Amid the chaos of an epidemic, those who survive a disease like COVID-19 carry within their bodies the secrets of an effective immune response. Virologists like me look to survivors for molecular clues that can provide a blueprint for the design of future treatments or even a vaccine.

Researchers are launching trials now that involve the transfusion of blood components from people who have recovered from COVID-19 to those who are sick or at high risk. Called convalescent-plasma therapy, this technique can work even without doctors knowing exactly what component of the blood may be beneficial.

For the pioneering work of the first treatment using therapeutic serum in 1891 (against diphtheria), Emil von Behring later earned the Nobel Prize in medicine. Anecdotal reporting of the therapy dates back as far as the devastating 1918-19 influenza pandemic, although scientists lack definitive evidence of its benefits during that global health crisis.

The extraordinary power of this passive immunization has traditionally been challenging to harness, primarily due to the difficulty of obtaining significant amounts of plasma from survivors. Due to scarce quantities, infusions of plasma pooled from volunteers were reserved for those most vulnerable to infection.

Fast forward to the 21st century, and the passive immunization picture changes considerably, thanks to steady advances in molecular medicine and new technologies that allow scientists to quickly characterize and scale up the production of the protective molecules.

The immune systems of COVID-19 survivors figured out how to combat and defeat the invading SARS-CoV-2 virus.

Neutralizing antibodies are one kind of immunological front-line response. These antibodies are proteins that are secreted by immune cells called B lymphocytes when they encounter an invader, such as a virus.

Antibodies recognize and bind proteins on the surface of virus particles. For each infection, the immune system designs antibodies that are highly specific for the particular invading pathogen.

For instance, each SARS-CoV-2 virus is covered by distinctive spike proteins that it uses like keys to unlock the doors to the cells it infects. By targeting these spikes imagine covering the grooves of a key with tape antibodies can make it nearly impossible for the virus to break in to human cells. Scientists call these kind of antibodies NAbs because they neutralize the virus before it can gain entry.

A holy grail for vaccinologists is figuring out how to spark the production of these ingenious antibodies. On first infection, your B lymphocytes train themselves to become expert producers of NAbs; they develop a memory of what a particular invader looks like. If the same invader is ever detected again at any time, your veteran B lymphocytes (known as memory B cells by this stage) spring into action. They rapidly secrete large quantities of the potent NAbs, preventing a second illness.

Vaccines capitalize on this ability, safely provoking an immune response and then relying on the immune systems memory to be able to fend off the real pathogen if you ever encounter it.

Passive immunization is a process in which neutralizing antibodies from one individual can be used to protect or treat another. A clever example of this process exploited by nature is breastmilk, which passes protective antibodies from the mother to the infant.

In addition to their potential preventative role, neutralizing antibodies are starting to prove beneficial in novel treatments for viral disease. Harnessing their protective power has been challenging, though, primarily because isolating enough antibodies to be effective is laborious.

Recent advances in the technology of molecular medicine at last allowed the kind of scale-up that enabled researchers to test the immunological principle. In 2014-15, Ebola virus disease surfaced in West Africa, triggering an epidemic that raged for over a year, killing more than 11,000 people. About 40% of those infected died. There were no treatments and no vaccine.

In the midst of the devastation came innovation: ZMapp, a mix of three synthetic NAbs showed early promising results in ameliorating disease in people infected with EBOV.

By the time Ebola again emerged from the rainforest, this time in 2018 in the Democratic Republic of Congo, the science was ready. In November 2018, doctors launched three parallel trials comparing three different antibody cocktails. Nine months later, spectacular results allowed for an immediate end of the experimental trials so the cocktails could be used in the field.

While ZMapp did not work as well as anticipated, the trials identified two other antibody-based therapies from two different companies that did suppress Ebola symptoms in infected patients. The earlier in their infection that patients received therapy, the better the protection.

Infectious disease experts around the globe heralded the results as a vital breakthrough.

At that time last fall, it would have been difficult to imagine that within six months thered be an even greater need for the powerful strategy of passive immunization.

While the SARS-CoV-2 virus is moving quickly, with almost 1 million confirmed infections worldwide as of this writing, the science is racing to catch up.

Days ago a report published by scientists working in Shenzhen, China, suggested that plasma which contains antibodies from survivors of COVID-19 was successful in treating five critically ill patients. At the end of March, the FDA approved the use of convalescent plasma in treating severely ill people here in the U.S. In addition, Mt. Sinai in New York has established a collaboration with the FDA and other hospitals to begin clinical trials to scientifically determine whether this strategy of passive immunization is viable.

While the rapid move to evaluate this novel treatment is a moment for celebration, the science must keep moving. Convalescent plasma, which is isolated from recently recovered survivors, is in too short of a supply to be broadly useful. The most potent neutralizing antibodies must be quickly characterized and then produced efficiently in large quantities. Several companies, as well as a number of powerhouse academic labs, aim to meet the challenge of identifying and generating these life-saving NAbs.

At the fore is Regeneron, the pharmaceutical company that designed the effective Ebola treatment. Although targeting a different virus, their overall strategy remains the same. Theyve isolated and characterized NAbs and plan to engineer a cocktail of the most potent molecules. The viral target of these antibodies is the SARS-CoV-2 spike protein; the NAbs work by preventing the virus from entering cells.

Clinical trials are planned for early summer, essentially three months time. It is a breakneck pace for the development of such a sophisticated tool of intervention.

As the U.S. enters the exponential phase of COVID-19s spread, this treatment cannot come soon enough.

[You need to understand the coronavirus pandemic, and we can help. Read our newsletter.]

Ann Sheehy, Professor of Biology, College of the Holy Cross

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Read this article:

Antibodies in blood of COVID-19 survivors can beat coronavirus and researchers are already using them for new treatments - Raw Story

Ann Sheehy, College of the Holy Cross

Amid the chaos of an epidemic, those who survive a disease like COVID-19 carry within their bodies the secrets of an effective immune response. Virologists like me look to survivors for molecular clues that can provide a blueprint for the design of future treatments or even a vaccine.

Researchers are launching trials now that involve the transfusion of blood components from people who have recovered from COVID-19 to those who are sick or at high risk. Called convalescent-plasma therapy, this technique can work even without doctors knowing exactly what component of the blood may be beneficial.

