Universityof Toronto researcherSachdev Sidhuand his collaborators are engineering antibody molecules that can neutralize the novel coronavirus in the body before it invades cells.

Sidhu (left) already leads a differentteam that received supportin the first round of federal funding. The goal of that project is to design antiviral medicines that block viral replication.

With our two funded projects, we are working to develop molecules that can target the virus both inside human cells and on the outside to prevent it from getting in, says Sidhu, who is a professor of molecular genetics in the Faculty of Medicine.

Other teams in Canada, as well as in the U.K. and U.S., are looking to infuse Covid-19 survivors blood plasma containing antibodies into patientsto aid their recovery. Plasma transfusion, however, is fraught with challenges, including variability in efficacy between different donors and risk of disease transmission. Synthetic antibodies, on the other hand, represent a defined drug in terms of molecular content, efficacy and dosing regimen.

Rini has previously helped to determine how antibodies bind to and inactivate the SARS virus, the coronavirus that caused the outbreak in Asia more than 15 years ago. Also on the team isAlan Cochrane, a professor in the department of molecular genetics and an HIV virologist with expertise in viral RNA processing.

The antibodies will be engineered to block the so-called S-protein that forms spikes on the virus's surface. The spikes lock on to a protein called ACE2 on the surface of human cells to gain entry. Coating viral particles with synthetic antibodies should prevent the spikes from binding to ACE2.

Sidhu and Rini will also engineer antibodies that bind ACE2 to make it inaccessible to the virus. This type of engineered immunity surpasses the capacity of the bodys natural immune system since antibodies that react against self-proteins have been filtered out. If successful, the approach may obviate worries about viral mutations that can render drugs ineffective to new emerging viral strains becausethe host protein ACE2 does not change over time.

Sidhus team has advanced a technology called phage display to rapidly create and select human antibodies with desired biological properties, including blocking the virussspike protein. Over the last decade, his team has created hundreds of antibodies with therapeutic potential some of which are in clinical development through spin-off companiesand large pharmaceutical firms.

The group has demonstrated success with both approaches for inhibiting viral entry, having developed neutralizing antibodies that target the Ebola virus as well as antibodies that target the human host receptor of hantavirus or hepatitis C. Moreover, other research has shown that antibodies targeting SARS, a related virus whose genetic material is over 80 per cent identical to the one causing COVID-19, can clear infection in cells and mice.

Using phage display, in which tiny bacterial viruses called phages are instructed to create vast libraries of diverse antibodies, the team will select the antibodies that can kill the virus in human cells before testing them on mice and, eventually, patients. Experiments on mice could start within three to six months, Sidhu says.

In addition to creating antibodies tailored to the new virus from scratch, the researchers will also modify existing SARS-blocking antibodies so that they attack COVID-19 and provide an additional route to the development of a therapeutic.

Given the global spread of the virus, its possible that it will become endemic and circulate in the population like seasonal flu. And, like the flu, it could mutate into new strains that will evade acquired immunity and the vaccines that are being developed. By generating a panel of different antibodies, the researchers aim to stay one step ahead of the virus.

Our advances in antibody engineering technologiesand access to the complete genomes of the COVID-19 virus and its relatives provides us with an opportunity to create tailored therapeutic antibodies at a scale and speed that was not possible even a few years ago, says Sidhu.

Ultimately, we aim to optimize methods to the point where the evolution of new drugs will keep pace with the evolution of the virus itself, providing new and effective drugs in response to new outbreaks.

Read more:
Researchers at U of T developing antibodies to 'neutralize' novel coronavirus before it invades cells - News@UofT

The coronavirus pandemic has hit older people far harder than those who are younger, but scientists are yet to fully understand why this is.

Many of the elderly people who have died have had pre-existing health conditions such as heart disease, lung disease and diabetes, all of which make fighting the virus more difficult, but many have not had any such health problems, and occasionally the virus has caused the deaths of younger, apparently healthy people.

Researchers around the world are racing to learn how the virus behaves, which health factors put people most at risk, and are trying to work out whether there may be genetic traits that could mean some people respond to the infection differently to others.

Sharing the full story, not just the headlines

There are various theories to suggest why the virus is so unusually and devastatingly selective.

Some scientists have suggested the greater the amount of virus that infects an individual known as the viral load could make a large difference to how the body is able to respond to infection.

Put simply,the larger the dose of the virus a person gets, the worse the infection is, and the least promising the outcome.

