The world desperately needs painkillers that aren't addictive or heavy with damaging side effects. A strong candidate has been found in the venom of a tarantula known as a Chinese bird spider, and fortunately no further tarantula involvement is required.

Venoms are exceptionally chemically complex, usually involving hundreds of different molecules. With so many animals having adopted them for hunting or defense, they provide a biochemical bonanza, including one of the most prescribed drugs in the world captopril.

Dr Christina Schroeder of the University of Queensland is hunting for a replacement for opioids such as fentanyl and oxycontin in treating chronic pains like back pain. She told IFLScience she has a particular interest in neuropathic pain, which can be such a severe side effect of chemotherapy some people discontinue treatment.

Although opioids are effective in producing pain relief, they come with unwanted side-effects like nausea, constipation and the risk of addiction, placing a huge burden on society, Schroeder said in a statement.

Having identified the 1.7 sodium channel as an important chronic pain relief target, Schroeder went looking for molecules to fit. She told IFLScience another team had already identified Huwentoxin-IV in bird spider venom as a candidate.

Schroeder set about modifying Huwentoxin-IV to make it more specific, seeking something that would block the channel she needed but not affect the body's eight other sodium channels, minimizing the risk of side effects.

The process proved particularly complex. We normally talk about receptors and molecules as a lock and key, Schroeder told IFLScience, But in this case we had to look at the whole frame around the lock. The doorframe in this analogy is the lipid membrane that surrounds the channel, which influences molecular binding.

In the Journal of Biological Chemistry, Schroeder has announced that the modified Huwentoxin-IV proved successful at blocking pain in mouse trials without obvious side-effects.It's not clear why the spiders target this particular channel in their venom, but Schroeder says the diversity of molecules they inject hits their prey from many angles at once, minimizing capacity to run away or fight back.

Schroeder assured IFLScience that even if a drug from her work eventually hits the market, there will be no spider farms to terrorize our dreams. The molecule will either be synthesized inorganically or produced by genetically modified bacteria. Indeed, Schroeder added, I don't much like spiders. I have a postdoc who enjoys finding animals and milking them, allowing her to concentrate on the chemistry undisturbed.

More preclinical research is required before studies can begin on humans, so a product is probably 15 years away. People are starting to understand how hard it is to get a drug on the market quickly now we need a vaccine so much, she said.

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The Painkiller We Really Need Might Come From Spider Venom - IFLScience

This article is part of Harvard Medical Schoolscontinuing coverageof medicine, biomedical research, medical education and policy related to the SARS-CoV-2 pandemic and the disease COVID-19.

Lung injury and acute respiratory distress syndrome have taken center stage as the most dreaded complications of COVID-19, the disease caused by the new coronavirus, SARS-CoV-2. But heart damage has recently emerged as yet another grim outcome in the virus'srepertoire of possible complications.

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COVID-19 is a spectrum disease, spanning the gamut from barely symptomatic infection to critical illness. Reassuringly, for the large majority of individuals infected with the new coronavirus, the ailment remains in the mild-to-moderate range.

Yet, a number of those infected develop heart-related problems either out of the blue or as a complication of preexisting cardiac disease. A report from the early days of the epidemic described the extent of cardiac injury among 41 patients hospitalized with COVID-19 in Wuhan, China: Five, or 12 percent, had signs of cardiovascular damage. These patients had both elevated levels of cardiac troponina protein released in the blood by the injured heart muscleand abnormalities on electrocardiograms and heart ultrasounds. Since then, other reports have affirmed that cardiac injury can be part of coronavirus-induced harm. Moreover, some reports detail clinical scenarios in which patients initial symptoms were cardiovascular rather than respiratory in nature.

How does the new coronavirus stoke cardiac damage?

The ways in which the new coronavirus provokes cardiac injury are neither that new nor that surprising, according to Harvard Medical School physician-scientists Peter Libby and Paul Ridker. The part that remains unclear is whether SARS-CoV-2 is somehow more virulent toward the heart than other viruses.

Libby and Ridker, who are practicing cardiologists at Brigham and Womens, say COVID-19-related heart injury could occur in any several ways.