For the pioneering work of the first treatment using therapeutic serum in 1891 (against diphtheria), Emil von Behring later earned the Nobel Prize in medicine. Anecdotal reporting of the therapy dates back as far as the devastating 1918-19 influenza pandemic, although scientists lack definitive evidence of its benefits during that global health crisis.

The extraordinary power of this passive immunization has traditionally been challenging to harness, primarily due to the difficulty of obtaining significant amounts of plasma from survivors. Due to scarce quantities, infusions of plasma pooled from volunteers were reserved for those most vulnerable to infection.

Fast forward to the 21st century, and the passive immunization picture changes considerably, thanks to steady advances in molecular medicine and new technologies that allow scientists to quickly characterize and scale up the production of the protective molecules.

The immune systems of COVID-19 survivors figured out how to combat and defeat the invading SARS-CoV-2 virus.

Neutralizing antibodies are one kind of immunological front-line response. These antibodies are proteins that are secreted by immune cells called B lymphocytes when they encounter an invader, such as a virus.

Antibodies recognize and bind proteins on the surface of virus particles. For each infection, the immune system designs antibodies that are highly specific for the particular invading pathogen.

For instance, each SARS-CoV-2 virus is covered by distinctive spike proteins that it uses like keys to unlock the doors to the cells it infects. By targeting these spikes imagine covering the grooves of a key with tape antibodies can make it nearly impossible for the virus to break in to human cells. Scientists call these kind of antibodies NAbs because they neutralize the virus before it can gain entry.

A holy grail for vaccinologists is figuring out how to spark the production of these ingenious antibodies. On first infection, your B lymphocytes train themselves to become expert producers of NAbs; they develop a memory of what a particular invader looks like. If the same invader is ever detected again at any time, your veteran B lymphocytes (known as memory B cells by this stage) spring into action. They rapidly secrete large quantities of the potent NAbs, preventing a second illness.

Vaccines capitalize on this ability, safely provoking an immune response and then relying on the immune systems memory to be able to fend off the real pathogen if you ever encounter it.

Passive immunization is a process in which neutralizing antibodies from one individual can be used to protect or treat another. A clever example of this process exploited by nature is breastmilk, which passes protective antibodies from the mother to the infant.

In addition to their potential preventative role, neutralizing antibodies are starting to prove beneficial in novel treatments for viral disease. Harnessing their protective power has been challenging, though, primarily because isolating enough antibodies to be effective is laborious.

Recent advances in the technology of molecular medicine at last allowed the kind of scale-up that enabled researchers to test the immunological principle. In 2014-15, Ebola virus disease surfaced in West Africa, triggering an epidemic that raged for over a year, killing more than 11,000 people. About 40% of those infected died. There were no treatments and no vaccine.

In the midst of the devastation came innovation: ZMapp, a mix of three synthetic NAbs showed early promising results in ameliorating disease in people infected with EBOV.

By the time Ebola again emerged from the rainforest, this time in 2018 in the Democratic Republic of Congo, the science was ready. In November 2018, doctors launched three parallel trials comparing three different antibody cocktails. Nine months later, spectacular results allowed for an immediate end of the experimental trials so the cocktails could be used in the field.

While ZMapp did not work as well as anticipated, the trials identified two other antibody-based therapies from two different companies that did suppress Ebola symptoms in infected patients. The earlier in their infection that patients received therapy, the better the protection.

Infectious disease experts around the globe heralded the results as a vital breakthrough.

At that time last fall, it would have been difficult to imagine that within six months thered be an even greater need for the powerful strategy of passive immunization.

While the SARS-CoV-2 virus is moving quickly, with almost 1 million confirmed infections worldwide as of this writing, the science is racing to catch up.

Days ago a report published by scientists working in Shenzhen, China, suggested that plasma which contains antibodies from survivors of COVID-19 was successful in treating five critically ill patients. At the end of March, the FDA approved the use of convalescent plasma in treating severely ill people here in the U.S. In addition, Mt. Sinai in New York has established a collaboration with the FDA and other hospitals to begin clinical trials to scientifically determine whether this strategy of passive immunization is viable.

While the rapid move to evaluate this novel treatment is a moment for celebration, the science must keep moving. Convalescent plasma, which is isolated from recently recovered survivors, is in too short of a supply to be broadly useful. The most potent neutralizing antibodies must be quickly characterized and then produced efficiently in large quantities. Several companies, as well as a number of powerhouse academic labs, aim to meet the challenge of identifying and generating these life-saving NAbs.

At the fore is Regeneron, the pharmaceutical company that designed the effective Ebola treatment. Although targeting a different virus, their overall strategy remains the same. Theyve isolated and characterized NAbs and plan to engineer a cocktail of the most potent molecules. The viral target of these antibodies is the SARS-CoV-2 spike protein; the NAbs work by preventing the virus from entering cells.

Clinical trials are planned for early summer, essentially three months time. It is a breakneck pace for the development of such a sophisticated tool of intervention.

As the U.S. enters the exponential phase of COVID-19s spread, this treatment cannot come soon enough.

[You need to understand the coronavirus pandemic, and we can help. Read our newsletter.]

Ann Sheehy, Professor of Biology, College of the Holy Cross

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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How researchers are trying to harness the blood of coronavirus survivors to beat infection - AlterNet

In the field of prevention, the work of Mexican molecular medicine researcher Laura Palomares stands out. And today, her team is developing a vaccine against SARS-CoV-2, based on the work they have been doing in recent years against dengue and zika.

I am convinced that the only way that we are going to be able to respond to this type of pandemic in a timely manner is going to be using platforms. I am referring to a vaccine, for which we already have the entire production, development, stability train, etc. , said the chemical engineer from the Instituto Tecnolgico y de Estudios Superiores de Monterrey (ITESM), that holds a masters in Biotechnology, and a doctorate in science from UNAM.

Many times we think that the laboratory is going to discover a vaccine to cure the patient, and it is not like that. This type of vaccine requires a lot of time and a lot of effort in developing the processes for production and characterization, before reaching the final patient, Laura Palomares added.

With this idea in mind, the also researcher at the Institute of Biotechnology (IBt) of UNAM has promoted the development of one of these technological and methodological platforms focused on the aforementioned Zika and Dengue viruses, conditions particularly significant for Mexico due to their high numbers of contagion, every year in different parts of the country.