A parallel school of thought is that genetic variations between humans differences in our DNA could affect how susceptible an individual is to the virus.

And another candidate for why apparently healthy young people are dying is they may have a highly reactive immune system, which is sent into overdrive fighting off the virus. In such a scenario, a huge inflammation storm could inadvertently overwhelm vital organs such as the lungs.

None of the theories compete with one another, and aspects of all of them, as well as innumerable other factors, could be at play in an individual case.

Viral load

No hype, just the advice and analysis you need

Dr Edward Parker of the London School of Hygiene and Tropical Medicine, explained how a high viral load can impact humans. He said: After we are infected with a virus, it replicates in our bodys cells. The total amount of virus a person has inside them is referred to as their viral load. For Covid-19, early reports from China suggest the viral load is higher in patients with more severe disease, which is also the case for Sars and influenza.

The amount of virus we are exposed to at the start of an infection is referred to as the infectious dose. For influenza, we know that that initial exposure to more virus or a higher infectious dose appears to increase the chance of infection and illness. Studies in mice have also shown that repeated exposure to low doses may be just as infectious as a single high dose.

He added: So all in all, it is crucial for us to limit all possible exposures to Covid-19, whether these are to highly symptomatic individuals coughing up large quantities of virus or to asymptomatic individuals shedding small quantities. And if we are feeling unwell, we need to observe strict self-isolation measures to limit our chance of infecting others.

Professor Wendy Barclay, the head of the Department of Infectious Disease at Imperial College London, said existing knowledge of viral load means healthcare workers can be at greater risk of infection.

In general with respiratory viruses, the outcome of infection whether you get severely ill or only get a mild cold can sometimes be determined by how much virus actually got into your body and started the infection off. Its all about the size of the armies on each side of the battle, a very large virus army is difficult for our immune systems army to fight off.

So standing further away from someone when they breathe or cough out virus likely means fewer virus particles reach you and then you get infected with a lower dose and get less ill. Doctors who have to get very close to patients to take samples from them or to intubate them are at higher risk so need to wear masks.

Genetic differences between those infected

Scientists are currently preparing to scour Covid-19 patients genomes for DNA variations that might indicate why some people are more at risk than others.

The findings could then be used to identify groups most at risk of serious illness and those who might be protected, and this knowledge could then inform the hunt for effective treatments.

A huge effort to pool DNA research from patients around the world is now on, with the ultimate goal being to build a body of evidence from people with no underlying health issues, but who have reacted differently to infection by the virus.

One promising strand of research into why some people are more susceptible to the coronavirus is on the gene variation for the cell surface protein angiotensin-converting enzyme 2 (ACE2), found on the outer membranes of cells, and which the coronavirus uses to enter cells in the lungs and airways.

Variations in production of ACE2 could make it easier or more difficult for the virus to enter and infect cells.

We see huge differences in clinical outcomes and across countries. How much of that is explained by genetic susceptibility is a very open question, geneticist Andrea Ganna, of the University of Helsinkis Institute for Molecular Medicine Finland, told Science Magazine.

Another fascinating line of inquiry is whether different blood types could lead to differing levels of susceptibility to the disease.

A Chinese research team reported in a non-peer-reviewed article that people with type O blood may be protected from the virus, and those with type A blood could be at greater risk.

Were trying to figure out if those findings are robust, Stanford University human geneticist Manuel Rivas told Science Magazine.

The first results from the investigations into genetic differences and susceptibility are expected in less than two months time.

Go here to see the original:
How 'viral load' and genetics could explain why young people have died from coronavirus - The Independent

Editor's note: Find the latest COVID-19 news and guidance in Medscape's Coronavirus Resource Center.

We've been told to avoid people who are obviously sick, coughing, and sneezing to prevent us from getting the new coronavirus.

But up to 25% of people infected may never have symptoms. And in others, their symptoms may not show up until 48 hours after being infected, according to new evidence. Yet researchers have said people in both groups may be "silent spreaders" of the virus.

Several recent studies have backed this up. One that studied transmission in Singapore and China found infection was transmitted between 2.55 and 2.89 days, respectively, before symptoms started.

Another that identified seven clusters of COVID-19 cases in which transmission likely occurred before symptoms found that 6.4% of cases were attributed to transmission before there were symptoms. Another study in China found that 12.6% of the transmissions could have occurred before symptoms began in the "source" patient.

"The initial epidemiologic [research] suggests that asymptomatic spreading is happening," says Timothy Schacker, MD, a vice dean for research and professor of medicine at the University of Minnesota Medical School.

