Category Archives: Molecular Medicine

Such a substantial change in average temperature over a fairly short period of history could have other, unforeseeable impacts. Parsonnet points out that there are more microbial organisms in us than there are human cells, which creates a complex ecosystem. And like a human-size version of climate change, were seeing probably a change in our ecosystem thats associated with this drop in temperature. Yet were only beginning to understand all the ways temperature influences that ecosystem to help determine how we function.

Our body temperature is controlled by the hypothalamus, which acts as a thermostat, keeping the temperature of vital organs fairly constant. (Its this core temperature that a thermometer approximates.) Temperature sensors in nerve endings, which produce the sensation of being hot or cold, prompt the hypothalamus to initiate adjustments like shivering to warm up or sweating to cool down. At any given time, your skin might be 10 degrees cooler or warmer than your core. And that difference and thus how much energy the body has to expend to keep the core stable seems to affect how the immune system functions. For instance, in 2013 Elizabeth Repasky of the Roswell Park Comprehensive Cancer Center and co-authors reported in P.N.A.S. that raising the room temperature improved the ability of laboratory mice to fight off cancer after they got it. Repasky and others are also experimenting with heating tumor cells to kill them or make them more susceptible to chemotherapy. Already, certain abdominal cancers are treated with hot chemotherapy, in which the drug is heated to 103 degrees, which has been shown to increase how much of it is absorbed by cancer cells. Separately, the heat from a fever may help fight infection, because, as Mark Dewhirst, an emeritus professor of radiation oncology at the Duke University School of Medicine, puts it, a lot of bacteria and other pathogens dont fare well at elevated temperatures.

Scientists struggle, though, to explain how a cooler average body temperature has been associated with longevity. A lower metabolic rate, and thus a lower temperature, has been linked to a longer life span in experimental settings with reduced calorie intake, when the body slows to conserve energy. But Bruno Conti, a professor of molecular medicine at the Scripps Research Institute, and colleagues have also found that mice genetically engineered to have a body temperature a half-degree lower than average lived longer than ordinary mice, even if they ate as much as they wanted. What other effects this has on an organism is unknown. For instance, he says, a brain at a lower temperature might not function as well.

At the same time, other bodily systems might benefit from being cooler. H. Craig Heller, a biology professor at Stanford, and colleagues have shown that muscle fatigue is caused by heat, which they believe triggers a temperature-sensitive enzyme that acts as a safety valve, stopping the production of chemicals that power muscle contractions in order to prevent the tissue from burning up. When Heller cools muscle during physical activity using special gloves that chill blood as it moves through the hands, the muscle just keeps on going, he says. Ive had freshmen doing more than 800 push-ups.

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What Does Our Body Temperature Say About Our Health? - The New York Times

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

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

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

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

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

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

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

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

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

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

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

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

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

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As most people rush to distance themselves from COVID-19, Canadian researchers have been waiting eagerly to get our (gloved) hands on the hated virus.

We want to learn everything we can about how it works, how it changes and how it interacts with the human immune system, so we can test drugs that may treat it, develop vaccines and diagnostics and prevent future pandemics.

This is what researchers live to do. Much of our everyday work is incremental. Its important and it moves the field forward, but to have a chance to contribute to fighting a pandemic is especially inspiring and exciting.

Viruses are fascinating. They are inert microscopic entities that can either hide out, innocuous and undetected, or wreak pandemic havoc.

They are simultaneously complex and simplistic, which is what makes them so interesting especially new, emerging viruses with unique characteristics. Researching viruses teaches us not only about the viruses we study, but also about our own immune systems.

The emergence of a new coronavirus in a market in Wuhan, China, in December 2019 set in motion the pandemic we are now witnessing in 160 countries around the world. In just three months, the virus has infected more than 360,000 people and killed more than 16,000.

The outbreak sent researchers around the world racing to isolate laboratory specimens of the virus that causes COVID-19. The virus was later named severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2.

In countries that experienced earlier outbreaks, including China, Australia, Germany and the United States, researchers were able to isolate the virus and develop their own inventories of SARS-CoV-2, but logistical and legal barriers prevented them from readily sharing their materials with researchers beyond their borders.

What Canadian researchers needed to join the fight in earnest was a domestic supply of clean copies of the virus preferably from multiple Canadian COVID-19 cases. Even in a pandemic, developing such a supply is not as easy as it might sound, and multiple teams in Canada set out to isolate and develop pure cultures of the virus, not knowing which would be successful, or when.

Ultimately two teams in Canada would isolate the virus for study: one at the University of Saskatchewan and one that featured researchers from McMaster University, Sunnybrook Health Sciences Centre and the University of Toronto.

Arinjay Banerjee, a postdoctoral research fellow at McMaster who typically works in my virology lab, volunteered his special expertise. We were proud to have him share his talent with the team in Toronto, where he set to work with physicians and researchers Samira Mubareka, Lily Yip, Patryk Aftanas and Rob Kozak.

For Banerjee, it was like a batter being called to the plate with the score tied in the bottom of the ninth. He had come to work at McMaster because of its Institute for Infectious Disease Research and its Immunology Research Centre, and because the university maintains a research colony of bats.

Banerjees PhD work at the University of Saskatchewan, and now at McMaster, has focused on bats and how their viruses, including coronaviruses, interact with bat and human antiviral responses. Over the past few years, studies have shown that bat coronaviruses have the capacity to infect human cells. Multiple researchers had predicted a coronavirus that would evolve and jump into humans.

Also read:Modis India isnt Maos China. Silly forecasts assume well let corona kill millions of us

Isolating a virus requires collecting specimens from patients and culturing, or growing, any viruses that occur in the samples. These viruses are obligate intracellular parasites, which means that they can only replicate and multiply in cells. To isolate a particular virus, researchers need to provide it with an opportunity to infect live mammalian cells, in tiny flasks or on tissue culture plates.

Viruses adapt to their hosts and evolve to survive and replicate efficiently within their particular environment. When a new virus such as SARS-CoV-2 emerges, it isnt obvious what particular environment that virus has adapted to, so it can be hard to grow it successfully in the lab.

We can use tricks to draw out a virus. Sometimes the tricks work and sometimes they dont. In this case, the researchers tried a method Banerjee and the team had previously used while working on the coronavirus that causes Middle Eastern Respiratory Syndrome: culturing the virus on immunodeficient cells that would allow the virus to multiply unchecked. It worked.

Since specimens from patients are also likely to contain other viruses, it is critical to determine if a virus growing in the culture is really the target coronavirus. Researchers confirm the source of infection by extracting genetic material from the virus in culture and sequencing its genome.

They compare the sequence to known coronavirus sequences to identify it precisely. Once a culture is confirmed, researchers can make copies to share with colleagues.