The result has been a vaccine created with recombinant DNA technology, which Palomares calls a chimera.

Lets put it in simple words, for people to understand: If we take away from the platform the zika and dengue viruses, and we put the coronavirus there, that way we can get a vaccine against SARS-Cov-2, says the member of the University Commission for Attention of the Coronavirus Emergency.

What took us two years in genetic engineering, adding on and taking off proteins, understanding how these capsids were going to be assembled, characterizing them, etc., all that we had already done. So now, we are replacing that with SARS-CoV-2, and that is precisely why we have advanced so much right now , Palomares continued.

The approach to the development of vaccines through platforms has also been the route taken by two vaccines against Covid-19 in the world that are currently under clinical evaluation: that of the North American company Moderna and that of the Chinese company CanSino Biologics, stated the expert.

The coronavirus vaccine is in the testing phase in animal models, a process in which the Zika and dengue vaccine has already been evaluated. If everything progresses positively, Palomares estimates that the first human tests could be carried out in three years.

In the case of the SARS-CoV-2 vaccine that she and her team are currently developing, they plan to collaborate wth the Mexican company Liomont, which has a manufacturing plant that would allow the production of this vaccine, this way Mexico does not have to depend on transnational companies.

So this pandemic is obviously terrible for us, because it is affecting the health of a large part of the population, but also a great opportunity to raise awareness, the researcher concluded.

comments

Read the original post:

Mexico is already testing its own Covid-19 vaccine - The Yucatan Times

Young, healthy people are dying of COVID-19 infections, even if most serious cases occur in the elderly and those with preexisting conditions. Now, scientists are looking to see if genes may explain why some people fall seriously ill while others show only mild symptoms, Science magazine reported.

Several ongoing projects aim to analyze and compare the DNA of those with severe COVID-19 infection to those with mild or asymptomatic cases. Differences may lie in genes that instruct human cells to build a receptor called ACE2, which the novel coronavirus relies on to enter cells, Science reported. Alternatively, it may be that genes that support the body's immune response to the virus differ between individuals, or that those with particular blood types carry protective genetic traits that shield them from illness, as suggested by a preliminary study from China.

For now, we don't know which genes might render people susceptible to serious COVID-19 infection, but given the pace of the pandemic, researchers could identify likely candidates within a few months, Andrea Ganna, a geneticist at the University of Helsinkis Institute for Molecular Medicine Finland (FIMM), told Science.

Related: 10 deadly diseases that hopped across species

Ganna and FIMM Director Mark Daly are heading an international effort to collect genetic data from COVID-19 patients, known as the COVID-19 Host Genetics Initiative. Several biobanks, including FinnGen in Finland and the 50,000-participant biobank at the Icahn School of Medicine at Mount Sinai in New York, have "expressed interest" in contributing data to the study, according to Science. Some groups working with the initiative plan to collect DNA samples from willing patients who are currently hospitalized with COVID-19 infections. Alessandra Renieri, a geneticist at the University of Siena in Italy, expects 11 Italian hospitals to participate in such a study with her own research group.

"It is my opinion that [host] genetic differences are a key factor for susceptibility to severe acute pneumonia," Renieri told Science. Jean-Laurent Casanova, a pediatrics researcher at the Rockefeller University, is organizing a similar effort within a global network of pediatricians. Their aim is to study "previously healthy" patients under age 50 who have developed severe COVID-19 infections, as their vulnerability to the virus likely lies in their genes, Casanova told Science.

As part of their own initiatives, the UK Biobank will also begin curating data from COVID-19 patients, and the Iceland-based company deCODE Genetics will partner with the country's government to do the same. In the U.S., the Personal Genome Project at Harvard University is recruiting volunteers to share their genetic data, tissue samples, health data and COVID-19 status, Science reported.

In the coming weeks and months, these and other projects may reveal why COVID-19 only triggers a transient cough in some people, while endangering the lives of many others.

Originally published on Live Science.

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Why are young, healthy people dying from COVID-19? Genes may reveal the answer. - Live Science

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.

See original here:

How sick will the coronavirus make you? The answer may be in your genes - Science Magazine

by Claire Callahan | 4/1/20 2:15am

People have always used humor as a response to current events, no matter how serious, and Dartmouth students' reactions to COVID-19 have been no different. Dartmouth's meme page, currently titled "Dartmouth Memes for Cold AF Teens," is chock-full of memes about the coronavirus and its effects on the student body.

The page was created by Luke Cuomo '20 during his freshman winter, when other colleges meme accounts were cropping up everywhere.

If you werent there when it happened, its hard to understand, he said. There was this whole meme page culture that was developing. It was a really interesting time.

Cuomo never expected that the page would still be so active four years later. But it is.

Jennifer Hinds, a graduate student in the program in experimental and molecular medicine at the Geisel School of Medicine, posted a photo that her husband took of a sign at a bus stop on campus that read NOTICE and nothing else. She captioned it, "Dartmouth COVID-19 tAsK fOrCE emails be like.

We could all enjoy a bitter laugh, she said of her thoughts when her post started to accumulate likes. But her meme wasnt just for laughs she felt it reflected a truth about Dartmouth.

[The College] started off handling [its response to COVID-19] in what I would call typical Dartmouth fashion, Hinds said. A lot of keywords and a lot of reassurances that dont actually point to any specific action.

As a graduate student, Hinds said she doesnt usually feel connected with the undergraduate student body, but in times like this, the meme page changes that.

Being involved in something like their meme group, especially in times like this when we're all suffering from the same thing, makes me feel like I can relate more to that group of people, she said.

Paul Hager 22 edited a photo of a singer performing to an empty Gold Coast lawn with students watching through Zoom and captioned it, Green Key 20S!! All enrolled students may invite two (2) registered guests to the Zoom (proper wristband required).

Hager made the meme while he was up late studying for an exam with his friends in their River apartment. He was surprised when it got a lot of attention.

I was like, I really made it, he said, laughing. This is my moment.

Hager finds humor in the more trivial repercussions of the pandemic.

Joking about specific absurdities that will happen because of what is objectively an absurd situation is kind of the best way of dealing with it, Hager said. It's not funny that there's this global virus, but just the idea of a concert playing for no one on Gold Coast lawn he trailed off as we cracked up.

