Category Archives: Molecular Genetics

Dr. Bettina Fries, right, a professor of medicine and the chief of the division of infectious diseases, and Agjah Libohova with a new face shield they developed for treating Covid-19 patients.

Stony Brook University Hospital will soon increase both the number of its health care providers and its hospital capacity, it was announced this week.

Representative Lee Zeldin's office said on Monday that the Army Corps of Engineers has paid a construction company $50 million to expand the hospital space by building climate-controlled tents on its campus. The project, which will add 1,038 beds to Stony Brook's capacity, is expected to be completed by April 18.

Stony Brook Medicine, which oversees all of Stony Brook University Medicine's educational and hospital functions, announced several initiatives and research activities this week related to the Covid-19 pandemic. These include clinical trials of treatments for the illness, the design and manufacture of a new face shield for medical workers, and the early graduation of senior medical students who have met the requirements in April.

The students will be rolled into Stony Brook University Hospital's staff under the supervision of residents, fellows, and attending physicians. The graduates will begin their residencies on July 1.

The university has developed the face shields through the efforts of Dr. Bettina Fries, a professor of medicine, molecular genetics, and microbiology and the chief of the division of infectious diseases, and Agjah Libohova, a neighbor of Dr. Fries who is a research and development specialist at Clear-Vu Lighting, a Long Island manufacturing company.

The company will mass-produce a shield using a prototype of one that Dr. Fries wears, starting with an order of 20,000 with plans to scale up to 40,000 a day for a total of 1.2 million per month. The shields will be available to caregivers at all of Stony Brook's affiliate hospitals.

In addition, the hospital is conducting its own research and trials into several initiatives now being looked at nationally. These include the sharing of ventilators between patients, trials of Remdesivir and Sarilumab, and harvesting and sharing plasma from those who have recovered from Covid-19. Remdesivir is a drug developed to treat the Ebola and Marburg viruses, and Sarilumab is a human antibody.

The university is also part of a national effort in which caregivers wear a device to collect physiological data that could help detect and predict the onset of the virus that causes Covid-19 in high-risk medical facilities.

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Stony Brook Hospital Expands Staff and Capacity - East Hampton Star

Biologist David Roos studied influenza as a grad student, and he typically kicks off his advanced course on infectious disease biology with a focus on that virus. Thats how he began this semester, too, with plans to also cover aspects of HIV and malaria.

Then COVID-19 emerged.

A small silver lining to this dark cloud of the pandemic is that its not a bad semester to be taking, or teaching, a class on infectious disease biology and public health, says Roos, the E. Otis Kendall Professor of Biology in Penns School of Arts and Sciences.

In the midst of the campus shutdown that compelled faculty to move their courses online, Roos has also shifted the content of his course, Molecular Mechanisms of Infectious Disease Biology, to encompass what is playing out all around us. Because the approach of the course emphasizes how to think rather than how to memorize biological pathways and proteins, says Roos, the scientific approaches students have already learned allow them to consider strategies for discovering, characterizing, and fighting this new disease.

We had already spent considerable time this semester discussing the cell biology, molecular genetics, evolution, and epidemiology of influenza, including the 1918 pandemic and subsequent outbreaks, says Roos, as well as the emergence, spread, and management of HIV.

From the first weeks of the semester in January, Roos began sharing information with his students about the novel coronavirus in class discussions and suggesting readings and online resources related to the escalating outbreak.

Even before COVID-19 was really on everyones radar, he says, we had been challenging ourselves with questions like, Imagine there is a new disease outbreak. What do you look for? What data do you need? How could you obtain this information?

Roos has a wealth of experience to inform his teachings, including three decades of laboratory research on the parasites that cause malaria and other diseases and, more recently, the responsibility for supporting genomic datasets for hundreds of parasite and fungal pathogens. Several of his former trainees have gone on to careers in public health, including at the U.S. Centers for Disease Control and Prevention and other government labs, and in the pharmaceutical and biotech sectors. He also directs teams managing a constantly expanding database related to viral and parasite disease (VEuPathDB.org, the Eukaryotic Pathogen, Host & Vector Genomics Resource) and clinical and epidemiological datasets (ClinEpiDB.org).