All this work must be done in secure, high-containment laboratories that mitigate the risk of accidental virus release into the environment and also protect scientists from accidental exposure. The more versions of a virus that can be isolated, the better. Having multiple virus isolates allows us to monitor how the virus is evolving in humans as the pandemic progresses. It also allows researchers to test the efficacy of vaccines and drugs against multiple mutations of the virus.

Transmission electron microscopic image of an isolate from the first U.S. case of COVID-19. The spherical viral particles, colourized blue, contain cross-sections through the viral genome, seen as black dots. (U.S. CDC)

Both the Saskatchewan and Ontario teams are now able to make and share research samples with other Canadian scientists, enabling important work to proceed, using a robust domestic supply that reflects the evolving virus in its most relevant mutations.

That in turn gives Canadian researchers a fighting chance to deliver a meaningful blow to COVID-19 while there is still time. Im glad our colleagues at other Canadian institutions will also have versions of the virus to use in their research.

There is still so much work for all of us to do.

Karen Mossman, Professor of Pathology and Molecular Medicine and Acting Vice President, Research, McMaster University

This article is republished from The Conversation.

Also read:Lesson from Black Death: Coronavirus will transform economic life for longer than we expect

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This is how my team isolated the new coronavirus to fight the global pandemic - ThePrint

The increased incidence of colorectal cancer (CRC) in younger adults is not simply a demographic shift but reflects potential biological changes in the disease as well as alterations in geographical distribution that need to be better understood, say UK researchers in a large population-based study.

Numerous recent studies from the US, as well as those in countries across Europe, Australia, New Zealand, and Canada, have shown that there has been an increase in CRC incidence in younger people in the past few decades.

As reported by Medscape Medical News, these studies suggest that, while the overall incidence of CRC may have stabilised, the incidence in adults aged under 50 years has risen sharply, at rates ranging from 1.5% to 8% per year.

Seeking to provide a more detailed picture of the shift, Adam Chambers, School of Cellular and Molecular Medicine, University of Bristol, and colleagues looked at data on more than 56,000 UK adults aged 2049 years diagnosed with the disease between 1974 and 2015.

The new research, published online by the British Journal of Surgery, showed that, following an initial dip in incidence, rates increased initially in adults aged 2029 years, followed by those aged 3039 years, at rates of up to 6% per year.

While gender and socioeconomic status did not appear to have an impact on the change in incidence rates, there were notable geographic variations, with the largest increases in southern England, and distal tumours were found to be the biggest driver of new cases.

Mr Chambers commented in a news release: "Age has always been a major risk factor for bowel cancer, with the majority of cases being diagnosed in patients over 60 and therefore bowel cancer screening has focused on older age groups.

"However, this study shows that over the past 30 years, there has been an exponential increase in the incidence of bowel cancer among adults under 50."

Co-author David Messenger, a consultant colorectal surgeon at Bristol Royal Infirmary, added: "Future research needs to focus on understanding why this trend is occurring and how it might be reversed, potentially through the development of cost-effective testing strategies that detect tumours at an earlier stage or polyps before they become cancerous."

Mr Messenger told Medscape News UK that, while this is a population-based study and cannot demonstrate cause and effect, he believes that there are likely to be multiple factors underlying the trend that are "not necessarily the same" for different countries or regions.

He believes that "undoubtedly some of it is dietary related and some of it also obesity related" but, unlike in, say, lung cancer, it is "much more difficult to pick apart" the relationship between lifestyle factors and the development of CRC.

He said that, "based on when weve seen the rise in incidence, it is probably something to do with how our lifestyles have changed really from the mid-60s onwards" because, for successive generations from that period, "youve got a cohort effect" of increasing incidence.

Mr Messenger also notes that the shift in tumour location and the shift in geographical distribution of cases suggests that "the biology of the disease in young adults is different", which could have healthcare implications if the increase in CRC incidence in younger patients continues.

The authors point out that, while increases in rates of CRC have been observed in younger adults across Europe and North America, there appear to be differences in the way the disease manifests in younger versus older populations.

They note that it therefore is "vital" that the epidemiology underlying the increase is better understood, "as young adults typically present with more advanced tumours that carry a poorer prognosis".

To investigate further, the team examined data from the UK-wide National Cancer Registration and Analysis Service database on all adults aged 2049 years diagnosed with CRC between 1974 and 2015.

They also obtained population estimates from the Office for National Statistics and the European Standard Population report to examine trends in age-specific incidence rates, stratified by sex, anatomic subsite, Index of Multiple Deprivation quintile, and geographical region.

The researchers identified a total of 1,145,639 new cases of CRC diagnosed during the study period, of which 2594 were in adults aged 2029 years, 11,406 among 3039 year olds, and 42,314 in those aged 4049 years.

Joinpoint regression analysis revealed that after an initial decrease, there was a notable increase in cases among individuals aged 2029 years, at an annual percentage change (APC) of 4.6% in women from 1986 and 5.1% in men from 1992.

In adults aged 3039 years, the increase started later, at an APC in women of 3.8% from 1995 and 6.0% in men from 2002.

The increases were smaller in adults aged 4049 years and started later, at an APC of 1.5% in women and 0.8% in men, beginning in 2003.

These results, the team writes, are "suggestive of an age cohort effect".

Looking at the data in more detail, they found that the incidence of proximal CRCs, primarily driven by caecal and ascending colon cancers, was increased in 2029 year olds, at an APC of 4.4% from 1995, and in 3039 year olds, at an APC of 5.8% from 2005, but not in 4049 year olds.

However, the increase in incidence rates for distal cancers was higher and more sustained, at an APC of 5.6% from 1991 for 2029 year olds, and an APC of 3.3% from 1995 to 2006 and 7.0% from 2006 for adults aged 3039 years. For those aged 4049 years, the APC was 1.4% from 2001.

While there were few differences noted when stratifying individuals by socioeconomic status, there were differences observed when the researchers looked at geographical region.

For example, incidence rates of proximal CRC among 2049 year olds were, in 1985, decreasing all across England apart from in London, with the South West recording an APC of -12.1%.

By 2015, however, incidence rates for proximal CRC were increasing fastest in the South East at an APC of 7.4%, in London by 6.5% per annum, and in the East at an APC of 6.0%.

The increase was even greater for distal cancers, with all southern regions showing annual increases in incidence rates of more than 5%, rising to an APC of 10.1% in the South West.

"It is difficult to explain why incidence rates are increasing more rapidly in young adults in the south given that risk factors such as obesity are increasing faster in northern regions," the team says.

While acknowledging there may be issues around access to healthcare at play, they add: "The role of environmental factors, such as diet, obesity, physical exercise and the gut microbiota, in the development of youngonset colorectal cancer is incompletely understood and requires further research."

Mr Messenger said the evidence nevertheless suggests that the biology of CRC in younger adults differs from that in their older counterparts.

"That then begs the question about what is happening in the UK that were seeing such pronounced increases in southern regions," particularly in terms of the dramatic increase in CRC cases in the distal large bowel.