While Hager wanted to make people laugh, he also wanted to create an analogy that would show how online classes were not a viable replacement for in-person instruction. No one would question the absurdity of an online Green Key why are remote classes any more palatable?

Jacob Kingsley 23 posted a meme that poked fun at Dean of the College Kathryn Lively for routinely sending emails that look essentially identical to updates from the COVID-19 task force.

I was glad to see that it did well and that other people resonated with the joke, he said. I wasn't the only one who was confused why we were getting a hundred emails a day.

I think everyone who is posting on [the meme page] is taking this seriously. It's just a way for us to work through this in a funny way and bring each other up in this time that kind of sucks.

But when Kingsley sent his meme in another group chat, an international student told him not to joke about Lively because international students depended on her emails to know where they would be living in the spring.

I was like, Oh, thats a good point, Kingsley said. But I think it was all just generally in good fun. I think everyone who is posting on there is taking this seriously. It's just a way for us to work through this in a funny way and bring each other up in this time that kind of sucks.

This is not the first time that the meme page has fixated on a single topic. The example that stands out to the pages creator is NapkinGate an incident during Cuomos freshman winter in which Dartmouth Dining Services took away the napkin dispensers on each table at its dining locations, a move that prompted strong reactions from students.

If you speak to any 20 and say NapkinGate, they know what you mean, and thats not something that could have happened without the meme page, he said. Theres this shared consciousness.

While humor connects us as we commiserate together, the reality is that the virus has affected Dartmouth students in very different ways.

Ashwini Narayanan 22 is from Bangalore, India and is currently back home after a stressful decision about where to spend the term. She has mixed feelings on how the College handled the situation for international students.

Clearly, there's not enough infrastructure, staffing, planning and communication from the College, she said. Two weeks after the initial chaos, though, she is more inclined to believe that theyre trying their best.

As an international student, Narayanan felt distanced from the rest of campus during the transition to remote classes.

It's a whole host of things that made our situation so unique, Narayanan said, citing the anxieties of traveling through high-risk countries, the effect on financial aid, accessibility of healthcare and concerns over being allowed back into the country if she left.

People that are affected by things that change their lives in really crazy ways may or may not use humor to cope with it, but it isn't someone else's right to joke about it for them. You can't take someone else's situation and turn it into your own joke.

Narayanan said she enjoys the occasional meme and thinks its funny to joke about online classes, but that theres also the question of who can joke about what.

People that are affected by things that change their lives in really crazy ways may or may not use humor to cope with it, but it isn't someone else's right to joke about it for them, she said. You can't take someone else's situation and turn it into your own joke.

Meanwhile, Cuomo advocates for turning our surroundings into comedy.

I think it would be illogical to say that we can't make fun of the circumstances because of the unfortunate factors of reality, Cuomo said. Like everything, it's a delicate balance. People's tastes differ, and there's an invisible line that you dont see until you hit it.

Cuomo and Narayanan dont disagree on this point they both appreciate the humor of the meme page while remaining cognizant of boundaries. Many Dartmouth students seem to agree that memes about the circumstances surrounding the virus are okay, but jokes that target a specific group of people are not.

Last week, Vanessa Mauricio 21, the communications vice president of Alpha Xi Delta sorority, sent an email to her sisters after someone sent a coronavirus joke about Italians in the sorority GroupMe.

Whenever you post in the GroupMe or online, it is a representation of not only yourself, but everyone who you're affiliated with at Dartmouth, she said. We're allowed to post memes, and some of them are hilarious and relatable, but it does start to affect more than just you when it targets specific groups that are affected.

Mauricio said that her mindset is influenced not only by her position in her sorority, but also by her ethnicity.

I am Chinese, she said. I havent really bared the criticism, but Trump has been calling it the Chinese virus, so there's been a rising fear against Chinese people in general.

But Mauricio enjoys the meme page she visits it when she wants to feel happy and connected.

If I just can't find a way to be happy or laugh, I'll go to the meme page and I'll chuckle to myself and it makes me feel better, she said. It's also a way to stay connected with the people that you are close to or want to be close to. It's like, Here, Im going to let you into my circle of humor.

Its not just about laughs, though. The meme page can be a source of actual information and conversation. Kingsley brought up comedians like John Oliver, who conduct in-depth and credible research as part of their shows.

People are turned off by the idea of mainstream media and watching the news when they know it's all going to be negative, he said. If you can get it in a more positive, funny format, it's much better and more accessible to a lot of people.

Kingsley said that we often struggle with ways to address overwhelming events, but humor is something that comes naturally.

We try to talk about it and think about it in ways that are accessible, he said, which, for our generation, is memes.

In many ways, humor is a luxury its the capacity to think past survival to something as frivolous as a meme.

One phrase from Cuomo struck me: the shared misery of Zoom. Dartmouth students are currently sharing feelings of absurdity, despair, hilarity and our generation is going to express those feelings in a way that is uniquely ours.

In many ways, humor is a luxury its the capacity to think past survival to something as frivolous as a meme. But in the openness of a Facebook page, where anyone can post, I find a surprising amount of hope and collaboration.

Without an open and accessible place to share this content, this would be a little more isolating, Cuomo said. It would make hard times a little bit harder.

See the original post here:

The Shared Misery of Zoom: Making Memes in a Time of Crisis - The Dartmouth

A key driver for the advent of proteomics was the realization that complexity is driven by protein variation. Contrary to expectation, the genome is thought to be predominantly invariant1; however, the proteome displays significant plasticity that is a product of protein complexation, post-translational modification (PTM), splicing, and both the spatial and temporal regulation of proteins.2 Proteomics is the concomitant and systematic study of numerous and diverse proteins. Given that the proteome is a readout of the changing state of cells, tissues, and therefore the organism, it underpins our understanding of both health and disease.

The sensitivity associated with Nanoflow-LC has contributed to its use in a variety of novel analytical settings that may have a sample limited input. Tissues are often heterogenous in nature, and the ability to interrogate cellular heterogeneity is vitally important, for example, microheterogeneity in tumor biology. Ultra-sensitive nanoflow-LC has been combined with FACS and bespoke nanodroplet sample preparation (nanoPOTS), enabling the identification of >700 proteins from a single HeLa cell. This proteome coverage (for a single cell) is more comprehensive than previously reported.17 This affords the possibility of investigating single cells and their microenvironment to help determine their contribution to disease progression.