Transitioning to video conference-style teaching has not posed a major barrier for Roos, whose database group is dispersed around the globe and relies on such technology on a daily basis.

Within several days of the Universitys announcement that Penn would be moving classes online for the remainder of the spring semester, Roos sent a note to his students offering an optional online meeting during spring break to smooth out any technological difficulties, to check in to see how they were faring, and to discuss some of the science behind the COVID-19 pandemic.

Most of our readings this semester focus on primary research literature, so I shared articles on the evolution of coronaviruses than can cause the common cold, previous epidemics like SARS and MERS, and recent preprints on the SARS-CoV-2 virus responsible for COVID-19, he says.

Recognizing the personal toll of the pandemic, and with many students now home with their families, Roos also invited questions from family members about coronavirus biology, the ongoing pandemic, and public health responses. Im not a practicing physician, so I cannot answer medical questions, says Roos, but I wanted to do my best to address whatever concerns they may have.

Abhinav Suri, who graduated from Penn last year with a double major in biology and computer science, is now taking the course remotely from his home in San Antonio as part of the post-baccalaureate Pre-Health Specialized Studies Program. While getting a firsthand view of the pandemic responsehis parents are both physiciansSuri, who plans to go to medical school, also appreciates how what hes been learning has given him a deeper understanding of the scientific approaches to fighting the novel coronavirus.

The research papers we read and the methodologies we learned in the first part of the class when we were dealing with influenza are coming full circle, says Suri. Now were talking about things like, How can scientists use these methodologies to make something along the lines of a vaccine or an antiviral for this disease? Its making our discussions even more relevant to whats going on in the world today.

As the pandemic continuesand classes do, tooRoos plans to work in additional readings, discussions, and probably exam questions relating to COVID-19.

The point I make at the beginning of this class is that in most university courses we do a pretty good job of teaching students the stuff we know, says Roos. But we dont always do a great job of teaching students how scientists figured all that stuff out. With this brand new virus now spreading throughout the world, its an important time to learn about the how.

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A quick pivot turns an infectious disease class into timely education - Penn: Office of University Communications

Michelle Kuppersmith's doctor recommended a bone marrow biopsy after suspecting she had a rare blood disorder. Though the biopsy was done by an in-network provider at an in-network hospital, Kuppersmith learned she was on the hook for $2,400 for out-of-network genetic profiling. Shelby Knowles for KHN hide caption

Michelle Kuppersmith's doctor recommended a bone marrow biopsy after suspecting she had a rare blood disorder. Though the biopsy was done by an in-network provider at an in-network hospital, Kuppersmith learned she was on the hook for $2,400 for out-of-network genetic profiling.

Michelle Kuppersmith feels great, works full time and exercises three to four times a week. So she was surprised when a routine blood test found that her body was making too many platelets, which help control bleeding.

Kuppersmith's doctor suspected the 32-year-old Manhattanite had a rare blood disorder called essential thrombocythemia, which can lead to blood clots, strokes and, in rare cases, leukemia.

Her doctor suggested a bone marrow biopsy, in which a large needle is used to suck out a sample of the spongy tissue at the center of the patient's hip bone.

Doctors examine the bone marrow under a microscope and analyze the DNA. The procedure allows doctors to judge a patient's prognosis and select treatment, if needed. Kuppersmith had heard the procedure can be intensely painful, so she put it off for months.

The biopsy performed by a provider in her insurance network, at a hospital in her network lasted only a few minutes, and Kuppersmith received relatively good news.

While a genetic analysis of her bone marrow confirmed her doctor's suspicions, it showed that the only treatment she needs, for now, is a daily, low-dose aspirin. She will check in with her doctor every three to four months to make sure the disease isn't getting worse.

All in all, Kuppersmith felt relieved.