He highlighted that, "typically, people have thought this is maybe a disease that is perhaps related to lower socioeconomic groups but weve not seen that in our study the increased rates have occurred equally across all socioeconomic groups in the younger adult age group".

However, Mr Messenger noted that, over time, there has been northsouth migration in England, as well as "increasing urbanisation in southern regions, particularly the South West".

He pointed to cities such as Bristol and towns along the M4 corridor, including Swindon, which are increasing in size and becoming more and more urbanised. In contrast, Middlesborough and Teeside are depopulating, a phenomenon he ascribes to internal migration.

Mr Messenger added that, as well as tumours in younger adults having a "greater propensity to be in the sigmoid and the rectum, theres some evidence that molecularly, they are slightly different; they dont necessarily exhibit microsatellite instability in the same way that you see with older adults".

He said that this observation cannot currently be fully explained, and is the focus of future research. There is also evidence to suggest that younger adults are more likely to present with metastatic or locally advanced disease.

He believes that screening could therefore help with identifying patients at an earlier stage, although not via the blanket use of flexible sigmoidoscopies or colonoscopies but rather greater application of faecal immunochemical testing, which is currently being used in the over-50s.

"The question is do we then roll that out to adults under 50 as a means of risk stratifying those groups, as to whether or not they should have endoscopic examination," Mr Messenger asked.

This would also be a way of obtaining more data on whether young adults really do present with more advanced disease.

"Weve got some idea that they might do worse because theyve got more advanced disease but that is really not set in stone and there is virtually no data on that in the UK, so thats really where things will be heading," he said.

If the current trends continue unchecked, Mr Messenger believes that the types of cases "that we see in 20 years time will look very different".

"At the moment, we think that about 5% of all bowel cancer occurs in adults under 50 but if you were to extrapolate out those rates of increase out to 2041we think it could account for anywhere from about 8% up to 30% of all cases, so youve got the potential in 20 years that patients with bowel cancer could be a very different group."

He continued: "This is anecdotal but Im seeing a lot more younger adults with advanced disease.

"So overall, globally in the population, probably the incidence will trickle down and everyone will think thats great, but actually if you look at it more deeply, those that are getting the cancers will be different. It will be younger adults with more advanced disease."

Mr Messenger said: "Suddenly were having a paradigm shift from where this is seen as a disease of middle age and elderly to then becoming a disease of a younger population."

The study was funded by the Medical Research Council, David Telling Charitable Trust and the Elizabeth Blackwell Institute.

No conflicts of interest declared.

Br J Surg 2020. doi 10.1002/bjs.11486

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Increase in Younger Bowel Cancer Cases Highest in Southern England - Medscape

LYON, France and CAMBRIDGE, Mass. , March 16, 2020 (GLOBE NEWSWIRE) -- ERYTECH Pharma (Nasdaq & Euronext: ERYP),a clinical-stage biopharmaceutical company developing innovative therapies by encapsulating therapeutic drug substances inside red blood cells, today announced the appointment of Melanie Rolli, M.D., to its Board of Directors and the intention to propose the ratification of her appointment at ERYTECHs next General Meeting of Shareholders. Dr. Rolli has more than 15 years of experience in the global biopharmaceutical and biotechnology industry, including in both Europe and the United States. Dr. Rollis appointment follows the resignation of Allene Diaz, who resigned from the Board effective September 30, 2019.

We are very pleased to welcome Melanie to our Board of Directors, commented Dr Jean-Paul Kress, Chairman of the Board of ERYTECH Pharma.We look forward to working with her to develop ERYTECHs business plans and strategy as ERYTECH advances its late-stage clinical programs and begins preparations for its transition into a commercial-stage company.

I am delighted to be joining ERYTECHs Board of Directors, said Dr. Rolli. It is an exciting time for ERYTECH as its lead product eryaspase is progressing through a pivotal Phase 3 clinical trial in one of the largest unmet medical needs in oncology. I look forward to working closely with the Board and leadership team in supporting the Companys plans.

Dr. Rolli currently serves as the Chief Executive Officer of PIQUR Therapeutics AG, a Basel, Switzerland-based clinical stage biotechology company dedicated to drug development of targeted therapies in various oncological and dermatological indications. Previously, she was at Novartis Pharmaceuticals AG for 14 years, where she held positions of increasing responsibilities across the Drug Development, Safety, and Medical Affairs functions. At Novartis, she spent eight years in the United States in global and local positions as the Medical Director in Primary Care, Respiratory, Womens Health and Dermatology and Oncology franchises.

Prior to joining Novartis, she worked as a post-doctoral cancer research physician at SCRIPPS Research Institute for Molecular and Experimental Medicine in La Jolla, California, and as a clinicial and researcher in Germany.

Dr. Rolli graduated from the University of Heidelberg with a doctorate in medicine and pharmacology.

About ERYTECH and eryaspase: http://www.erytech.com

ERYTECH is a clinical-stage biopharmaceutical company developing innovative red blood cell-based therapeutics for severe forms of cancer and orphan diseases. Leveraging its proprietary ERYCAPS platform, which uses a novel technology to encapsulate drug substances inside red blood cells, ERYTECH is developing a pipeline of product candidates for patients with high unmet medical needs. ERYTECHs primary focus is on the development of product candidates that target the altered metabolism of cancer cells by depriving them of amino acids necessary for their growth and survival.

The Companys lead product candidate, eryaspase, which consists of L-asparaginase encapsulated inside donor-derived red blood cells, targets the cancer cells altered asparagine and glutamine metabolism. Eryaspase is in Phase 3 clinical development for the treatment of second-line pancreatic cancer and in Phase 2 for the treatment of first-line triple-negative breast cancer. An investigator-sponsored Phase 2 study in second-line acute lymphoblastic leukemia is ongoing in the Nordic countries of Europe.

ERYTECH produces its product candidates for treatment of patients in Europe at its GMP-approved manufacturing site in Lyon, France, and for patients in the United States at its recently opened GMP manufacturing site in Princeton, New Jersey, USA.

ERYTECH is listed on the Nasdaq Global Select Market in the United States (ticker: ERYP) and on the Euronext regulated market in Paris (ISIN code: FR0011471135, ticker: ERYP). ERYTECH is part of the CAC Healthcare, CAC Pharma & Bio, CAC Mid & Small, CAC All Tradable, EnterNext PEA-PME 150 and Next Biotech indexes.