Biomarker discovery is often complicated by methodological challenges, where low concentrations of analytes must be determined in a complex matrix. Poor ovarian response is typically difficult to predict. Biomarker discovery studies (conducted during IVF treatment) on follicular fluid were performed using a highresolution orbitrap mass spectrometer coupled to a nanoflowLC system. Numerous proteins were identified (1079), and three of these proteins (renin, pregnancy zone protein, and sushi repeat-containing protein (SRPX)) were identified as predictors of a poor response.19Imaging mass spectrometry (IMS) is an emerging technique for mapping the spatial distribution of analytes (e.g., lipids) across tissue. However, various technical challenges have limited its application to proteomics. Applying these methods would have traditionally relied on labels that require prior knowledge of protein targets. Label-free LC-nanoflow proteomics has been used to analyze tissue voxels, prepared from mouse uterus prior to blastocyst implantation. This generated quantitative cell-type-specific images for more than 2000 proteins with a spatial resolution of 100 m.20Tooth enamel is the densest, hardest, and most mineralized human tissue. Analysis of its proteome is further complicated by the meager (<1%) presence of proteinaceous material. Amelogenin is a dimorphic and abundant tooth protein and expressed from both X and Y chromosomes. Gender may, therefore, be revealed by sequencing the gender dimorphic peptide regions. The analysis of enamel is crucial in archeological or forensic specimens where no other tissue is available and DNA may be irreparably degraded. In these circumstances, the amount of sample available may also be severely restricted. Unique peptides have been identified by acid etching single teeth and peptide identification made possible using nanoflow LC-MS. This workflow has enabled the identification of major structural enamel peptides, including amelogenin isoforms, in teeth obtained from Anglo-Saxon burials (600900 AD).21Given the drive toward increasingly small sample sizes, both micro and nano-LC are expected to play larger roles in research proteomics and will therefore remain fundamental to the advancement of biomedical science.

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The Rise of Micro and Nanoflow In Proteomics - Technology Networks

Coronavirus appears to pose a particular threat to men. Middle-aged and older men, and those with underlying health conditions that affect the immune system, are being especially badly hit by the virus. And while scientists cant say for certain why the current pandemic is discriminating by sex, it isnt a total surprise.

The discrepancy was first seen in China. An analysis of 44,672 confirmed cases from late 2019, when the virus first emerged in the city of Wuhan, up to February 11, found the death rate among men was 2.8 per cent, compared to 1.7 per cent among women. Italy whose death toll surpassed Chinas on March 19 has followed a similar trend with a case fatality rate of 10.6 per cent in men, compared with six per cent in women, according to the country's national health institute.

Men were also disproportionately likely to die during the Sars and Mers outbreaks, which were caused by similar coronaviruses. More women than men suffered from severe acute respiratory syndrome (Sars) in Hong Kong in 2003, but an analysis of all 1,755 cases showed that the death rate among men was 50 per cent higher. During the influenza pandemic of 1918, which killed an estimated 50 million people, adult men were also more likely to die than women.

While scientists dont know whats causing the gender disparity in this current pandemic, smoking and drinking have been floated as possible theories. Historically, men smoke more than women and the difference is particularly large in China, where nearly 50 percent of men but less than three per cent of women smoke.

People who smoke are more likely to develop chronic lung and heart diseases, which are tied to worse outcomes if they contract Covid-19. One of the main reasons for death is that your lungs are no longer working and if your lungs are already damaged because of smoking, theres less reserve before the lungs no longer are sufficiently effective at keeping you oxygenated, says Paul Hunter, a professor in medicine at the University of East Anglia.

A study of 1,099 patients in China with Covid-19, published in the New England Journal of Medicine in February 2020, found that smokers made up about 26 per cent of those that ended up in intensive care or died of the disease. Smokers are also more likely to contract the novel Sars-Cov-2 coronavirus in the first place as they transmit it from hand to mouth when touching their lips and because they may share contaminated cigarettes.

In Italy, however, the sex differences among smokers are much smaller than China with 28 per cent of men smoking and 19 per cent of women smoking. This may suggest that there is some other as yet unidentified factor at play.

Women mount stronger immune responses than men except during pregnancy to avoid attacking and rejecting the foetus growing inside them which could be another plausible explanation for the emerging picture of male susceptibility to the Covid-19 disease. In a series of experiments in 2016 and 2017, microbiologists from the University of Iowa infected male and female mice with the coronavirus that caused Sars, and as had happened in humans, male mice were more likely to die. But when the team removed the ovaries from females, their death rates shot up suggesting that the hormone oestrogen somehow protected them from Sars.

Hormones could also play a part in how the novel coronavirus, whose genetic makeup is around 79 per cent similar to the Sars virus, interacts with human airways. Ian Hall, a professor of molecular medicine at the University of Nottingham explains that Sars-Cov-2 uses a spike protein to attach to a receptor protein called ACE2 on the surface of human respiratory cells. There could be differences in the way in which the virus interacts with its key receptor in the airways, which might make male individuals more susceptible, he says, noting that its just one theory. Research into the shape of this spike protein and all the ways it folds and shifts with the ACE2 receptor could not only shed light into how the virus infects men and women differently but may also offer a route into treatment.

If we can identify that key difference, and then we could potentially design a drug which might remove that difference, then that would hopefully reduce the risk in males down to the same risk as you see in females, says Hall.

Ultimately, biology, lifestyle and behaviour are all likely to play a role in the spread and impact of Covid-19. But it will only be possible to understand the exact differences between men and women once more countries produce and make available sex-disaggregated statistics on infection and mortality.

Global Health 50/50, an initiative that advocates for gender equality in health, has been collecting Covid-19 infection figures from the 25 countries with the highest number of cases, but so far only 12 countries provide details on male and female fatality. Sarah Hawkes, professor of global public health at University College London, who is also co-director of the initiative, points out that some countries including the UK and US have failed to provide crucial data. They definitely have the data, but I dont know why theyre not putting it out in a sex-disaggregated manner, she says. Its not just a statistical exercise. As a doctor, Id want to know if there was this quite different risk of death and equally, Id want to know whos getting infected.