Then she got a notice saying her insurer refused to pay for the genetic analysis, leaving her responsible for a $2,400 payment.

The patient: New York resident Michelle Kuppersmith, 32, who is insured by Maryland-based CareFirst Blue Cross Blue Shield. She works as director of special projects at a Washington-based watchdog group. Because she was treated in New York, Empire Blue Cross Blue Shield which covers that region handled part of her claim.

Total amount owed: $2,400 for out-of-network genetic profiling

The providers: Kuppersmith had her bone marrow removed at the Mount Sinai Ruttenberg Treatment Center in New York City, which sent her biopsy sample to a California lab, Genoptix, for testing.

Medical services: Bone marrow biopsy and molecular profiling, which involves looking for genetic mutations

What gives: The field of molecular diagnostics, which includes a variety of gene-based testing, is undergoing explosive growth, said Gillian Hooker, president of the National Society of Genetic Counselors and vice president of clinical development for Concert Genetics, a health IT company in Nashville, Tennessee.

A report from Concert Genetics, a company that helps clients manage genetic testing, found there are more than 140,000 molecular diagnostic products on the market, with 10 to 15 added each day.

The field is growing so quickly that even doctors are struggling to develop a common vocabulary, Hooker said.

Kuppersmith underwent a type of testing known as molecular profiling, which looks for DNA biomarkers to predict whether patients will benefit from new, targeted therapies. These mutations aren't inherited; they develop over the course of a patient's life, Hooker said.

Medicare spending on molecular diagnostics more than doubled from 2016 to 2018, increasing from $493 million to $1.1 billion, according to Laboratory Economics, a lab industry newsletter.

Charges range from hundreds to thousands of dollars, depending on how many genes are involved and which billing codes insurers use, Hooker said.

Based on Medicare data, at least 1,500 independent labs perform molecular testing, along with more than 500 hospital-based labs, said Jondavid Klipp, the newsletter's publisher.

In a fast-evolving field with lots of money at stake, tests that a doctor or lab may regard as state-of-the-art an insurer might view as experimental.

Worse still, many of the commercial labs that perform the novel tests are out-of-network, as was Genoptix.

Stephanie Bywater, chief compliance officer at NeoGenomics Laboratories, which owns Genoptix, said that insurance policies governing approval have not kept up with the rapid pace of scientific advances. Kuppersmith's doctor ordered a test that has been available since 2014 and was updated in 2017, Bywater said.

Although experts agree that molecular diagnostics is an essential part of care for patients like Kuppersmith, doctors and insurance companies may not agree on which specific test is best, said Dr. Gwen Nichols, chief medical officer of the Leukemia & Lymphoma Society.

Tests "can be performed a number of different ways by a number of different laboratories who charge different amounts," Nichols said.

Insurance plans are much more likely to refuse to pay for molecular diagnostics than other lab tests. Laboratory Economics found Medicare contractors denied almost half of all molecular diagnostics claims over the past five years, compared with 5-10% of routine lab tests.

With so many insurance plans, so many new tests and so many new companies, it is difficult for a doctor to know which labs are in a patient's network and which specific tests are covered, Nichols said.

"Different providers have contracts with different diagnostic companies," which can affect a patient's out-of-pocket costs, Nichols said. "It is incredibly complex and really difficult to determine the best, least expensive path."

Kuppersmith said she has always been careful to check that her doctors accept her insurance. She made sure Mount Sinai was in her insurance network, too. But it never occurred to her that the biopsy would be sent to an outside lab or that it would undergo genetic analysis.

She added: "The looming threat of a $2,400 bill has caused me, in many ways, more anxiety than the illness ever has."

The resolution: Despite making dozens of phone calls, Kuppersmith got nothing but confusing and contradictory answers when she tried to sort out the unexpected charge.

An agent for her insurer told her that her doctor hadn't gotten preauthorization for the testing. But in an email to Kuppersmith, a Genoptix employee told her the insurance company had denied the claim because molecular profiling was viewed as experimental.