Forward-looking information

This press release contains forward-looking statements with respect to the clinical development plans of eryaspase, including ERYTECHs plans for transition into a commercial-stage company. Certain of these statements, forecasts and estimates can be recognized by the use of words such as, without limitation, believes, anticipates, expects, intends, plans, seeks, estimates, may, will and continue and similar expressions. All statements contained in this press release other than statements of historical facts are forward-looking statements, including, without limitation, statements regarding the ERYTECHs business strategy including its clinical development of eryaspase; the status of the TRYbeCA1 trial including the timeline for patient enrollment, expansion of trial into the United States and intended activities with respect to the interim analysis; the potential of ERYTECHs product pipeline; the timing of ERYTECHs preclinical studies and clinical trials and announcements of data from those studies and trials; ERYTECHs anticipated manufacturing capacity and ability to meet future demand and ERYTECHs anticipated cash runway and sufficiency of cash resources. Such statements, forecasts and estimates are based on various assumptions and assessments of known and unknown risks, uncertainties and other factors, which were deemed reasonable when made but may or may not prove to be correct. Actual events are difficult to predict and may depend upon factors that are beyond ERYTECH's control. There can be no guarantees with respect to pipeline product candidates that the candidates will receive the necessary regulatory approvals or that they will prove to be commercially successful. Therefore, actual results may turn out to be materially different from the anticipated future results, performance or achievements expressed or implied by such statements, forecasts and estimates. Further description of these risks, uncertainties and other risks can be found in the Companys regulatory filings with the French Autorit des Marchs Financiers (AMF), the Companys Securities and Exchange Commission (SEC) filings and reports, including in the Companys 2018 Document de Rfrence filed with the AMF in March 2019 and in the Companys Annual Report on Form 20-F filed with the SEC on March 29, 2019 and future filings and reports by the Company. Given these uncertainties, no representations are made as to the accuracy or fairness of such forward-looking statements, forecasts and estimates. Furthermore, forward-looking statements, forecasts and estimates only speak as of the date of this press release. Readers are cautioned not to place undue reliance on any of these forward-looking statements. ERYTECH disclaims any obligation to update any such forward-looking statement, forecast or estimates to reflect any change in ERYTECHs expectations with regard thereto, or any change in events, conditions or circumstances on which any such statement, forecast or estimate is based, except to the extent required by law.

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ERYTECH Announces the Appointment of Dr. Melanie Rolli to its Board of Directors - BioSpace

In the absence of vaccines or antiviral drugs, researchers at Johns Hopkins University in Baltimore say the key to slowing and treating the coronavirus might be hidden in the blood of those whove already recovered from the disease.

The method of using convalescent serum essentially harvesting virus-fighting antibodies from the blood of previously infected patients dates back more than a century, but has not been used widely in the United States in decades.

During the Spanish flu epidemic of 1918, scientists reported that transfusions of blood products obtained from survivors led to a 50 percent drop in deaths among severely ill patients. A similar strategy was used to treat and slow the spread of polio and measles outbreaks decades ago, but the technique fell out of favor in the 1950s with the innovation of modern vaccine science and antiviral drugs, said Dr. Arturo Casadevall, chair of the molecular microbiology and immunology department at the Johns Hopkins Bloomberg School of Public Health.

When Casadevall learned in December that a new coronavirus was spreading rapidly in China, he started telling colleagues that it might be time to revive the antiquated treatment.

Im an infectious disease doctor who is interested in history, Casadevall said. I knew the history of what was done in the early 20th century with epidemics. They didnt have vaccines then, they didnt have any drugs then just like the situation we face now. But physicians then knew that, for certain conditions, you could take the blood of the immune and use it to prevent disease or treat those who became ill.

In a paper published Friday in the Journal of Clinical Investigation, Casadevall and a colleague, Dr. Liise-anne Pirofski, argued that collecting blood serum or plasma from previously infected people might be the best hope for treating severe cases of COVID-19, the disease caused by the virus, at least until a better treatment can be developed.

Theres some evidence from recent history that suggests the approach could work.

In 2003, doctors in China used plasma from recovered patients to treat 80 people suffering from the viral disease known as severe acute respiratory syndrome, or SARS an earlier coronavirus and found that the treatments were associated with improved outcomes and shorter hospital stays. In 2014, the World Health Organization published guidelines for using donated plasma to treat people infected with Ebola after the treatments showed promise.

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In an interview with Stat News last month, a top Food and Drug Administration official said convalescent plasma might be helpful in the fight against the new coronavirus. Although the treatment is not a cure, Casadevall says it might be an important stopgap.

Researchers in the U.S. and across the globe have been scrambling to develop drugs for the coronavirus, but federal officials say those treatments are likely months or in the case of a vaccine more than a year away. That leaves hospitals with few options other than ventilators to treat COVID-19 patients suffering from respiratory failure, stoking concerns nationally that a surge of severely ill patients in the coming weeks could overwhelm emergency rooms and intensive care units.

The approach definitely has merit, and whats remarkable about it is its not a new idea; its been with us for a good hundred years or longer, said Dr. Jeffrey Henderson, an assistant professor of medicine and molecular microbiology at the Washington University School of Medicine in St. Louis. I think we dont know until we have experience and case reports with this particular disease whether it will be effective, but just based on its track record with a number of other viruses, I think it has a very good chance of working.

Henderson said part of what makes the treatment attractive is its simplicity. Although there is danger in giving a patient the wrong type of blood, safety advancements over the past two decades have made adverse outcomes rare. And hospitals have the tools needed to begin harvesting and transfusing patients with blood serum right away, he said.

The Johns Hopkins team is planning to submit its plan for approval by the FDA, but Casadevall said they dont anticipate problems since the method has been used in the past and relies on standard blood-banking technology. He hopes to begin collecting serum from recovered patients within four to six weeks.

Patients tend to make large numbers of antibodies against an infecting pathogen, and these antibodies often circulate in the blood of survivors for months or years afterward. By collecting and transfusing a survivors serum or plasma the liquid portion of blood left once cells and platelets have been removed doctors could potentially boost an ailing patient's immune response, Casadevall said.

Doctors in China have begun treating COVID-19 patients with plasma harvested from survivors and have reported somewhat positive results, especially when the method is applied early in the disease, though it has not been tested widely.

The usage of plasma will probably reduce the time needed to treat the disease from five to 10 days to three to five days, said Dr. Zhang Wenhong, the leader of a medical team sent from Shanghai to Wuhan to help tackle the outbreak, in an interview with Al-Jazeera last week.

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Casadevall argues that convalescent serum could also be given to front-line health care workers to help protect them from becoming ill.

To implement his plan, academic hospitals would need to work collaboratively with blood banks to set up research protocols and treatment guidelines. Doctors at Johns Hopkins started that work weeks ago, Casadevall said, and they have begun drafting guidelines that can be copied by hospitals across the country.

Hes already been in touch with doctors at the Mayo Clinic in Minnesota, he said.

At the local level, hospitals and blood banks have everything they need to do this, Casadevall said. But what would really help is coordination from the federal government.

First, Casadevall said, the U.S. must immediately begin widespread testing, because its impossible to collect blood serum from survivors if public health officials dont know whos been infected. Second, Casadevall said federal officials may need to oversee the interstate shipment of blood products. He can imagine a scenario where blood banks in Seattle, which has been at the epicenter of the U.S. outbreak for weeks, might be in a position to send excess blood products to other cities where outbreaks are still ramping up.