First, people with preexisting heart disease are at a greater risk for severe cardiovascular and respiratory complications from COVID-19. This is hardly a surprise. Research has shown that infection with the influenza virus poses a more severe threat for people with heart disease than those without cardiac problems. Research also shows that heart attacks can actually be brought on by respiratory infections such as the flu.

Second, people with previously undiagnosed heart disease may be presenting with previously silent cardiac symptoms unmasked by the viral infection. In people with existing heart-vessel blockages, infection, fever and inflammation can destabilize previously asymptomatic fatty plaques inside the heart vessels. Fever and inflammation also render the blood more prone to clotting, while also interfering with the bodys ability to dissolve clotsa one-two punch akin to throwing gasoline on smoldering embers.

Its like one big stress test for the heart, said Ridker, who is the Eugene Braunwald Professor of Medicine at Brigham and Womens Hospital.

Third, some people may experience heart damage that mimics heart attack injury even if their arteries lack the fatty, calcified flow-limiting blockages known to cause classic heart attacks. This scenario, called myocardial infarction type 2, can occur when the heart muscle is starved for oxygen, which in the case of COVID-19 may be triggered by a mismatch between oxygen supply and oxygen demand. Fever and inflammation accelerate heart rate and increase metabolic demands on many organs, including the heart. That stress is compounded if the lungs are infected and incapable of exchanging oxygen and carbon dioxide optimally. This impaired gas exchange can further diminish oxygen supply to the heart muscle.

Finally, there is a subset of people with COVID-19some of them previously healthy and with no underlying cardiac problemswho develop fulminant inflammation of the heart muscle as a result of the virus directly infecting the heart. This type of inflammation could lead to heart rhythm disturbances and cardiac muscle damage as well as interfere with the hearts ability to pump blood optimally.

The propensity of certain viruses to attack the heart muscle and cause viral myocarditis is well known, Libby said, adding that the most notorious viral offender has been the Coxsackie B virus. Nonetheless, a recent case report from Italy underscores the notion that the new coronavirus could also infect the heart and affect heart muscle function in healthy adults even after the acute phase of the infection has resolved and even in the absence of lung damage.

There are definitely some people who develop acute fulminant myocarditisin which the virus infects the heart muscle itself or the cells within the heartand causes a horrible inflammatory reaction, said Libby, who is also the Mallinckrodt Professor of Medicine at Brigham and Womens Hospital. This can be life threatening, and it can happen in people who don't have any preexisting risk factors.

Libby and Ridker, however, say this out-of-the-blue scenario in otherwise healthy individuals is likely rare relative to the overall number of people with COVID-19 who experience heart problems.

The frenemy within

For Ridker and Libby, who have studied the immune pathways of cardiovascular disease for decades, the cardiac involvement in COVID-19 is yet another striking example of the widespread effects of inflammation on multiple organs and systems.

Inflammation is a critical defense response during infection, but it has a dark side. Infections can set off a cascade of immune signals that affect various organs.

Libby and Ridker hypothesize that any infection in the bodya festering boil, an injured joint, a viruscan become a source of inflammation that activates the release of inflammatory proteins known as cytokines and calls up armies of white blood cells and other messenger molecules that, in an effort to fight the infection, disrupt normal processes. When these inflammatory molecules reach the welcoming soil of a fatty deposit in the blood vessel wallone that is already studded with resident inflammatory white blood cellsthe cytokines can boost the local inflammatory response and trigger a heart attack.

Our work has shown that cytokines can impinge on these cells in the plaque and push it through a round of further activation, Libby said.

The inflammatory chemicals released during infection can also induce the liver to ramp up the production of important proteins that defend the body from infection. These proteins, however, make the blood more prone to clotting, while also reducing the secretion of natural clot-dissolving substances. The tiny clots that may form can clog the small blood vessels in the heart and other organs, such as the kidneys, depriving them of oxygen and nutrients and setting the stage for the multisystem failure that can occur in acute infection.