A spokesperson for New York-based Empire Blue Cross Blue Shield, which handled part of Kuppersmith's claim, said her health plan "covers medically necessary genetic testing."

New York, one of 28 states with laws against surprise billing, requires hospitals to inform patients in writing if their care may include out-of-network providers, said attorney Elisabeth Benjamin, vice president of health initiatives at the Community Service Society, which provides free help with insurance problems.

A spokesperson for Mount Sinai said the hospital complies with that law, noting that Kuppersmith was given such a document in 2018 nearly one year before her bone marrow biopsy and signed it.

Benjamin said that's not OK, explaining: "I think a one-year-old, vague form like the one she signed would not comply with the state law and certainly not the spirit of it."

Instead of sending Kuppersmith a bill, Genoptix offered to help her appeal the denied coverage to CareFirst. At first, Genoptix asked Kuppersmith to designate the company as her personal health care representative. She was uncomfortable signing over what sounded like sweeping legal rights to strangers. Instead, she wrote an email granting the company permission to negotiate on her behalf. It was sufficient.

A few days after being contacted by KHN, Kuppersmith's insurer said it would pay Genoptix at the in-network rate, covering $1,200 of the $2,400 charge. Genoptix said it has no plans to bill Kuppersmith for the other half of the charge.

The takeaway: Kuppersmith is relieved her insurer changed its mind about her bill. But, she said: "I'm a relatively young, savvy person with a college degree. There are a lot of people who don't have the time or wherewithal to do this kind of fighting."

Patients should ask their health care providers if any outside contractors will be involved in their care, including pathologists, anesthesiologists, clinical labs or radiologists, experts said. And check if those involved are in-network.

"Try your best to ask in advance," said Jack Hoadley, a research professor emeritus at Georgetown University. "Ask, 'Do I have a choice about where [a blood or tissue sample] is sent?'"

Ask, too, if the sample will undergo molecular diagnostics. Since the testing is still relatively new and expensive most insurers require patients to obtain "prior authorization," or special permission, said Dr. Debra Regier, a medical geneticist at Children's National Hospital in Washington and an associate with NORD, the National Organization of Rare Diseases. Getting this permission in advance can prevent many headaches.

Finally, be wary of signing blanket consent forms telling you that some components of your care may be out-of-network. Tell your provider that you want to be informed on a case-by-case basis when an out-of-network provider is involved and to consent to their participation.

Bill of the Month is a crowdsourced investigation by Kaiser Health News and NPR that dissects and explains medical bills. Do you have a perplexing medical bill you want to share with us? Tell us about it here.

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Bill Of The Month: Pricey Genetic Test For Essential Thrombocythemia : Shots - Health News - NPR

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

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

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.

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How 'viral load' and genetics could explain why young people have died from coronavirus - The Independent

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

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13 Company Profiles

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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

(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.

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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

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2020 Bloomberg L.P.

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Its Still Hard to Predict Who Will Die From Covid-19 - Yahoo Finance

Ever since the earliest reports of a pneumonia-like illness spreading within Hubei province in China, the resemblance to the SARS outbreak of 2002-2003 has been uncanny: probable origins in the wild-animal markets of China; an illness that in some people resembles the common cold or a flu, but in others leads to pneumonia-like symptoms that can cause respiratory failure; community transmission that often occurs undetected; super-spreader events; and reported vertical transmission in high-rises or other living spaces where the waste systems are improperly engineered or drain catch-basins are dry, allowing aerosolized particles to pass from one floor of a building to another (see The SARS Scare for an in-depth description of the epidemiology and virology of the SARS outbreaks of 2002-2003 and 2003-2004).

At first, this latest outbreak was referred to as a novel coronavirus, then in the media as COVID-19 (formally, the name for the disease in an infected person who has become sick, a distinction analogous to that between a person who is HIV positive and one who has developed AIDS). Now that the virus has been characterized and its relationship to SARS firmly established, its designation is SARS-CoV-2severe acute respiratory syndrome coronavirus 2.