Women make up 70 per cent of the workforce in the health and social sector and, according to Hawkes, could be more exposed to the virus because of gendered roles. In many societies, its women who provide frontline care. Its women who are involved in looking after sick relatives or friends in their homes, she says. So am I seeing a spike in the number of young women who have been infected and what can I do about that? There are so many reasons why youd want to see this data.

Data on infection and death rates broken down by sex and age also help doctors and nurses plan and monitor critical care capacity in hospitals, says Hall. It does help in terms of planning critical care capacity because one needs to know how many people are likely to deteriorate. We have to match the number of patients who potentially might need critical care with the number of ventilators that are available in different spaces in the hospital.

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Why is coronavirus killing more men than women? - Wired.co.uk

COVID-19 is a respiratory disease which primarily targets people's airways.

As a result, most people who come down with the illness report difficulty breathing and a new cough as symptoms.

These mirror complaints of heavy smokers, who may find themselves at an increased risk from the virus.

READ MORE:'Quit smoking now!' Expert warns habit could increase coronavirus risk

According to Professor Gordon Dougan, of Cambridge University's Department of Medicine, more study is needed on the effects of COVID-19 on smokers.

He said while there is not yet clear evidence of the effects smoking has, smokers do suffer from impaired lung function.

Professor Dougan said: It is unlikely that anyone knows for sure yet how smoking might impact on susceptibility to COVID infection, as it is too early to call.

"We need to compare smokers versus no-smokers or countries with different incidences of smoking, and this will take time."

I would recommend that people stop smoking but, having lost my own sister to lung cancer, know it is not easy.

"I also respect people have a personal choice.

Other health experts have warned smokers are at an increased risk of developing illnesses such as COPD or cardiovascular disease, both risk factors for death amongst COVID-19 sufferers.

Ian Hall, Professor of Molecular Medicine at the University of Nottingham, said smokers should consider dropping the habit, adding withdrawal will not make them more susceptible to the virus.

While tobacco may result in vulnerability to the effects of COVID-19, manufacturers have committed to snuffing the disease out.

British American Tobacco, which makes cigarette brands such as Lucky Strike and Dunhill, said it has a potential vaccine in the works.

The company said it was attempting to develop a tobacco-based vaccine with doses available by summer 2020.

They said: If testing goes well, BAT is hopeful that, with the right partners and support from government agencies, between one and three million doses of the vaccine could be manufactured per week, beginning in June.

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Smoking and coronavirus: How dangerous is smoking amid coronavirus outbreak? - Express

The U.S. Food and Drug Administration (FDA) has approved the use of two anti-malaria drugs to treat patients infected by the new coronavirus.

On Sunday, the U.S. Department of Health and Human Services (HHS) said in a statement that chloroquine and hydroxychloroquine could be prescribed to teens and adults with COVID-19 "as appropriate, when a clinical trial is not available or feasible," after the FDA issued an Emergency Use Authorization. (EUA) That marked the first EUA for a drug related to COVID-19 in the U.S., according to the statement.

Currently, there are no specific drugs for COVID-19 which, as shown in the Statista graph below (accurate as of March 26), has sickened over half a million people. According to Johns Hopkins University, over 720,000 cases have been confirmed, more than 34,000 people have died, and over 152,000 have recovered since the pandemic started in China late last year.

Both chloroquine and hydroxychloroquine are used to treat diseases including malaria, and have "shown activity in laboratory studies against coronaviruses, including SARS-CoV-2 (the virus that causes COVID-19)," the HHS stated.

"Anecdotal reports suggest that these drugs may offer some benefit in the treatment of hospitalized COVID-19 patients. Clinical trials are needed to provide scientific evidence that these treatments are effective."

Under the EUA, health care providers and patients must be given fact sheets outlining the known risks and drug interactions of the medications.

The HSS said it accepted 30 million doses of hydroxychloroquine sulfate from an arm of the pharmaceutical company Novartis, and one million of chloroquine phosphate from Bayer Pharmaceuticals to be used for treating hospitalized COVID-19 patients or in clinical trials.

"These and other companies may donate additional doses, and companies have ramped up production to provide additional supplies of the medication to the commercial market," the HHS said.

"Given the importance of understanding the efficacy of these medications for the treatment and prevention of COVID-19, federal agencies, such as the National Institutes of Health and ASPR's Biomedical Advanced Research and Development Authority (BARDA), are working together to plan clinical trials."

The Strategic National Stockpile will ship the drugs to states, according to the statement.

The HHS said it hoped the donated drugs would "ease supply pressures" for the medications, and that it was working with manufacturers to boost production to ensure those who depend on them to treat conditions such as malaria, lupus, and rheumatoid arthritis have access.

The decision comes after FDA commissioner Stephen Hahn said that the agency would "take a closer look" at chloroquine in "a large pragmatic clinical trialto actually gather that information and answer that question that needs to be asked and answered," after President Donald Trump said chloroquine and hydroxychloroquine showed promise in COVID-19 patients.

Last week, the authors of a paper published in the Journal of Zhejiang University concluded that hydroxychloroquine is no better a treatment for coronavirus than currently used methods.

Vineet Menachery, Assistant Professor in the Department of Microbiology & Immunology at the University of Texas Medical Branch who was not involved in the research, cautioned to Newsweek last week that the paper involved a small number of participants. And while the patients didn't improve and it doesn't appear to worsen COVID-19, there are concerns about its side effects.

He told Newsweek: "Like the papers to date on hydroxychloroquine and chloroquine, there isn't much concrete data."

As experts investigate the potential benefits of the drugs, health officials last week urged members of the public not to self-medicate, after an Arizona man who took chloroquine phosphate in the form of a fish tank cleaner died.

Ian Hall, professor of molecular medicine at the University of Nottingham told Newsweek: "I am slightly surprised by this approach, as at present we don't know if these drugs are effective. Whilst there is some laboratory work and also anecdotal evidence in patients they may be effective, there are also preliminary trial data suggesting they may not work.

"All drugs have potential side effects, and we obviously want to avoid side effects in patients who are already ill with COVID19. Hence in my view the most important thing to do is to undertake formal clinical trials to find out if there is a role for these drugs in the management of different groups of patients with COVID-19."

Hall said: "Ultimately we hope a vaccine will be available, and initial studies have already commenced in healthy volunteers, but it is likely to be at least six months before we may have a vaccine for wider use."