Thus, immune-mediated injury to the heart and other organs could be collateral damage because of the bodys overwhelming systemic immune responsea condition known as cytokine storm, which is marked by the widespread release of cytokines that can cause cellular demise, tissue injury and organ damage.

COVID-19 and blood pressure medications

SARS-CoV-2 invades human cells by latching its spike protein onto the ACE2 receptor found on the surface of cells in the airways, lungs, heart, kidneys and blood vessels. The ACE2 protein is an important player in the renin-angiotensin-aldosterone system, which regulates blood vessel dilation and blood pressure. Two classes of drugs widely used to treat high blood pressure and heart diseaseACE inhibitors and angiotensin receptor blockersinteract with the ACE2 receptor. A possible concern related to COVID-19 stems from the notion that these blood pressure medications could increase the number of ACE2 receptors expressed on cells, possibly creating more molecular gates for the virus to enter. Some experts have wondered whether the use of such drugs could render people who take them more susceptible to infection. Conversely, others have postulated that the abundance of ACE2 receptors may enhance cardiovascular function, exercising a protective effect during infection.

The answer is far from clear, but a recent review suggests these medicines may play a dual role in COVID-19on the one hand, enhancing susceptibility to infection and, on the other, protecting the heart and ameliorating lung damage from the disease.

Libby and Ridker cautioned that patients who take such life-saving medications should stay on them or at least have a careful discussion with their cardiologists. This is because these drugs have clear and well-established benefits in hypertension and certain forms of heart disease, while their propensity to make humans more susceptible to SARS-CoV-2 remains speculative for the time being.

But what remains speculative today will crystalize in the weeks and months to come, Ridker and Libby said, because the science is moving forward rapidly, with new papers coming out daily and a growing pool of patients to draw observations from.

In 12 to 18 months we're going to have a great deal of information, but right now our job is to, number one, keep people from getting COVID-19 by strict adherence to now-familiar containment measures, Libby said. Then, we need to get people who get the disease through this acute phase.

The need for rigorous randomized trials done quickly and effectively is acute, they said. Until the evidence from these trials begins to coalesce, clinicians will have to navigate the uncharted territory of delivering cardiac care in the time of pandemic with caution but also with resolve.

We don't have the comfort of our usual databases, so we have to rely on our clinical skills and judgment. But we have to do so in all humility because often data dont bear out our logical preconceptions, Libby said. Yet, we must act.

RelatedEnding the Pandemic

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Coronavirus and the Heart - Harvard Medical School

Dr. Garry Ferroniis a bit of a legend. He is professor emeritus (retired) at the Northern Ontario School of Medicine and was a microbiology professor when I was a molecular biology student at Laurentian University. Most of my classmates and I were in awe of Ferroni.

His area of expertise is medical microbiology and infectious diseases. He has a PhD from the University of Waterloo and spent his career doing research and teaching at LU and NOSM.

At NOSM, he was the founding division head of medical sciences, as well as a professor, and he worked with colleagues in Sudbury and Thunder Bay to develop the infectious diseases curriculum for the medical program.

The Star reached out to Ferroni with some questions on COVID-19. Ever the helpful teacher, he was happy to oblige.

Q. In lay person terms, what is the novel coronavirus?

A. COVID-19 is caused by a virus officially named SARS-CoV-2, which stands for severe acute respiratory syndrome coronavirus 2. This virus is being referred to in the media as COVID-19 or novel coronavirus. It is the newest virus in a family of viruses called coronaviruses, so named because club-shaped protrusions from their surface give them a crown-like appearance.

Most of them infect animals such as bats, pigs and camels, but a few have managed to jump to humans.

In humans, they tend to cause mild upper respiratory tract infections diagnosed as the common cold. The exceptions are the coronaviruses that cause SARS, Middle East Respiratory Syndrome (MERS) and COVID-19. These coronaviruses are more adept at invading the lower respiratory tract where they can cause a very severe pneumonia.