Will public-health measures be sufficient to contain its spread? How infectious is it? What is the incubation period? Is this a pandemic? What role does the immune-system response play in the progression of the disease? Which populations are most at risk? Can scientists develop a vaccine, and how quickly? These are some of the questions that scientists worldwide are asking, and that a collaboration among Harvard University and Chinese researchers will address as part of a $115-million research initiative funded by China Evergrande Group, which has previously supported Universitygreen-buildings research at the Graduate School of Design, research onimmunologic diseases, and work inmathematics. (See below for the University press release describing the initiative.)

Harvard Magazinespoke with some of the researchers involved in fighting the first SARS outbreak, and those who will be collaborating with Chinese colleagues, in what is already a worldwide effort to control SARS-CoV-2.

Michael Farzan 82, Ph.D. 97, who in 2002 was an assistant professor of microbiology and molecular genetics at Harvard Medical School (HMS) studying the mechanism that viruses use to enter cells, was the first person to identify the receptor that SARS used to bind and infect human cells. SARS-CoV-2 is a close cousin to SARS, and uses the same human receptor, ACE2, reports Farzan, who is now co-chair of the department of immunology and microbiology at Scripps Research. The ACE2 receptor is expressed almost exclusively in the lungs, gastrointestinal tract, and the kidneys, which explains why the disease is so effectively transmitted via both the respiratory and fecal-oral routes.

But there are subtle differences in the new virus behind the current outbreak, he explained in an interview. The viruss receptor binding domainthe part that attaches to the human receptorhas undergone a lot of what we call positive selection, meaning there has been a good deal of evolutionary pressure on that region from natural antibodies, probably in bats or some other animal host that is a reservoir for this disease. So while the virus retains its ability to bind ACE2, Farzan explains, it no longer binds the same antibodies. That is unfortunate, because as the first SARS epidemic wound down, HMS professor of medicine Wayne Marasco had identified a single antibodyfrom what was then a 27-billion antibody librarythat blocked the virus from entering human cells. (Marasco is actively testing new antibodies, hoping to find one that will have the same effect on SARS-CoV-2.) Still, we are not starting from square one, says Farzan.

In animal studies,Remdesivir [a new and experimental antiviral drug] has seemed to work against SARS-like viruses, he says. Its effectiveness will probably hinge on getting it early enough, in the same way that the antiviral drug Tamifluis most effective against the seasonal flu when given to patients early in the course of infection.

And there is a reasonable hope that a vaccine canbe developed, Farzan adds, because the part of the virus that binds the human receptor is exposed and accessible, making it vulnerable to the immune systems antibodies. In addition, the viral genome is relatively stable. That means SARS CoV-2 wont evolve much over the course of an epidemic, so a vaccine that is relatively protective at the beginning of an epidemic will remain effective until its end.

Another reason for optimismdespite the long road to deploying any vaccine in humansis that the science that allows researchers to understand the viruss structure, life cycle, and vulnerabilities is progressing far more rapidly today than during the first SARS outbreak 17 years ago. So, too, is the understanding of the human immune response to the virus, and of the most effective public-health strategies based on the epidemiology of the disease.

When epidemiologists assess the severity of an epidemic, they want to know how effectively the disease can propagate in a population. The first measure they attempt to calculate is the reproductive number (R0)the number of people that an infected individual will in turn infect in an unexposed population, in the absence of interventions. When the reproductive number is greater than 1 (meaning each infected person in turn infects more than one other person), more and more people become infected, and an epidemic begins. Public-health interventions are therefore designed to lower the rate of transmission below 1, which eventually causes the epidemic to wind down. The second number epidemiologists focus on is the serial intervalhow long it takes one infected person at a particular stage of the disease to infect another person to the point of the same stage of the disease. The serial interval thus suggests how rapidly the disease can spread, which in turn determines whether public-health officials can identify and quarantine all known contacts of an infected individual to prevent their retransmitting the disease to others.