And finally, Casadevall said, government officials would need to help spread the word. He believes people whove had the coronavirus and recovered will be eager to donate plasma if they believe it could help elderly patients and health care workers.

This is by no means a panacea, Casadevall said. But at a time when the message has been, Theres nothing you can do but wash your hands, this is an opportunity to do something proactive that can help fight this.

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Doctors push for treatment of coronavirus with blood from recovered patients - NBCNews.com

The researchers involved in isolating the virus: Dr. Rob Kozak and Dr. Samira Mubareka of the University of Toronto, and Dr. Arinjay Banerjee of McMaster University.

handout/Sunnybrook Hospital

Two teams of Canadian scientists have isolated the coronavirus that causes COVID-19 and successfully reproduced it in the laboratory.

The accomplishment means that researchers who are looking to test screening methods, therapies and vaccines now have Canadian sources that can provide access to the global pathogen without them having to undertake the complicating step of shipping live virus across international borders.

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The significance for us is that it serves as a tool," said Samira Mubareka, a microbiologist at Sunnybrook Health Sciences Centre in Toronto and member of one of the teams. Now that we have this virus in hand it means that we have material for a number of things."

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Dr. Mubareka and her colleagues at McMaster University in Hamilton and the University of Toronto worked in a facility in the Toronto area with the appropriate containment level to handle the new coronavirus safely. They announced their feat on Thursday.

On Friday, Paul Hodgson, associate director of business development at the Vaccine and Infectious Disease Organization-International Vaccine Centre in Saskatoon, confirmed to The Globe and Mail that the joint federal-provincial facility had quietly reached the same milestone a few weeks earlier and is now using its version of the virus for a vaccine development effort.

Samples of the Saskatoon-derived version of the coronavirus are now available for approved research groups through the National Microbiological Laboratory in Winnipeg. The Ontario group also plans to generate its version for distribution.

The spread of the novel coronavirus that causes COVID-19 continues, with more cases diagnosed in Canada. The Globe offers the dos and don'ts to help slow or stop the spread of the virus in your community.

In both cases, the virus was isolated from clinical samples obtained from patients at Sunnybrook, the first hospital in Canada to treat someone with COVID-19. However, the Toronto and Saskatoon isolates are from different patients and so may vary in ways that will be important for scientists looking to detect or target the virus.

They are also different from a version of the virus isolated by the U.S. Centers for Disease Control and Prevention and documented in a paper posted online last week. That version is intended to be the reference strain for scientists working in the United States.

I think having multiple virus isolates is incredibly valuable, Dr. Hodgson said. We can see whether one vaccine or therapy works across all the virus strains ... if there are known [genetic] variations.

Dr. Mubareka said that for the Ontario-based team, the process of isolating the virus began with a relatively standard procedure that did not work the first time. Hurdles along the way had to be surmounted with some additional scientific tricks. The group ultimately succeeded in getting the virus to reproduce in animal cells that were engineered to have no immune response and specially treated to enhance the likelihood of infection.

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The first sign that the method was working surfaced when the group spotted plaques in their cell cultures patches of dead cells that were destroyed by the virus.

We did the infection from clinical specimens on a Friday, said Arinjay Banerjee, a postdoctoral researcher at McMaster Universitys Institute for Infection Disease Research. Then to go back on Monday and see all [the] cells dead that was pretty exciting. That was step one.

Dr. Mubareka said that one of the first uses for the isolate would be to act as a control to make sure that tests used by health-care workers to identify the virus are performing as expected. It could also serve as a challenge strain for antiviral drugs and vaccines currently in development.

Karen Mossman, a professor of pathology and molecular medicine at McMaster, said that researchers there would be working with the isolates to better understand details about the biology of COVID-19, including how the virus works to counteract the human immune response.

She added that there was a certain irony in trying so hard to create a virus that everyone else is trying to get rid of.

Dr. Hodgson said the virus isolated in Saskatoon has now been used to establish the virus in ferrets that can be used to test the efficacy of vaccines in living organisms before human clinical trials commence.

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Last week, the western facility received a $1-million grant to advance its work as part of a funding competition organized by the Canadian Institutes for Health Research, which selected 47 teams working on various aspects of the COVID-19 outbreak.

The Ontario collaboration was not among the winners and, until now, a lack of funding has been the teams biggest challenge, Dr. Mubareka said.

On Friday, the federal agency said it would be able to support 49 additional projects with a portion of the $1.1-billion COVID-19 response package announced earlier in the week by Prime Minister Justin Trudeau. Among them is a proposal by Dr. Mossmans group at McMaster to study the biology of how the virus interacts with its hosts and to model this interaction in laboratory experiments

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Two Canadian teams of scientists isolate coronavirus to speed research effort - The Globe and Mail

Henry Ford Health System plans to rapidly expand its life-extending precision medicine program in Detroit after the Jeffries family pledged $25 million to create a specialized center.

The $25 million donation, provided by developer Chris Jeffries and his wife, Lisa, is the largest single gift from individuals in Henry Ford's 105-year history and one of the largest in the nation for a precision medicine program, Henry Ford officials said.

"We are incredibly grateful to Lisa and Chris Jeffries for their generosity," Wright Lassiter III, president and CEO of Henry Ford Health System, said in a statement. "We are experiencing a momentous era in medicine, a radical shift from the traditional approach to cancer care. This gift will help us consolidate and advance our collective efforts to create unprecedented access to advanced, highly personalized treatments for our patients and members."

But in the past three months, precision medicine or precision health, as neurosurgeon Steven Kalkanis, M.D., CEO of the Henry Ford Medical Group, likes to call it is now available for a whole host of new treatments besides those for cancer.

"Hot off the press. There have been animal studies and now clinical studies, only in the last several months, where precision health is ready for prime time and for human beings," said Kalkanis, who also is Henry Ford's chief academic officer.

Over the past decade, precision medicine has been evolving as a new type of medical care that initially focused on treating patients with various forms of cancer, including brain, lung, colon and pancreatic. It works like this: By analyzing patients' own molecular profile and the genetic mutations of their tumors, doctors are able to use the information to develop personalized treatments that could be more effective than standard care.

Doctors are now using precision medicine approaches to treat many other conditions, including cystic fibrosis, asthma, depression, heart disease, autoimmune diseases and multiple sclerosis, Kalkanis said.

"We have a whole era opening up to treat a host of other chronic diseases, using precision medicine to identify patients' molecular profiles, but potentially using existing drugs for everything from asthma to high blood pressure to depression," Kalkanis said. "However, the majority (of precision medicine) is still about designing a tailored drug regimen for individual patients."

Kalkanis said patients with some chronic conditions will one day soon be able to take a blood test and have their molecular profile entered into a database of existing drugs that may be able to match to an existing drug or to new ones being created in real time.