So how exactly is the virus being spread?

"People think, 'If I don't feel bad, I don't have it and can't give it to anyone,' and that is now misguided thinking," says Chad Petit, PhD, an assistant professor in the department of biochemistry and molecular genetics at the University of Alabama at Birmingham School of Medicine, who studies viruses.

Researchers don't yet have all the answers. But an expert panel from the National Academy of Sciences told White House officials Wednesday night that the virus can possibly be spread through talking or just breathing.

A letter from the Academy reads in part: "Currently available research supports the possibility that SARS-CoV-2 could be spread via bioaerosols generated directly by patients' exhalation."

Robert Mason, MD, at National Jewish Hospital in Denver, says it's little things like touching your nose or touching your eyes, then touching a doorknob or other common surface, that can help spread it, or clearing your throat. "If you have a large number of people doing little things," that's a problem, he says.

After a person is exposed, "the virus is propagating in your body, but your immune system has not recognized that something is going on systemically," says Petit. "That's why you don't get a fever right away. Just because you don't have symptoms doesn't mean you don't have the virus."

The Singapore researchers say the spread of the virus before there are symptoms might happen "through generation of respiratory droplets or possibly through indirect transmission. Speech and other vocal activities such as singing have been shown to generate air particles, with the rate of emission corresponding to voice loudness." They cite the report about singers in Washington State attending choir practice, with 40 of 60 later testing positive for the virus.

Basically, the infection is transmitted from the silent spreaders the same ways obviously sick people do, Petit says. "If somone sneezes or coughs and wipe their nose, and those droplets get on you or your hands and you touch your face that's thought to be the most common route of transmission at the moment," he says, although the virus shed on surfaces can also be infectious.

People who have mild symptoms may pass it off as allergies or a slight cold, he says.

The CDC says that people are thought to be the most contagious when they are symptomatic, or sickest. But as more information emerges about how the virus spreads, more people are taking to wearing masks. On Wednesday, Los Angeles Mayor Eric Garcetti said he was not waiting on revised guidance and advised residents to wear non-medical masks when out doing essential tasks such as grocery shopping.

Academy of Sciences member Harvey Fineberg, MD, told CNN he will start wearing a homemade mask when he goes food shopping, saving the surgical masks for health care providers.

Evidence of transmission by silent spreaders reinforces the importance of measures already in place, experts agree. That means continuing to use social distancing, frequent hand-washing, and disinfecting household surfaces.

WebMD senior writer Brenda Goodman contributed to this report.

More here:
How COVID-19 Silent Spreaders May Be Infecting Others - Medscape

Much is still unknown about the novel coronavirus, as you knowbut experts are gathering more and more interesting info every day about the virus, how it behaves, and where it came from. One surprising tp of investigation? The new coronavirus and snakes.

While most scientists are in agreement that the virus started in animalsbats, specificallyand jumped to humans, researchers are still trying to figure out the details on how exactly that transfer went down. Since the first cases of COVID-19 were identified in December (the number of cases is now over 693,000 worldwide, according to the World Health Organization report from March 30), experts have looked into bats, pangolins (aka anteaters!), and, yup, snakes as all potential players in the spread of the virus.

While the scientific community has largely ruled out snakes as being directly involved in the transfer of the virus to humans, research on the role reptiles played in the outbreak has helped scientists better understand other aspects of this virus. Here, everything you need to know about snakes and novel coronavirus.

A little background info: The novel coronavirus is a zoonotic virus, which means it belongs to a class of diseases that are able to be transferred from animals to humans and vice-versa. About 80 percent of viruses that exist are zoonotic, says Richard J. Kuhn, PhD, a professor of biological sciences at Purdue University. (Other diseases like Ebola, Zika, and the flu are all zoonotic viruses as well.) In the case of novel coronavirus, researchers have determined that bats were the likely original host.

But these diseases often jump from the origin animal to humans with the help of an intermediate host, meaning an animal that isnt the first carrier of a virus, but one that contracts it and then transfers the virus to another animal, or a human. That's why you may have seen headlines about snakes and the novel coronavirus recently.

In a study published in the Journal of Medical Virology in January, researchers compared parts of the novel coronavirus RNA to the RNA of suspected hosts of the virus and found similarities between that of the novel coronavirus and the RNA of certain snakes (specifically, the Chinese krait and cobra).