Marc Lipsitch, a professor of epidemiology at the Harvard Chan School of Public Health (HSPH), and director of the schoolsCenter for Communicable Disease Dynamics, helped lead one of the two teams that first calculated the reproductive number of SARS in the 2002-2003 outbreak. SARS had an R0 of 3, he recalls: each case led to three others. In that outbreak, about 10 percent of those who became sick died. The good news is that SARS CoV-2 appears to have a much lower R0 than SARS, ranging from the high ones to low twos, and only 1 percent to 2 percent of those who become sick have died. On the other hand, the serial intervalstill being worked outappears to be shorter, meaning the new virus has the potential to spread faster.

In the current epidemic, Lipsitch notes a further concern: the fact that the incubation-period distribution and the serial-interval distribution are almost identical. Thats a mathematical way of saying that people can start transmitting the virus even when they are pre-symptomatic, or just beginning to exhibit symptoms. That makes tracing and quarantining contacts of infected individualsa classic, frontline public-health measurenearly impossible.

Tracing, quarantining, and other public-health interventions, such as distancing measures (closing workplaces or asking employees to work from home, for example) proved sufficient to defeat SARS in the early 2000s. But with SARS-CoV-2, public-health measures alone may prove inadequate. Controlling this version of SARS may require antivirals, stopgap antibody therapies, and ultimately, vaccines, deployedtogetherwith robust public-health containment strategies.

Unfortunately, SARS-CoV-2 is almost certainly already a pandemic, Lipsitch continues: demonstrating sustained transmission in multiple locations that will eventually reach most, if not all places on the globe. The disease appears to be transmitting pretty effectively, probably in Korea, probably in Japan, and probably in Iran. He has estimated that 40 to 70 percent of the adult global population will eventually become infected.

That said, Infected is different from sick, he is careful to point out. Only some of those people who become infected will become sick. As noted above, only about 1 percent to 2 percent of those who have becomesickthus far have died, he says. But the number of people who areinfectedmay be far greater than the number of those who are sick. In a way, he says, thats really good news. Because if every person who had the disease was also sick, then that would imply gigantic numbers of deaths from the disease.

I'm very gratified, Lipsitch continues, to see that both China and Harvard recognize the complementarity between public health and epidemiology on the one hand, and countermeasure-development on the other hand. We can help target the use of scarce countermeasures [such as antivirals or experimental vaccines] better if we understand the epidemiology; and we will understand the epidemiology better if we have good diagnostics, which is one of the things being developed in this proposal. These approaches are truly complementary.

In the short term, Lipsitchwho has sought to expand the modeling activities of the Center for Communicable Disease Dynamics to better understand the current outbreaks epidemiologysays, It would be great toexpand collaborations with Chinese experts. Longer term, I see a really good opportunity for developing new methods for analyzing data better, as we have in previous epidemics. After the first SARS outbreak, for example, epidemiologists developed software for calculating the reproductive number of novel diseases; that software now runs on the desktop computers of epidemiologists around the world. And in 2009, during an outbreak of swine flu in Mexico, Lipsitch and others developed a method for using the incidence of the disease among awell-documented cohort of travelerswho had left Mexico, to estimate the extent of the disease among amuch larger and less well surveyedpopulation of Mexican residents.

What they found then was that the estimated number of cases in Mexican residents likely exceeded the number of confirmed cases by two to three orders of magnitude. The same method is being used to assess the extent of SARS-CoV-2 in China right nowso far without any hiccups. In the Mexican case, Lipsitchreports, the estimates suggested that severe cases of the disease were uncommon, since thetotal numberof cases was likely much larger than the number ofconfirmedcases. So I think we have learned from each epidemic how to do more things. And in between them, you solidify that less visible, less high-profile research that builds the foundation for doing better the next time. His group, for example, has been developing ways to make vaccine trials faster and better once a vaccine candidate exists.