"We have found, in one of our clinical trials, that a (patient had a) rare type of brain cancer with a mutation impacting glucose levels. We used an existing diabetes drug and the patient went into remission," Kalkanis said.

Why the Jeffries donated

Chris Jeffries' father, Gerald was diagnosed with a highly malignant brain tumor in 2001.

Treated initially by neuro-oncologist Tom Mikkelsen and later Kalkanis and the Hermelin Brain Tumor Center team, Gerald was given only nine to 11 months to live, but using a precision medicine approach, he lived another five years until he died in December 2006.

"That meant so much to us. It's impossible to describe," Chris Jeffries said in a statement. Lisa Jeffries also lost her stepfather to cancer.

A native of Flint, Chris Jeffries is co-founder of Millennium Partners, a real estate development company that specializes in mixed-use, urban living and entertainment centers in Boston; San Francisco; Miami; Washington D.C.; Los Angeles; and New York.

Last year, the Jeffries donated $33 million to the University of Michigan Law School, where Chris was a 1974 graduate. The donation is earmarked for student support, including scholarships and other forms of financial aid, summer funding programs, and debt management. It was the largest private donation to the law school in its history, UM said.

Kalkanis said Gerald Jeffries was one of the first cohorts of patients in Henry Ford's personalized medicine program long before it was called precision medicine, in the early 2000s.

"He was enrolled in a clinical trial at Henry Ford 10 to 15 years ago and treated with a novel drug based on his unique cancer characteristics," Kalkanis said. "Because of that, he lived way beyond his life expectancy. The family was very supportive of our program and especially wanted to provide this same hope to others once they learned of the enhanced capability of precision medicine."

Since Gerald Jeffries was treated and Henry Ford developed its precision medicine approach, Kalkanis said there have been a number of patients who have outlived their prognoses. He said doctors can now give patients and families more hope than ever.

"We went through the precision medicine protocol, based on his own unique biomarkers and using a novel drug," he said. "Today these tests have become much more accessible. (For instance), a decade ago, it cost $5,000 (for testing). Now it costs several hundred for the tests" that can lead to the novel, personalized treatment.

Henry Ford's precision medicine program

For years, Henry Ford has been at the forefront of the precision medicine revolution, making world-class, targeted cancer treatments available at its national destination referral center, the Henry Ford Cancer Institute, officials said.

"By analyzing genetic and non-genetic factors, we can gain a better understanding of how a disease forms, progresses and can be treated in a specific patient," Mikkelsen, who is Henry Ford's medical director of the Precision Medicine Program and Clinical Trials Office, said in a statement.

"As of now, we can check for more than 500 genomic markers, which helps us understand the pattern of changes in a patient's tumor cells that influence how cancer grows and spreads," Mikkelsen said. "I'm confident this gift will lead to advancements that provide hope for patients with even the most complex diagnoses."

Kalkanis said the $25 million donation, which is expected to be received over the next several years, will enable Henry Ford to do a number of things.

"It takes investment to build out our biodepository with tissue samples, test them, look for biomarkers and see if (patients are) eligible for certain drugs," Kalkanis said. "We need to design our lab platform that is FDA-approved and recruit the best and brightest scientists and clinicians (specializing in) other cancer types."

Based on the current projection of about four to five chronic diseases and about 10 subspecialties that can be addressed by precision medicine, Kalkanis estimated Henry Ford will recruit two to three scientists and clinicians each year for the next few years.

"We are launching the search process for key researchers and working with the lab and pathology group for tests this calendar year," he said. "We should be up and running over the next year."

Adnan Munkarah, M.D., Henry Ford's executive vice president and chief clinical officer, said taking research in the lab and translating it to patient care is a standard process at Henry Ford.

"(It) is a critical element to help us treat many of the most challenging conditions our patients face," Munkarah said in a statement. "Translational research is bench-to-bedside, meaning it allows patients to benefit from discoveries in real time. That is an essential part of our history and commitment to medicine and academics not only offering the latest innovations in medicine, but also playing a leading role in their development."

Precision medicine is an approach to patient care that allows doctors to select treatments most likely to help patients based on a genetic understanding of their disease.

"The support of our donors is the fuel behind our clinical innovations and the breakthroughs that are improving people's lives," Mary Jane Vogt, Henry Ford's senior vice president and chief development officer, said in a statement. "It is remarkable to work with donors who believe in a better tomorrow and the power of a unified approach to medicine."

The Jeffrieses said they believe Henry Ford will achieve transformational advancements in cancer treatment using precision medicine and personalized treatments.

"The team at Henry Ford is second to none," said Chris Jeffries. "We believe this gift will lead to other families having more time together, as I had with my father. Defeating cancer requires a concerted effort from everyone and we hope to make as big an impact on that goal as possible."

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Henry Ford to expand precision medicine program with help of $25 million donation - ModernHealthcare.com

In the race to develop a treatment for the rapidly spreading illness Covid-19, dozens of drugs are being tested around the world. Its an urgent mission because the latest data suggests that some 20 percent of people infected have serious illness, and around 1 percent may die.

Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told Congress on Wednesday that Covid-19 is 10 times more lethal than the seasonal flu.

The danger stems from the pathogen itself: a virus called SARS-CoV-2.

Teeny tiny viruses are one of the biggest threats that humanity has ever faced. They are behind some of the most devastating pandemics ever known. Even with all of modern medicine, we have only eradicated one virus, smallpox, which required a decades-long global mass vaccination effort.

SARS-CoV-2, the brand new foe, is spreading fast even as entire countries, like Italy, are locking down to prevent its transmission. Estimates of its potential impact vary, but Brian Monahan, the attending physician of the US Congress, told lawmakers Wednesday he expects between 70 million and 150 million people in the US to get infected with the virus over time.

Right now, doctors are using general treatment measures to control the symptoms of Covid-19, but theres not yet a specific vaccine or cure.

Several factors make viruses like SARS-CoV-2 a particularly pernicious threat to humans. The good news is scientists have learned more about how they attack. Theyve also come up with ways to keep some of the deadliest of these tiny germs in check and are slowly inching toward cures. The question now is whether that research will bear fruit in time to blunt the blow of the Covid-19 pandemic and help us get ahead of the next outbreak.

Viruses are the most bizarre germs. Using just a handful of molecules, they assemble into all kinds of tiny shapes, and with just a small set of instructions, they can wreak havoc across entire ecosystems and threaten crop harvests. They can travel between hosts through the air, water, soil, and droplets. They mutate rapidly. And they are truly everywhere, from the oceans to the skies.

Compared to infectious agents like bacteria and fungi, viruses are much smaller and simpler. In fact, viruses can even make other germs sick. Yet theyre so simple that most scientists dont even consider them to be living organisms.