Robin May, professor of infectious diseases and director of the Institute of Microbiology and Infection at the U.K.'s University of Birmingham, told Newsweek: "Like many things about this pandemic, the decision regarding chloroquine is a very tough one to make. Early data showed promising results with this drug, but a more recent study from China showed no evidence of efficacy. Both studies are very small, though, so the jury is still very much out.

"What is very much needed at this stage is a randomized clinical trial to establish efficacy of chloroquinebut of course, this is a challenging and long-term undertaking. In the meantime, the FDA has approved the drug for situations where alternatives are not available."

May continued: "It is critical to emphasize, however, that chloroquine can have substantial side effects, particularly if the dosing is not correct.

"The individual risk/benefit will be something that clinicians will take into account on a patient by patient basis and consequently it is absolutely essential that patients do not self-medicate in the meantime, which can have life-threatening consequences."

Andrew Preston, reader in microbial pathogenesis at the U.K.'s University of Bath, told Newsweek there is a sound basis for the use of the drugs, and the anti-viral effects of chloroquine have been demonstrated in a number of laboratory studies involving the close relatives of SARS-CoV-2the SARS and MERS viruses.

"However, while providing a rationale for the FDA decision, laboratory tests on isolated cells are a long way from showing efficacy in patients," he said.

Preston explained clinical trials "involve numbers of study participants (patients in this case) of the appropriate size to given statistically significant results." The participants are randomly assigned the treatment or a control "in which the two groups are well matched for as many parameters as possible." Those might include age, gender, underlying conditions, study centers like hospitals where precise care may differ, days since onset of symptoms, and medications taken.

Such steps haven't been followed when it comes to using chloroquine or hydroxychloroquine in COVID-19 patients, he said, and therefore it has not been possible to properly determine whether either drug had an effect, or not.

"Unfortunately, proper clinical trials take time to set up and to conduct. A number are already underway, and initial results from these can be expected in the coming days and weeks," said Preston.

Fortunately, both drugs have been used in humans, meaning doctors know they are well-tolerated, as well as the side effects and appropriate dosing levels.

"Thus, the huge concerns regarding patient safety are lifted in terms of using chloroquine and hydroxychloroquine," he said. "In this regard, many will see it as a case of 'can do no harm, but might do some good' and combined with the relative cheapness of the drugs, this probably contributed to the FDA's decision."

Preston said: "The desperate clinical need for treatment options for COVID-19, and the pressure that authorities are under to provide answers/solutions, and to be shown to providing them, it is perhaps understandable as to why the FDA has moved to approve chloroquine and hydroxychloroquine use, before the firm evidence supporting their use is available."

This article has been updated with comment from Professor Ian Hall, Professor Robin May, and Andrew Preston.

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FDA Says Hydroxychloroquine and Chloroquine Can Be Used to Treat Coronavirus - Newsweek

A magnified coronavirus germ illustration sits beside laboratory glassware during coronavirus vaccine research work inside the Pasteur Institute laboratories in Lille, France, on Monday, March 9, 2020. The euro-area economy may be headed for its first recession in seven years as the coronavirus outbreak takes an increasing toll on businesses and consumer confidence. Photographer: Adrienne Surprenant/Bloomberg via Getty Images

Long before vaccines became a thing, inoculation which is intentionally introducing a pathogen or antigen that can cause a disease into a living organism to stimulate the production of antibodies was current practice in Africa, China and India some 2,000 years ago.

According to The National Centre for Biotechnology Information (NCBI), smallpox, caused by the variola virus, appeared around 10,000 BC, at the time of the first agricultural settlements in north-eastern Africa. The virus spread around the world with disastrous effects on humankind; yet, survivors of smallpox seemed to then be immune from the virus.

This is when inoculation, also called variolation, started. The inoculator usually used a lancet wet with fresh matter taken from a ripe pustule of some person who suffered from smallpox. The material was then subcutaneously introduced on the arms or legs of the non-immune person, says NCBI. And the practice had some degree of effectiveness. Many inoculated people did become immune to smallpox, but some also died while others even started a new epidemic.

Still, there was hope and by 1796 British physician Edward Jenner, who had observed how milkmaids were generally immune to smallpox he assumed this was probably because of the pus in the blisters that milkmaids received from cowpox (a disease similar to smallpox, but much less virulent), decided to insert pus from a cowpox pustule into an eight-year-old boys arm.

The boy not only survived the experiment but also became immune to smallpox. Although the experiment proved conclusive, the vaccine wasnt born yet. The Royal Society, the UKs scientific academy, needed more proof and vaccination only became widespread two years later. And it took almost another two centuries to eradicate the smallpox entirely; it was eliminated in 1979, with the last case seen in Somalia two years earlier.

Today, as Covid-19 rapidly spreads across the world, the search for a vaccine against the novel virus is hastening. An article published by The Guardian newspaper on 25 March explained that: About 35 companies and academic institutions are racing to create a vaccine, at least four of which already have candidates they have been testing in animals. The first of these produced by Boston-based biotech firm Moderna will enter human trials imminently.

The process to create a vaccine is a complex one: as the Institut Pasteur in France explains, scientists need to understand more about the virus, the face of the virus, in order to recreate the pathogen and extract antigens, the virus toxins that spark an immune response in the body, and hopefully find antibodies that may have therapeutic applications.

The Guardian Laura Spinney reported that this process can be achieved by using live, weakened forms of the virus, or part or whole of the virus once it has been inactivated by heat or chemicals.

Professor Ed Rybicki, from the Department of Molecular & Cell Biology and Institute of Infectious Disease and Molecular Medicine at the University of Cape Town, adds that novel viruses require experimental investigational work, such as growing the novel virus in culture which is often not easy characterising it by sequencing it, fortunately [it is] very quick these days, and can be done without culturing it, then by looking at its components and how they relate to known viruses.

Yet, as it sometimes happened with inoculation, the live form can continue to evolve in the host, for example, potentially recapturing some of its virulence and making the recipient sick, while higher or repeat doses of the inactivated virus are required to achieve the necessary degree of protection.

Another option, Spinney notes, is to extract the genetic code for the protein spike on the surface of Sars-CoV-2 (Covid-19), which is the part of the virus most likely to provoke an immune reaction in humans, and pasting it into the genome of a bacterium or yeast forcing these microorganisms to churn out large quantities of the protein.

