Its overwhelmingly the world record, said Anthony Fauci, the director of the National Institute Of Allergy And Infectious Diseases. In total, 45 subjects are set to receive the test vaccine in the coming weeks.

The speed is due to the ground-breaking area of viral genetics, whereby scientists can work on the vaccine after receiving its genetic sequence by email, without the need for a sample of the virus itself. Human cells are then genetically reprogrammed for the production of the coronavirus protein. Essentially, the body creates something that looks like the virus and so can learn how to fight it in a way that is entirely safe: a punching bag instead of a puncher. You essentially bypass the virus bit, says Klenerman.

But its very cutting-edge techniques may prove to be the problem. Its an elegant solution when modelled on a computer, but while these things sometimes work quite well in preclinical models, adds Klenerman, theyre not quite so powerful in humans. There are also question marks over how quickly production could be scaled up.

Another American company Inovio are using the same technology, as areCureVacin Germany. The latter sparked international headlines last month when it was reported that the Trump administration offered the company large sums of money for exclusive rights to any Covid-19 vaccine they developed.

Germany is not for sale, German economy minister Peter Altmaier told broadcaster ARD in reaction to the news.

Currently, no vaccine made from genetic material has ever been approved for use and even the most optimistic estimates put a vaccine coming from this technique at 18 months away.

Perhaps the biggest irony of most modern vaccines is that so few have been put into widespread use, coming as they often do so long after the initial outbreak, by which time its often been contained or people have developed immunity (or, rather, the survivors have). This is what happened with many severe acute respiratory syndrome (sars) and ebola vaccines funding vanished when the panic subsided.

There is always that potential, says Klenerman. Hopefully these will be quick enough that youll be able to see if they work or not.

In the short- and medium-term, the only hope is existing drugs ones already approved for other purposes or already known to be largely safe. These wont make you immune, but can be administered to diagnosed patients and may end up saving many more lives than a vaccine arriving when the damage has already been done.

Earlier this month the World Health Organization launched Solidarity, a global megatrial of the four most promising treatments.

The most hopeful of these is Remdesivir. Originally designed to combat ebola, it shuts down viral reception by inhibiting a key viral enzyme. The only problem was, it didnt work on ebola. Yet later lab and animals studies showed that it did prove effective on both sars and mars two incredibly close relations to sars-cov-2. In fact, the very first patient in the States with Covid-19 was given it when his condition worsened and improved the next day. It can also be given at high doses without risk of toxicalities.

Jiang Shibo of Fudan University, an expert in coronavirus therapeutics, has said that Remdesivir has the best potential to be used in clinics.

Creator Gilead Sciences recently courted controversy after applying and being granted orphan drug status for Remdesivir, meaning years of exclusivity and the ability to set whatever price it sees fit. Gilead Sciences later asked the FDA to rescind the status after a public backlash, with presidential candidate Bernie Sanders calling the move truly outrageous.

WHO was all set to exclude another compound chloroquine and hydroxychloroquine from its global megastudy, but changed its mind in mid-March as the drugs received significant attention in many countries. It was curious, as it seemed the least promising of the bunch.

One person who has certainly had their attention on it is the American president Donald Trump, who has repeatedly talked up the medication, calling it a game changer. In fact, he has talked it up so much that people have taken the non-medical version of chloroquine chloroquine phosphate, a chemical used to clean fish tanks in apparent attempts to self-medicate, with several ending up in emergency rooms as a result and one man from Arizona dying.

And yet its hard to understand what Trump sees in it. The decades-old antimalarial which works by decreasing the ability of the virus cells to ingest other cells has been used in trials against two other viral diseases (dengue and chikungunya) without success, while no evidence suggests it works with Covid-19 either.

One of the main mysteries that remain, says Klenerman, is why some people develop mild symptoms, while for others it's severe. It is, he says, currently a big, big area of research to try to understand what process is happening in the patients that leads them to develop severe disease, whereas some people will have a mild or even a completely asymptomatic course.

Right now, there are advanced technologies that can pick apart our immune responses against the virus piece by piece, cell by cell, molecule by molecule, with the hope of understanding it. The solution may be a medication we already have. I just hope we make some progress very quickly.

How to take control of your coronavirus anxiety

Best hand sanitiser and hand soap to keep bacteria at bay

How I passed the time in coronavirus-related self-isolation

Read more:
The race to find the coronavirus cure - British GQ

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

View original content to download multimedia: http://www.newswire.ca/en/releases/archive/March2020/31/c7291.html

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