Dr. Garry Ferroni is a retired professor from NOSM and Laurentian University. He taught microbiology and infectious diseases. In fact, he helped establish the curriculum for the medical school.supplied photo

Q. Do we know how the virus was transmitted from animal to human? How is it transmitted from person to person?

A. The assumption is the COVID-19 virus was transmitted from animal to human, and the animal often mentioned is the bat. There are some who suggest that animals called pangolins might be an intermediary host, which means the virus moved from an unknown animal to pangolins and then to humans.

The possibility that an exotic animal market in Wuhan, China, provided the opportunity for animal to human transmission has not been proven. At this point, the origin of the virus just isnt known. Studies of the sequence of the viruss genetic material (genome) relative to other coronavirus genomes do indicate the COVID-19 virus arose naturally as opposed to being created in a research laboratory.

It is likely that infected persons transmit the virus to other persons via respiratory droplets in their coughs and sneezes (such droplets might even be discharged by talking and deep breathing) and by direct contact, such as hand-shaking and hugging. It follows that infected persons would contaminate surfaces and objects via droplets and direct contact. If we touch or handle these and then touch our faces, we can introduce the virus into our bodies, the entry sites being the mouth, nose and eyes. Knowing how infectious agents are transmitted allows us to protect ourselves and our contacts.

Registered nurses Karen Hatton, left, and Theresa Murray stand inside a shelter associated with the drive-through option for coronavirus testing on Walford Road.Jim Moodie/Sudbury Star

Q. How long does the virus live on different surfaces, such as plastic, metal, produce?

A. Viruses can survive on surfaces for a limited period of time, but they cannot multiply. They must invade the cells of an appropriate organism to multiply. Not surprisingly, there is not a lot of information on the survival of the COVID-19 virus when it is outside of the human host.

Studies at or supported by the National Institute of Allergy and Infectious Diseases and the Centers for Disease Control and Prevention, both of which are American institutions, have shown survival in aerosols for up to a few hours; on copper for up to a few hours; on cardboard for up to one day; and on plastic and stainless steel for up to a few days.

Concerning produce, as other pathogens can be found transiently on fruits and vegetables as a result of contamination, we should expect this to be true for COVID-19 as well, and we should wash and rinse our produce thoroughly. This means there should be no more tasting of grapes or cherries in the supermarket.

Q. There is lots of (mis-) information online about ways to kill the virus, particularly around heat and the use of saunas. Can you dispel some of those myths?

A. With a few exceptions possibly, cold temperatures do not kill viruses. Heat, on the other hand, definitely kills viruses, but the minimum temperature and exposure time to accomplish this vary from virus to virus.

Generally, 60-minute exposures to temperatures above 60 C kill most viruses, as would shorter exposures to higher temperatures. Nevertheless, using these moderate temperatures to try to eliminate viruses is not very practical.

Viruses are killed by a variety of disinfectants and by hand sanitizers that contain at least 60 per cent alcohol. In the process of proper hand-washing, employing soap and warm water, viruses are physically removed from the skin. Coronaviruses are actually killed because soap removes their membranous envelope that allows them to attach to host cells to initiate infection.

Q. Why and how does the virus make people sick (in lay terms)?

A. COVID-19 is a severe acute infection of the respiratory tract. A likely progression of the disease is as follows:

Upon entering the body, the virus establishes itself in the upper respiratory tract (nose and throat).

Around five to six days after exposure, the first symptoms occur, one or more of fever, dry cough, fatigue, aching muscles, sore throat and nasal congestion. In more serious cases the virus moves into the lower respiratory tract (the lungs) to cause a pneumonia that is indicated by shortness of breath.

The development of the disease is due to the ability of the virus to infect and kill cells that line the respiratory tract, including the air sacs in the lungs, and to an exaggerated response by the immune system that causes extreme inflammation in the lungs. This affects our ability to breathe.

Age and overall health are factors in the severity of the disease. Older adults and those with chronic diseases of the lungs and heart, for example, are most likely to experience serious disease, whereas healthy children are least likely.

An inspirational message is displayed in a window of a home in Sudbury on April 16.John Lappa/Sudbury Star

Q. What about treatment and prevention?

A. Treatment of a viral disease like COVID-19 requires administering an effective antiviral agent or administering antibodies that eliminate the virus. Antibodies are proteins produced by the immune system in response to infection, and for some diseases, they can be made available for therapeutic use.