At the time of the study, that RNA similarities were thought to be indications that snakes were a natural reservoir for the virus, explains Haitao Guo, PhD, a professor of microbiology and molecular genetics at the University of Pittsburgh. A "disease reservoir" is an environment or organism in which a pathogen can live and reproduce, the Centers for Disease Control and Prevention (CDC) explains.

The short answer is no. Snakes hunt bats in the wild, and snakes were sold in the Wuhan seafood market, which is where scientists believe the virus first jumped to humans, notes Guo. So it seemed plausible that a snake could have come in contact with an infected bat (or bat feces) and served as the intermediate host.

But, as scientists have done more research, many have raised questions about methodology and parameters of the initial snake study, Guo explains. Additionally, a study published by the American Chemical Society noted that coronaviruses usually only infect birds and mammals.

What's more: Reptiles dont normally play a role at all in viral outbreaks like this one. Neither Guo nor Kuhn could think of any examples where a reptile played a major role in a viral outbreak in humans. This is partly due to the fact that reptiles are cold-blooded and mammals are warm-blooded, explains Kuhn. This temperature difference would affect the virus ability to replicate in a new species, which means that in order for the virus to actually infect a human from a reptile, it would have to evolve much more than if it was jumping from another mammal to another human.

Research published within the past month points to pangolins, a scaly anteater found in parts of Asia and Africa, as a more likely candidatethough this is still up for debate in the scientific community.

For one thing, pangolins are also mammals. Plus, the dried scales of pangolins are often sold in wet markets, and likely were sold in the Wuhan market. The aforementioned American Chemical Society study also found genetic similarities between a coronavirus found in pangolins and the current novel coronavirus presenting in humans. However, the similarities are not strong enough for researchers to say for certain that the pangolin is the secret missing piece in the transmission of the novel coronavirus from animals to humans.

Per the latest CDC guidelines, the best way to avoid getting sick and help stop the spread of germs is by washing your hands with soap and water for 20 seconds, avoiding touching your face or hands, and disinfecting often-touched surfaces. Also, continue practicing social distancing and stay 6 feet away from other people if you do have to go out for groceries or supplies.

If you do feel sick, self-quarantine for at least two weeks. Even if you dont feel sick, if youve been in contact with someone who has tested positive for COVID-19, the best thing you can do to protect others is to *stay home.*

See the rest here:
What Does The Novel Coronavirus Have To Do With Snakes? - Women's Health

Dublin, April 06, 2020 (GLOBE NEWSWIRE) -- The "U.S. Hematologic Malignancies Testing Market: Focus on Product, Disease, Technology, End User, Country Data and Competitive Landscape - Analysis and Forecast, 2018-2025" report has been added to ResearchAndMarkets.com's offering.

This report projects the market to grow at a significant CAGR of 14.60% during the forecast period, 2019-2025. The U.S. hematologic malignancies market generated $723.9 million revenue in 2018, in terms of value.

The U.S. hematologic malignancies market growth has been primarily attributed to the major drivers in this market, such as rising incidence of hematologic malignancies, favorable reimbursement scenario, and increase in funding in the hematologic malignancies market. However, there are factors hindering the growth of the market, such as lack of training professionals, high pricing pressure, and issue pertaining to the analytic validity of genetic testing.

Key Questions Answered in this Report:

Market Segmentation

Key Companies in the U.S. Hematologic Malignancies Market

The key manufacturers that have been contributing significantly to the U.S. hematologic malignancies market include Abbott Laboratories, Illumina, Inc., F. Hoffmann-La Roche Ltd, Bio-Rad Laboratories, Inc., Sysmex Corporation, Cancer Genetics Inc., QIAGEN N.V., ICON plc, Quest Diagnostics Incorporated, Invitae Corporation, Opkp Health, Laboratory Corporation of American Holdings, NeoGenomics Laboratories, Inc., ASURAGEN, INC., ArcherDX, Inc., Adaptive Biotechnologies, ARUP Laboratories, and Invivoscribe, Inc, among others.