It can take years to find the right vaccine and although few companies and institutes around the world have already started human trials, results will only be known in a few months without any assurance that theyll work.

Rybicki explains that the human testing phases, following quite extensive animal testing for toxicity, immunogenicity and dosing, are broken into three phases:

First, there needs to be safety trials in a few human volunteers; 20-80 people, healthy volunteers who are monitored for reaction frequently. Some data can be gathered on immunogenicity in these trials, says Rybicki.

The second step is trials over several hundred people screened by strict criteria, usually not in a disease risk group, where more safety but also primarily immunogenicity and dosing schedule and amounts are trialled. These trials generally include randomized dosing, with placebo groups.

Finally, Efficacy trials, on thousand or multiple thousands of people, in at-risk groups of people; randomised double-blind placebo-controlled trials, that look for lower incidence of infection in vaccinated vs placebo groups generally after the trial is finished.

But there can be many hiccups along the way. Rybicki says the main challenges are investigation of the components of the virus, getting them made, and money to do the work!

In the case of Covid-19, the challenge is also the novelty of the virus. Spinney explains that In contrast, Sars-CoV-2 is a novel pathogen in humans, and many of the technologies being used to build vaccines are relatively untested too. No vaccine made from genetic material RNA or DNA has been approved to date, for example. So the Covid-19 vaccine candidates have to be treated as brand new vaccines.

When asked about collaborations between institutes and research centres around the world, Rybicki says that: A collaboration between various centres is proposed; what is happening right now in terms of response is a scramble to develop and roll out tests mainly nucleic-acid based by the NICD and partners, and to sequence virus isolates by NICD and various academic groups.

We started quite early here at UCT with proposing a South African programme for vaccine development: this would have involved mine and Professor Anna-Lise Williamsons groups and partners like Professor Wolfgang Preiser at Stellenbosch University, in making several candidate vaccines (our groups) and doing neutralisation tests on animal serum injected with these candidates (Preiser). We expanded this into a proposal to Department of Science and Innovation (DSI) which included Professors Jonathan Blackburn, Ed Sturrock, Wendy Burgers and Dr Mani Margolin from UCT, which aimed at a One Health type of approach, where we would produce and test proteins as possible components of serological test kits, some of which could also be used as vaccines. This got subsumed by a national effort apparently led by the South African Medical Research Council (SAMRC) and DSI on trying to co-ordinate response efforts which seem to have as their priority the development and deployment of PCR-based testing, with serological reagent provision very necessary for bedside blood tests and testing to see who is already immune more on a back burner, and vaccines a maybe for the future.

On the progress made, Rybicki explains that their group has been able to create through cell culture and plants a candidate reagent or vaccine based on the S or spike protein of SARS-CoV-2. He is confident that this could give the basis of a reagent supply to other institutions or companies for the formulation of serological assays. ML

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Vaccines: what are they and how do they work? - Daily Maverick

Scientists all over the world are working on finding ways to quickly test and develop vaccines for COVID-19.

The first step was finding and isolating the virus so other scientists and researchers can begin working with the live virus and come up with vaccines that may be able to defeat this illness.

In Canada, a joint team of researchers from Sunnybrook Hospital, the University of Toronto and McMaster University quickly collaborated to become one of the first in the country to isolate the COVID-19 virus. With that breakthrough, other Canadian researchers have started their work on combatting the disease.

Today we are talking with Dr. Karen Mossman, now in self isolation, who is a professor of pathology and molecular medicine and vice president of research at McMaster University.

She talks about what it took to isolate the virus, what creating a vaccine entails and what is giving her hope about all the work being done.

Listen here or subscribe at Apple Podcasts, Spotify or wherever you listen to your favourite podcasts.

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A (now isolated) scientist who isolated the COVID-19 virus explains the fight for a vaccine - Toronto Star

Scientists at Sunnybrook Hospital, the University of Toronto, and McMaster University successfully isolated and cultured SARS-CoV-2, the virus that causes the COVID-19 disease, from two patients, accelerating progress toward a COVID-19 vaccine.

The discovery was announced on March 12, and comes almost three months after the outbreak of COVID-19, which started as an epidemic in Wuhan, China in December 2019. One day earlier, on March 11, the World Health Organization (WHO) had declared the virus spread across the globe to be a pandemic.

Research teams from all across the world have started accepting grants to work on developing a potential vaccine. Even though COVID-19 shares genomic and structural similarities with severe acute respiratory syndrome better known as SARS another strain of coronavirus that was identified and previously researched in 2003, the WHO has said that it would take at least 18 months to develop a vaccine.

Dr. Rob Kozak, a clinical microbiologist at U of T and at Sunnybrook Hospital, told Sunnybrook News that researchers from these world-class institutions came together in a grassroots way to successfully isolate the virus in just a few short weeks.

Lab-grown copies of the virus will help researchers around the world enhance their understanding of the virus biology and evolution in order to develop better treatments and a potential vaccine.

One of the primary uses of the isolated virus will be as a control group to see whether the tests currently being used by health care providers are performing as expected, according to Dr. Samira Mubareka, an infectious diseases physician and microbiologist whos at U of T and Sunnybrook.

Researchers can also use the isolated virus to measure the effectiveness of the vaccines and drugs that are currently in development.

As Kozak explained to U of T News, From a bigger picture standpoint, having a virus isolate that can be shared with other labs to perform other experiments to better understand the virus and how to stop it is critical.

Karen Mossman, a professor of pathology and molecular medicine at McMaster University, told The Globe and Mail that she and her colleagues would be using the isolated virus to understand how COVID-19 counteracts the human immune response.

As of time of publication, the virus has infected more than 662,000 people in over 177 countries and regions, and caused more than 30,800 deaths. While there is more work to be done, there is cause for hope, as the isolation of SARS-CoV-2 could eventually help quell the outbreak and save many lives worldwide.

Now that we have isolated the SARS-CoV-2 virus, we can share this with other researchers and continue this teamwork, said Dr. Arinjay Banerjee, Natural Sciences and Engineering Research Council of Canada postdoctoral fellow at McMaster University, to Sunnybrook News, emphasizing that this collaboration will continue.

The more viruses that are made available in this way, the more we can learn, collaborate and share, he added.

Tags: coronavirus, COVID-19

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COVID-19 breakthrough: researchers from U of T and McMaster successfully isolate virus - Varsity