Currently, neither type of therapy is available, but research and trials are in progress. The major preventative would be a vaccine and this is being pursued.

Q. Does this virus show much capacity for mutation? Should we be concerned about mutation?

A. The genome of a virus can be altered by a change in the base sequence, a process called mutation. It can also be altered by a process called genetic recombination, in which a second virus contributes some of its genome to another genome. Genetic recombination can happen if the two different viruses infect a host cell at the same time.

Mutations tend to cause minor changes in the characteristics of the virus, whereas genetic recombination can result in major changes. It is these major changes that can produce a new strain of the virus capable of causing a pandemic, as there is no immunity to the new strain. Given that coronaviruses have been shown to mutate and to undergo genetic recombination, and to move from one animal species to another, we should expect the same of the COVID-19 virus. This means, of course, that a disease similar to COVID-19 could emerge in the future.

Q. Once youve been sick, are you immune to the virus?

A. It is a reasonable assumption that individuals who have had the disease will have a substantial period of immunity, if not life-long immunity, to subsequent exposure to the same strain of the virus. Moreover, immunity as a result of having had a disease is superior to that acquired by any immunization procedure (vaccine), which should be true for COVID-19 as well.

Q. Can you predict how this virus will travel through the human population? Do you foresee a second/third/fourth wave of sickness?

A. It is difficult to predict virus movement through the population, but if we look at what has happened thus far in our province and in countries further into the pandemic we see that: older adults and individuals with certain chronic conditions get seriously ill; certain sites in a community, for example, long-term care facilities, can have high densities of infection; individuals who provide essential services are exposure-prone; and hospitals can be overwhelmed with patients needing intensive care.

Past influenza pandemics tell us there can be more than one wave of illness, each separated by a few months. Because the reasons for a second or even third wave are not always known in advance, it is difficult to predict waves. It is much easier to account for them after the fact.

Q. What are the best- and worst-case scenarios?

A The best-case scenario would be if our preventive measures had a major positive impact and terminated this outbreak within a few months. For this scenario, as for some others, there would be the issue of individuals at highest risk and without immunity emerging from isolation into a population where some might still be harboring COVID-19. The development of a vaccine or effective anti-viral medication would eliminate this as an issue.

The worst-case scenario would be to experience for an extended period of time what is currently happening in Italy, Spain and the USA.

Q. There has been media attention on the need to strip and change clothes when you come home. Is this necessary? What other measures, besides washing hands, maintaining distance and stifling coughs, should we be putting into practice?

A To protect ourselves, family members and others, it is important to adopt effective procedures and behaviours. As respiratory droplets discharged by infected persons travel in the air for a metre or so, maintain a safe space of two metres. Cough and sneeze into the bent arm or into a tissue. Avoid touching ones face to prevent introducing the virus into your body. Wash hands properly with soap and warm water, frequently and at critical times. Sanitize hands at critical times with sanitizer containing at least 60 per cent alcohol.

If you decide to wear a mask when you are in public, sanitize your hands before putting the mask on and just before and just after taking the mask off, and be aware the mask might collect infectious droplets. Do not use masks designed for health care workers because of their limited supply.

We should be aware that clothing can become contaminated if the two-metre barrier is broken and by contact with or transfer from surfaces and objects. Individuals should assess their own probability of exposure and that of their children, and decide if changing clothes is necessary.

The Public Health Sudbury and Districts website (phsd.ca) should be visited frequently and the recommendations for isolation and in-person socializing followed.

sud.editorial@sunmedia.caTwitter: @SudburyStar

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Sudbury Accent: The best and worse case scenarios for COVID-19 - The Sudbury Star

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Some labs remain active, with focus switched to COVID-19

A School of Medicine lab member packs up items in a lab in the Couch Biomedical Research Building. Research in most of the universities' labs has been ramped down due to the COVID-19 pandemic.

When Washington University Vice Chancellor for Research Jennifer K. Lodge, PhD, first sounded the alarm about the disruptive impact COVID-19 likely would have on labs across the university, the research community heeded her warning, taking steps to shut down lab work and move as much as possible online.