Key Topics Covered:

1 Product Definition

2 Market Scope

3 Research Methodology

4 Epidemiology of Hematological Malignancies in U.S.

5 U.S. Hematologic Malignancies Testing Market: Value and Volume Data 2019 (U.S. State Regions)5.1 Midwest U.S.5.2 Mid Atlantic5.3 The Southwest5.4 New England5.5 The West5.6 The South

6 Market Dynamics6.1 Market Drivers6.1.1 Rising Incidence of Hematologic Malignancies6.1.2 Increasing Adoption of Inorganic Growth Strategies in the Market6.1.3 Favorable Reimbursement Scenario in the U.S. hematologic Malignancies Testing Market6.1.4 Increase in Funding in Hematologic Malignancies Testing Market6.2 Restraints6.2.1 High Pricing Pressure6.2.2 Lack of Trained Professionals6.2.3 Issues Pertaining to the Analytical Validity of Genetic Testing for Cancers6.3 U.S. Market Opportunities6.3.1 An Underlying Relaxation in Revised 2018 PAMA Criteria6.3.2 Informatics and Technological Innovation for Larger Consumer Base6.3.3 Technological Advancements in the Field of Molecular Diagnostics

7 Competitive Landscape7.1 Key Strategies and Developments7.1.1 Synergistic Activities7.1.2 Approvals7.1.3 Product Launches and Enhancements7.1.4 Merger, Acquisitions & Expansions7.2 Product Scenario7.3 Funding Scenario7.4 Market Share Analysis7.5 Growth Share Analysis (Opportunity Mapping)7.5.1 By Company7.5.2 By Product

8 Industry Insights8.1 Regulatory Framework8.1.1 Legal Requirements and Framework in the U.S.8.2 Reimbursement Scenario8.2.1 Protecting Access to Medicare Act (PAMA) Criteria for Advanced Diagnostic Laboratory Tests (ADLT)8.3 Physicians' Perceptions

9 U.S. Hematologic Malignancies Testing Market (by Product) 2018-2025 ($ Million)9.1 Services9.2 Kits9.2.1 NGS-Based Gene Panels9.2.1.1 Leukemia9.2.1.2 Lymphoma9.2.1.3 Multiple Myeloma9.2.1.4 Myeloproliferative Neoplasms9.2.1.5 Myelodysplastic Syndromes9.2.2 NGS-Based Molecular Clonality Testing9.2.2.1 Leukemia9.2.2.2 Lymphoma9.2.2.3 Multiple Myeloma9.2.2.4 Myeloproliferative Neoplasms9.2.2.5 Myelodysplastic Syndromes9.2.3 NGS-Based Translocation Testing9.2.3.1 Leukemia9.2.3.2 Lymphoma9.2.3.3 Multiple Myeloma9.2.3.4 Myeloproliferative Neoplasms9.2.3.5 Myelodysplastic Syndromes9.2.4 NGS-Based Mutation Testing9.2.4.1 Leukemia9.2.4.2 Lymphoma9.2.4.3 Multiple Myeloma9.2.4.4 Myeloproliferative Neoplasms9.2.4.5 Myelodysplastic Syndromes9.2.5 NGS-Based Minimal Residual Disease (MRD) Testing9.2.5.1 Leukemia9.2.5.2 Lymphoma9.2.5.3 Multiple Myeloma9.2.5.4 Myeloproliferative Neoplasms9.2.5.5 Myelodysplastic Syndromes

10 U.S. Hematologic Malignancies Testing Market (by End User)10.1 Specialty Clinics and Hospitals10.2 Diagnostic Laboratories10.3 Reference Laboratories10.4 Research Institutions

11 U.S. Hematologic Malignancies Testing Market (by Disease)11.1 Leukemia11.2 Lymphoma11.3 Multiple Myeloma11.4 Myeloproliferative Neoplasms11.5 Myelodysplastic Syndromes

12 U.S. Hematologic Malignancies Testing Market (by Technology)12.1 Next-generation Sequencing (NGS)12.2 Polymerase Chain Reaction (PCR)12.3 Fluorescence In-Situ Hybridization (FISH)12.4 Immunohistochemistry (IHC)12.5 Flow Cytometry12.6 Other Technologies

13 Company Profiles

Story continues

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/xcrdeu

Research and Markets also offers Custom Research services providing focused, comprehensive and tailored research.

CONTACT: ResearchAndMarkets.comLaura Wood, Senior Press Managerpress@researchandmarkets.comFor E.S.T Office Hours Call 1-917-300-0470For U.S./CAN Toll Free Call 1-800-526-8630For GMT Office Hours Call +353-1-416-8900

Link:
United States Hematologic Malignancies Testing Industry (2018 to 2025) - Featuring Illumina, Invitae Corporation & Invivoscribe Among Others -...

(Bloomberg Opinion) -- In every epidemic, some die, others become ill and recover, and the luckiest live through infection without symptoms. In todays pandemic, we are seeing this play out before our eyes. Although the initial epidemiological data show that Covid-19 is more severe in older people, men and those with pre-existing conditions such as heart and lung disease, not everyone with severe disease has these risk factors. And not everyone at risk has the same symptoms, prognosis or outcome.