A vaccine is the best long-term hope for controlling a disease like SARS-CoV-2. Higgins professor of microbiology and molecular genetics David Knipe, who like Lipsitch will participate in the newly announced collaboration, works on vaccine delivery from a molecular perspective. Knipe has developed methods to use the herpes simplex virus (HSV) as a vaccine vector and has even made HSV recombinants that express the SARS spike proteinthe part of the virus that binds the human ACE2 receptor. He now seeks to make HSV recombinants that express the new coronavirus spike protein as a potential vaccine vector.

But Knipe also studies the initial host-cell response to virus infection, which is sometimes called the innate immune response. And he has used HSV vectors that expressed the first SARS spike protein to study how it activates innate immune signaling. That is important because inSARS 1, initial symptoms lasted about a week, but it was the second phasecharacterized by a massive immune-system response that began to damage lung tissuethat led to low levels of oxygen saturation in the blood, and even death.The inflammation in the lungs is basically a cytokine storm, an overwhelming and destructive immune response thats the result of innate signaling, Knipe explains. So were going to look at that with the new coronavirus spike protein, as well. This could help to determine the actual mechanism of inflammation, and then we can screen for inhibitors of that that might be able to alleviate the disease symptoms.

The idea, he says, is to stop theinflammatoryresponse now killing people in the respiratory phase of the disease by targeting the specific molecular interaction between the virus and the host cell. This, he explains, aligns with one of the principal initial goals of the collaboration, which is to support research both in China and at Harvard to address the acute medical needs of infected individuals during the current crisis.

In the last days of 2019 and the first days after the New Year, we started hearing about a pneumonia-like illness in China, says Dan Barouch, an HMS professor of medicine and of immunology known for his anti-HIV work, whose lab has developed a platform for rapid vaccine development. (During the Zika virus outbreak of 2016, for example, his group was the first to report, within a month, a vaccine protective in animal models.) When the genome of the virus was released on Friday, January 10, we started reviewing the sequence that same evening, working through the weekend. By Monday morning, we were ready to grow it.

His concern about this latest outbreak was that the rate of spread seemed to be very rapid. In addition, the outbreak had the clinical features of an epidemic. We reasoned that this might make it difficult to control solely by public-health measures, he says, particularly because the virus can be transmitted by asymptomatic individuals. Thus, if the epidemic is still spreading toward the end of this year or early 2021, by which point a vaccine might be available, Barouch explains, such a remedy could prove essential. Historically, when viral epidemics don't self-attenuate, the best method of control is a vaccine.

Although Barouchs lab is working on DNA and RNA vaccines, a new technology that has the potential to cut vaccine development times in half, large-scale manufacturing using so-called nucleotide vaccines is unproven. That's why I think there needs to be multiple parallel vaccine efforts, he emphasizes. Ultimately, we don't know which one will be the fastest and most protective. At the moment, he reports, there are at least a half dozen scientifically distinct vaccine platforms that are being developed and he believes that vaccine development for this pathogen will probably go faster than for any other vaccine target in human history.

Ever since I graduated from medical school, he points out, there have been new emerging or re-emerging infectious disease outbreaks of global significance with a surprising and disturbing sense of regularity. There is Ebola. There was Zika. There were SARS, MERS; the list keeps growing. With climate change, increasing globalization, increasing travel, and population shifts, the expectation is that epidemics will not go away, and might even become more frequent.

In this global context, Barouch emphasizes the importance of a collaborative response that involves governments, physicians, scientists in academiaandin industry, and public-health officials. It has to be a coordinated approach, he says. No one group can do everything. But I do think that the world has a greater sense of readiness this time to develop knowledge, drugs, and therapeutics very rapidly. The scientific knowledge that will be gained from the vaccine efforts [will] be hugely valuable in the biomedical research field, against future outbreaks, and in the development of a vaccine to terminate this epidemic.

University provost Alan Garber, a physician himself, adds that Global crises of such magnitude demand scientific and humanitarian collaborations across borders. Harvard and other institutions in the Boston area conduct research on diagnostics, virology, vaccine and therapeutics development, immunology, epidemiology, and many other areas.With its tremendous range of expertise and experience, our community can be an important resource for any effort to address a major global infectious disease outbreak. Our scientists and clinicians feel an obligation to be part of a promising collaboration to overcome the worldwide humanitarian crisis posed by this novel virus.