Those in position to do so began pivoting their research to the novel coronavirus that has caused an unprecedented shutdown of public life across the globe. In a very short span of time, the universitys scientific community has responded to the pandemic with extraordinary research collaborations, all the while finding new ways to keep faculty, staff and students connected as they shift work out of the lab and into cyberspace.

For all of us who are passionate about our research, we know that ramping down and pausing our work is very difficult, said Lodge, a professor of molecular microbiology who also serves as associate dean of research for the School of Medicine. At the same time, this unusual situation may provide a rare opportunity for researchers to slow down our typically fast pace and think deeply about our science and connect with colleagues in ways we havent before.

Scientific research is a complex endeavor, and figuring out how to slow or stop research that might involve living cells or mice is not a simple task. The Office of the Vice Chancellor for Research is constantly updating its coronavirus information website, Guidance for Researchers on COVID-19, and recommends that investigators frequently refresh the site to check for updates on the fast-changing advice and resources available to researchers, including updates from funding agencies, such as the National Institutes of Health (NIH). The office also has held virtual town hall meetings via Zoom to keep researchers up to date.

Sarah K. England, PhD, the Alan A. and Edith L. Wolff Professor of Medicine, has moved much of her lab online and set up a small, rotating group of people to take care of lab tasks that need to continue, even during a shutdown. Englands lab focuses on studies of the uterus and factors that might lead to preterm birth.

We immediately made sure everyone has access to their data online, through Box, so that we all can work remotely, England said. Fortunately, quite a few people in my lab can focus on writing or new project planning. We still have a skeleton crew going into the lab to check on things we absolutely must check on. We set up an online calendar showing when people are going in so theres no overlap and we can maintain safe physical distancing. Its been helpful to have somebody there because we also were able to collect PPE to donate to coronavirus-focused clinical efforts.

Farshid Guilak, PhD, a professor of orthopedic surgery, described similar steps taken in his lab. Many labs, including his and Englands, are trying to maintain special colonies of mice. Even though active research may have stopped, it is important to continue caring for these groups of mice with special genetics and other characteristics that make them unique, so that work can ramp up again quickly when researchers are able to return to the lab. As a backup, researchers also have cryopreserved embryos of such specialized mice to ensure their survival.

Fortunately, at this point, we are able to continue to feed our mice their special diets, Guilak said. We study models of obesity and how that might increase the risk of developing arthritis. Were doing our best to minimize the impact of not having our typical access to the mice.

This lab in the Couch Biomedical Research Building normally would be bustling with activity but has been quieted due to a research rampdown ordered in response to the COVID-19 pandemic.

The School of Medicines COVID-19 task force orchestrating research into the novel coronavirus is led by Jeffrey Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics; William G. Powderly, MD, the J. William Campbell Professor of Medicine and director of the Institute for Clinical and Translational Sciences (ICTS); and Sean Whelan, PhD, the Marvin A. Brennecke Distinguished Professor and head of the Department of Molecular Microbiology. A major focus of this work includes creating mouse models of COVID-19 infection and vaccine development.

In addition, researchers who study other viruses, lung infections or have other related expertise are turning their labs resources to the novel coronavirus. Shabaana Khader, PhD, a professor of molecular microbiology, studies tuberculosis (TB); and Jacco Boon, PhD, an associate professor of medicine, is focused on influenza viruses. Both are uniquely positioned to trade research into one dangerous lung infection for another.

Because we study other types of respiratory viruses, our lab is ideally equipped to conduct basic research on the COVID-19 virus, Boon said. We can grow the virus in our facility and, once we have animal models, we can start testing new compounds and antibodies for potential treatments. One challenge is that mice dont have the lung receptor that this virus targets to infect human lungs. One solution could be to genetically modify mice to express the human lung receptor.

Khader studies the lungs immune response to tuberculosis (TB) infection. Her team could, potentially, help shed light on how the immune system in the lungs reacts to coronavirus infection. As part of her TB research, Khader works with a collaborator at the Texas Biomedical Research Institute, Deepak Kaushal, PhD. Kaushal studies TB infection in macaques, nonhuman primates that have the lung receptor for COVID-19 infection.