Why do people manifest such differences? And why is it not possible to predict an individuals experience? To address this complex question, it is important to first get our terminology right. Infection means acquisition of the coronavirus after exposure to it. Infection is not synonymous with exposure or with disease. Disease is a clinical state associated with cough, fever and other symptoms that ranges from mild to severe. These symptoms arise from damage to tissues and the immune system. Death occurs when there is so much damage that the body cannot maintain blood oxygenation and other necessary functions.

In past epidemics, death and survival were attributed to providence or fortune. Modern medicine and science provide a better understanding of why infection can lead to such different outcomes. Among individuals in the same risk group the same age, say differences in infection outcome can result from five different variables outside their control.

The first of these is microbial dosage or inoculum, the number of viral particles that cause infection. Small numbers of viral particles are more likely to be contained effectively by the bodys defenses. Then, infection may cause no symptoms or only mild disease. In contrast, a large number of particles can lead to increased viral growth, overwhelming the immune system and causing more severe disease.

Genetics may also influence susceptibility to severe infection. Viruses often gain access to host cells via surface proteins, which vary in presence and nature from person to person. Someone with no such surface proteins may be resistant to infection. In the case of HIV, for example, some people lack the receptors needed for viral infection and are not susceptible to the virus.

A third variable that influences infection outcome is the route by which a virus enters the body. Its possible that virus inhaled in the form of aerosolized droplets triggers different immune defenses than does virus acquired by touching contaminated surfaces and then touching ones face. The nose and the lung differ in local defenses, so the route of infection could significantly affect the outcome.

The fourth variable is the strength of the coronavirus itself. Viruses differ in virulence their capacity to damage host tissues or immunity even when they are all the same species. This is why flu seasons vary in severity from year to year. The varieties of a virus such as coronavirus differ depending on small genetic characteristics and how these affect the interaction with human hosts. As the coronavirus spreads from person to person, it may undergo unique changes in its genetic structure that enhance or attenuate its capacity to do harm. Strains that are more virulent could lead to more severe disease.

Finally, peoples immune status especially their history of prior infectious diseases crucially determines how they respond to a new infection. The immune system remembers previous encounters with microbes, and that affects how it fights and responds to new ones. In the case of dengue, infection with one type of the virus can make the individual more susceptible to infection with a different type of the same virus. In other situations, a recent infection with a virus can affect susceptibility to an unrelated new infection. For example, having had the flu before coronavirus infection could change the course of Covid-19 disease in unpredictable ways. When a persons immune system has no memory of an infectious agent, it may be unable to rapidly respond, and this may allow the invader to escape detection, giving it more time to cause damage.

Taken together, these variables create a complex picture. The amount of virus, our genes, the route of infection, the variety of the virus and our immunological history combine to produce outcomes ranging from asymptomatic infection to death. And because these parameters can vary so much from infected person to infected person, its impossible to predict who will live and who will die. Therefore, despite accumulating evidence that most who acquire the coronavirus will not develop severe disease, the uncertainty of who is at grave risk enhances the pandemics terror.

Story continues

In this regard, todays situation is similar to past pandemics in which the matter of who would live and who would die was also mysterious and led people to attribute outcomes to fortune or supernatural intervention. However, Covid-19 is different than the 1918 flu, in that today a robust scientific establishment can quickly analyze whats happening and help figure out how best to prevent and treat infections. Science is humanitys lifeline. In the days ahead, physicians, scientists, epidemiologists and many more will work hard to understand individual susceptibility to coronavirus. The Covid-19 pandemic will teach us a great deal of new science that will make us better prepared for the next outbreak.

This column does not necessarily reflect the opinion of Bloomberg LP and its owners.

Arturo Casadevall is a Bloomberg Distinguished Professor of molecular microbiology and immunology and infectious diseases at the Bloomberg School of Public Health and the School of Medicine at Johns Hopkins University.

Liise-anne Pirofski is a professor of medicine and chief of infectious diseases at Albert Einstein College of Medicine and Montefiore Medical Center.

For more articles like this, please visit us at bloomberg.com/opinion

Subscribe now to stay ahead with the most trusted business news source.

2020 Bloomberg L.P.

Go here to read the rest:
Its Still Hard to Predict Who Will Die From Covid-19 - Yahoo Finance