The official Harvard press release follows:

Harvard University Scientists to Collaborate with Chinese Researcherson Development of Novel Coronavirus Therapies, Improved Diagnostics

At a glance:

Since its identification in December, the novel coronavirus has quickly evolved into a global threat, taking a toll on human health, overwhelming vulnerable health care systems and destabilizing economies worldwide.

To address these challenges, Harvard University scientists will join forces with colleagues from China on a quest to develop therapies that would prevent new infections and design treatments that would alleviate existing ones.

The U.S. efforts will be spearheaded by scientists at Harvard Medical School, led by DeanGeorge Q. Daley, working alongside colleagues from the Harvard T.H. Chan School of Public Health. Harvard Medical School will serve as the hub that brings together the expertise of basic scientists, translational investigators and clinical researchers working throughout the medical school and its affiliated hospitals and institutes, along with other regional institutions and biotech companies.

The Chinese efforts will be led by Guangzhou Institute of Respiratory Health and Zhong Nanshan, a renowned pulmonologist and epidemiologist. Zhong is also head of the Chinese 2019n-CoV Expert Taskforce and a member of the Chinese Academy of Engineering.

Through a five-year collaborative research initiative, Harvard University and Guangzhou Institute for Respiratory Health will share $115 million in research funding provided by China Evergrande Group, aFortuneGlobal 500 company in China.

We are confident that the collaboration of Harvard and Guangzhou Institute of Respiratory Health will contribute valuable discoveries to this worldwide effort, said Harvard University President Lawrence Bacow. We are grateful for Evergrandes leadership and generosity in facilitating this collaboration and for all the scientists and clinicians rising to the call of action in combating this emerging threat to global well-being.

Evergrande is honored to have the opportunity to contribute to the fight against this global public health threat, said Hui Ka Yan, chair of the China Evergrande Group. We thank all the scientists who responded so swiftly and enthusiastically from the Harvard community and are deeply moved by Harvard and Dr. Zhongs teams dedication and commitment to this humanitarian cause. We have the utmost confidence in this global collaborative team to reach impactful discoveries against the outbreak soon.

While formal details of the collaboration are being finalized, the overarching goal of the effort is to elucidate the basic biology of the virus and its behavior and to inform disease detection and therapeutic design. The main areas of investigation will include:

With the extraordinary scale and depth of relevant clinical and scientific capabilities in our community, Harvard Medical School is uniquely positioned to convene experts in virology, infectious disease, structural biology, pathology, vaccine development, epidemiology and public health to confront this rapidly evolving crisis, Daley said. Harnessing our science to tackle global health challenges is at the very heart of our mission as an institution dedicated to improving human health and well-being worldwide.

We are extremely encouraged by the generous gesture from Evergrande to coordinate and supportthe collaboration and by the overwhelmingly positive response from our Harvard colleagues, said Zhong, who in 2003 identified another novel pathogen, the severe acute respiratory syndrome (SARS) coronavirus and described the clinical course of the infection.

We look forward to leveraging each of our respective strengths to address the immediate and longer-term challenges and a fruitful collaboration to advance the global well-being of all people, Zhong added.

Harvard University ProvostAlan M. Garbersaid outbreaks of novel infections can move quickly, with a deadly effect.

This means the response needs to be global, rapid and driven by the best science. We believe that the partnershipwhich includes Harvard and its affiliated institutions, other regional and U.S.-based organizations and Chinese researchers and clinicians at the front linesoffers the hope that we will soon be able to contain the threat of this novel virus, Garber said. The lessons we learn from this outbreak should enable us to respond to infectious disease emergencies more quickly and effectively in the future.

Excerpt from:
Harvard and the Guangzhou Institute of Respiratory Health Team to Fight SARS-CoV - Harvard Magazine