For instance, the poliovirus is just 30 nanometers wide. The SARS-CoV-2 virus behind Covid-19 is about 120 nanometers. Meanwhile, the E. coli bacterium is more than 16 times larger than SARS-CoV-2, and the human red blood cell is 64 times larger. A human cell uses 20,000 different types of proteins. HIV uses just 15. SARS-CoV-2 uses 33.

With all that extra space, larger pathogens like bacteria store the molecular tools they need to make copies of themselves and to fight off infections of their own. These tools are also what make bacteria vulnerable to antibiotics, drugs that interfere with molecular mechanisms in bacteria but not those of human cells, so they have a targeted effect.

But antibiotics dont work on viruses. Thats because viruses dont reproduce on their own. Rather, they invade cells and hijack their hosts machinery to make copies of themselves.

Bacteria are very different from us, so theres a lot of different targets for drugs. Viruses replicate in cells, so they use a lot of the same mechanisms that our cells do, said Diane Griffin, a professor of microbiology and immunology at the Bloomberg School of Public Health at Johns Hopkins University. So its been harder to find drugs that target the virus but dont damage the cell as well.

Theres also a huge variety of viruses, and they mutate quickly, so tailored treatments and vaccines against a virus can lose effectiveness over time.

Another factor that makes viruses so difficult to treat is how our bodies respond to them. Once the immune system detects a virus, it makes antibodies. These are proteins that attach to a virus or a virus-infected cell, marking it for destruction or preventing it from infecting new cells.

The problem is that a virus can cause a lot of damage and infect other people before the immune system readies its defenses. When those defenses kick in, they can cause other problems like fever and inflammation. And by the time these symptoms show up, the virus may already be in decline, or it may be too late to act.

Often at the time that virus diseases present themselves, its fairly far into the replication of that virus in that person, Griffin said. Many symptoms of the virus disease are actually manifestations of the immune response to the disease, so often things are sort of starting to get better at the time that you actually even figure out somebody has a virus infection.

Researchers use two broad strategies to combat viral infections: slowing down the damage from the virus, and speeding up and strengthening the bodys countermeasures.

Antiviral drugs are one approach to slowing down viruses. Like antibiotics, these are drugs that hamper the virus without causing much collateral damage. The majority of antivirals are targeting the viruses [themselves]. That means the components of the viruses, the viral enzymes, the surface proteins, said Pei-Yong Shi, a biochemistry and molecular biology professor at the University of Texas Medical Branch. By attacking different parts of the virus, antiviral compounds can prevent a virus from entering cells or they can interfere with its reproduction.

For example, remdesivir, under development by Gilead Sciences, is being studied as a way to treat Covid-19. It works by blocking the SARS-CoV-2 virus from copying its genetic material, RNA, the instructions the virus uses to replicate itself. Remdesivir resembles a component of RNA, but when its taken up by the virus, it causes the copying process to stop. Crucially, remdesivir fools the virus, but not human cells.

Protease inhibitors are another class of antiviral drugs, like lopinavir and ritonavir used to treat HIV (the -vir suffix is used to denote an antiviral drug, similar to how -cillin denotes an antibiotic). These compounds block an enzyme in the virus that normally trims proteins down, allowing the virus to infect other cells. When the enzyme is blocked, the virus doesnt mature properly, rendering it inert.

Researchers are also studying how to use antibodies to a given virus collected from engineered animals or from people previously infected with the same virus. By administering antibodies as a treatment, the recipients immune system can get a head start on identifying and eliminating the viral threat rather than waiting to build up its own antibodies.

There are also drugs like interferons that trigger a general immune response. These are a series of signaling molecules that make cells in the body more resistant to infection, inhibiting the spread of a virus while the rest of the immune system catches up. Its mainly used to control persistent infections like hepatitis B.

But interferons can have severe side effects like inflammation, so it requires fine-tuning to treat a virus without doing more harm than good. Doctors have used interferon with other antiviral drugs to treat Covid-19 in China and researchers are investigating this approach as another potential therapy.

Doctors can also use a number of different therapies to limit the immune systems response to viruses, like fever and inflammation, which can sometimes cause more damage to a patient than the virus itself. Anti-inflammatory drugs like corticosteroids and chloroquine are often used to lessen these symptoms.

And there are also vaccines for some viruses and efforts to develop new ones. These are treatments that coach the immune system to detect and fight off a virus before an infection takes place. These are powerful tools for controlling viruses across an entire population, but theyre tricky to optimize for a rapidly changing pathogen, and they require extensive, time-consuming testing to ensure they are safe for a wide segment of the population.

However, even if effective treatments enter the market, the virus will likely remain a threat. As weve learned with influenza (another respiratory disease caused by viruses), despite updated vaccines, new treatments, and a long history of public health responses, there are still between 12,000 and 60,000 flu deaths each year in the US. Covid-19 could remain a persistent threat, too.

To be clear, the best way to fight a virus is to prevent infections in the first place. And that depends on public health measures during an outbreak, like quarantines and social distancing, as well as personal tactics like robust, 20-second hand-washing with soap.

While there is a large and growing body of research on drugs to control viruses, they are still few and far between. We dont have that many antiviral drugs for acute infections, Griffin said. You often dont have any choice except to let it run its course.

Developing new drugs can take years of testing, and by then, an outbreak may have faded, or another more threatening pathogen may have emerged. Even viruses for which we do have antiviral drugs, like influenza, the illness often isnt detected in time to make it worth the treatment.

Other viruses like HIV can be controlled with drugs, but not eliminated, as hidden reservoirs of the virus remain in the body.

And within a population, there are always people who are more susceptible to infections, like people with depressed immune systems. For them, treatments and vaccines may not work, so they depend on the people around them to be immunized and to take proper infection control procedures.

All of which brings us back to prevention as the most effective way to combat viruses within a population. That means global coordinated action can be one of the best strategies to control the smallest pathogens. And simple tools like soap and water can be more effective at fighting a pandemic than the best drugs.

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Is there a cure for coronavirus? Why Covid-19 is so hard to treat - Vox.com

A computer image created by Nexu Science Communication together with Trinity College in Dublin, shows a model structurally representative of a betacoronavirus which is the type of virus linked to COVID-19.

Source: NEXU Science Communication | Reuters

Research has gone digital, and medical science is no exception. As the novel coronavirus continues to spread, for instance, scientists searching for a treatment have drafted IBM's Summit supercomputer, the world's most powerful high-performance computing facility, according to the Top500 list, to help find promising candidate drugs.

One way of treating an infection could be with a compound that sticks to a certain part of the virus, disarming it. With tens of thousands of processors spanning an area as large as two tennis courts, the Summit facility at Oak Ridge National Laboratory (ORNL) has more computational power than 1 million top-of-the-line laptops. Using that muscle, researchers digitally simulated how 8,000 different molecules would interact with the virus a Herculean task for your typical personal computer.

"It took us a day or two, whereas it has traditionally taken months on a normal computer," said Jeremy Smith, director of the University of Tennessee/ORNL Center for Molecular Biophysics and principal researcher in the study.

Simulations alone can't prove a treatment will work, but the project was able to identify 77 candidate molecules that other researchers can now test in trials. The fight against the novel coronavirus is just one example of how supercomputers have become an essential part of the process of discovery. The $200 million Summit and similar machines also simulate the birth of the universe, explosions from atomic weapons and a host of events too complicated or too violent to recreate in a lab.

The current generation's formidable power is just a taste of what's to come. Aurora, a $500 million Intel machine currently under installation at Argonne National Laboratory, will herald the long-awaited arrival of "exaflop" facilities capable of a billion billion calculations per second (five times more than Summit) in 2021 with others to follow. China, Japan and the European Union are all expected to switch on similar "exascale" systems in the next five years.

These new machines will enable new discoveries, but only for the select few researchers with the programming know-how required to efficiently marshal their considerable resources. What's more, technological hurdles lead some experts to believe that exascale computing might be the end of the line. For these reasons, scientists are increasingly attempting to harness artificial intelligenceto accomplish more research with less computational power.

"We as an industry have become too captive to building systems that execute the benchmark well without necessarily paying attention to how systems are used," says Dave Turek, vice president of technical computing for IBM Cognitive Systems. He likens high-performance computing record-seeking to focusing on building the world's fastest race car instead of highway-ready minivans. "The ability to inform the classic ways of doing HPC with AI becomes really the innovation wave that's coursing through HPC today."

Just getting to the verge of exascale computing has taken a decade of research and collaboration between the Department of Energy and private vendors. "It's been a journey," says Patricia Damkroger, general manager of Intel's high-performance computing division. "Ten years ago, they said it couldn't be done."

While each system has its own unique architecture, Summit, Aurora, and the upcoming Frontier supercomputer all represent variations on a theme: they harness the immense power of graphical processing units (GPUs) alongside traditional central processing units (CPUs). GPUs can carry out more simultaneous operations than a CPU can, so leaning on these workhorses has let Intel and IBM design machines that would have otherwise required untold megawatts of energy.

IBM's Summit supercomputer currently holds the record for the world's fastest supercomputer.

Source: IBM

That computational power lets Summit, which is known as a "pre-exascale" computer because it runs at 0.2 exaflops, simulate one single supernova explosion in about two months, according to Bronson Messer, the acting director of science for the Oak Ridge Leadership Computing Facility. He hopes that machines like Aurora (1 exaflop) and the upcoming Frontier supercomputer (1.5 exaflops) will get that time down to about a week. Damkroger looks forward to medical applications. Where current supercomputers can digitally model a single heart, for instance, exascale machines will be able to simulate how the heart works together with blood vessels, she predicts.

But even as exascale developers take a victory lap, they know that two challenges mean the add-more-GPUs formula is likely approaching a plateau in its scientific usefulness. First, GPUs are strong but dumbbest suited to simple operations such as arithmetic and geometric calculations that they can crowdsource among their many components. Researchers have written simulations to run on flexible CPUs for decades and shifting to GPUs often requires starting from scratch.

GPU's have thousands of cores for simultaneous computation, but each handles simple instructions.

Source: IBM

"The real issue that we're wrestling with at this point is how do we move our code over" from running on CPUs to running on GPUs, says Richard Loft, a computational scientist at the National Center for Atmospheric Research, home of Top500's 44th ranking supercomputerCheyenne, a CPU-based machine "It's labor intensive, and they're difficult to program."

Second, the more processors a machine has, the harder it is to coordinate the sharing of calculations. For the climate modeling that Loft does, machines with more processors better answer questions like "what is the chance of a once-in-a-millennium deluge," because they can run more identical simulations simultaneously and build up more robust statistics. But they don't ultimately enable the climate models themselves to get much more sophisticated.

For that, the actual processors have to get faster, a feat that bumps up against what's physically possible. Faster processors need smaller transistors, and current transistors measure about 7 nanometers. Companies might be able to shrink that size, Turek says, but only to a point. "You can't get to zero [nanometers]," he says. "You have to invoke other kinds of approaches."

If supercomputers can't get much more powerful, researchers will have to get smarter about how they use the facilities. Traditional computing is often an exercise in brute forcing a problem, and machine learning techniques may allow researchers to approach complex calculations with more finesse.

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Take drug design. A pharmacist considering a dozen ingredients faces countless possible recipes, varying amounts of each compound, which could take a supercomputer years to simulate. An emerging machine learning technique known as Bayesian Optimization asks, does the computer really need to check every single option? Rather than systematically sweeping the field, the method helps isolate the most promising drugs by implementing common-sense assumptions. Once it finds one reasonably effective solution, for instance, it might prioritize seeking small improvements with minor tweaks.

In trial-and-error fields like materials science and cosmetics, Turek says that this strategy can reduce the number of simulations needed by 70% to 90%. Recently, for instance, the technique has led to breakthroughs in battery design and the discovery of a new antibiotic.

Fields like climate science and particle physics use brute-force computation in a different way, by starting with simple mathematical laws of nature and calculating the behavior of complex systems. Climate models, for instance, try to predict how air currents conspire with forests, cities, and oceans to determine global temperature.

Mike Pritchard, a climatologist at the University of California, Irvine, hopes to figure out how clouds fit into this picture, but most current climate models are blind to features smaller than a few dozen miles wide. Crunching the numbers for a worldwide layer of clouds, which might be just a couple hundred feet tall, simply requires more mathematical brawn than any supercomputer can deliver.

Unless the computer understands how clouds interact better than we do, that is. Pritchard is one of many climatologists experimenting with training neural networksa machine learning technique that looks for patterns by trial and errorto mimic cloud behavior. This approach takes a lot of computing power up front to generate realistic clouds for the neural network to imitate. But once the network has learned how to produce plausible cloudlike behavior, it can replace the computationally intensive laws of nature in the global model, at least in theory. "It's a very exciting time," Pritchard says. "It could be totally revolutionary, if it's credible."

Companies are preparing their machines so researchers like Pritchard can take full advantage of the computational tools they're developing. Turek says IBM is focusing on designing AI-ready machines capable of extreme multitasking and quickly shuttling around huge quantities of information, and the Department of Energy contract for Aurora is Intel's first that specifies a benchmark for certain AI applications, according to Damkroger. Intel is also developing an open-source software toolkit called oneAPI that will make it easier for developers to create programs that run efficiently on a variety of processors, including CPUs and GPUs.As exascale and machine learning tools become increasingly available, scientists hope they'll be able to move past the computer engineering and focus on making new discoveries. "When we get to exascale that's only going to be half the story," Messer says. "What we actually accomplish at the exascale will be what matters."

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Next-gen supercomputers are fast-tracking treatments for the coronavirus in a race against time - CNBC