When we receive lung samples from his group, we will be using single cell technology to study the lung immunology of this disease, Khader said. We will be able to look at the immune response over time and how it might change from the first few days of infection to longer time points. So, my lab is shutting down our TB operations and ramping up COVID-19 work.

Even investigators whose research might seem to have little to do with respiratory viruses are exploring aspects of COVID-19, such as investigating ways the pandemic is influencing childhood development. Deanna M. Barch, PhD, the Gregory P. Couch Professor and head of the Department of Psychological & Brain Sciences, co-leads the Adolescent Brain and Cognitive Development Study, a national study with multiple clinical sites involving a broad sample of children across the country. As much as possible, the studys assessments have been moved online.

We are adding assessments that directly address COVID-19 in terms of its impacts on families and kids, Barch said. We would like to understand what factors may predict resilience in this stressful situation and how that might impact brain development over time.

Lori A. Setton, PhD, the Lucy and Stanley Lopata Distinguished Professor and chair of the Department of Biomedical Engineering, said that several professors in her department also have pivoted their research to COVID-19, including studying the heart arrhythmia that some patients experience.

She also talked about supporting faculty members who are teaching online for the first time while ramping down work in their labs.

I held drop-in coffee hours on Zoom, so faculty members could tell me what they needed to help with the transition, Setton said. Many lab groups are holding virtual happy hours to have more casual discussions about their transitions to remote work and their research strategies moving forward. There are a lot of humorous and uplifting stories about these transitions that it has helped to share.

Setton, Khader, England, Guilak and others also talked about the importance of maintaining social ties during this time of social distancing, and providing support for their lab members physical and mental well-being.

Labs are little communities, and many of our trainees are far from home, so were concerned about everyones mental health, Guilak said. Were trying to check in with everybody on a regular basis. Were continuing our regular lab meetings online and then having smaller group meetings every week. Several of our trainees have started their own journal clubs. All of this is over Zoom or otherwise online, but its important to maintain the connections.

Added England: Many of our people have young children at home, and were trying to make sure everyone has the time and ability to adjust to the challenges of working from home for a while.

Many labs and groups around campus have found ways to use Slack to stay connected. Guilak said his lab has a Slack channel called Positivity, where they share photos of kids and pets and trade recipes and cooking tips.

I am inspired by the response of the Washington University community to this unprecedented situation, Lodge said. Thank you to those who have switched their work to COVID-19. And thank you to everyone who has taken steps to ramp down all other research in their labs and work remotely to keep as many people off campus as possible. Together, we are doing our best to bend the curve and help protect our clinical colleagues on the front lines fighting this virus.

Postdoctoral researchers Brett Case, PhD, (left) and Adam Bailey, MD, PhD, wear full personal protective equipment to study the COVID-19 virus. Washington University School of Medicine in St. Louis physicians and researchers are preparing for COVID-19 cases and working on drugs and vaccines to fight the disease.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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Research in most university labs moved from bench to internet - Washington University in St. Louis Newsroom

A team at Stanford Medicine has developed gadgets that can be fitted in an ordinary toilet to screen urine and feces and upload the encrypted health data. The technology may be particularly useful for monitoring individuals at high risk of developing particular illnesses.

Many people will be uncomfortable with the idea of cameras and sensors in their toilet. It may seem like an unthinkable intrusion into what is perhaps the most private of all activities.

But a team of developers at Stanford Medicine in Stanford, CA, believe the clinical benefits of their smart toilet could be far-reaching.

They are also confident that their toilet can safeguard the privacy of users.

Technologies that continually monitor a persons health play a growing role in healthcare.

Existing devices include smartwatches for collecting data, such as heart rate, and wearable blood pressure monitors. A skin patch is in development that tracks movement, heart rate, and breathing.

The thing about a smart toilet, though, is that unlike wearables, you cant take it off, says Prof. Sanjiv Gambhir, chair of radiology at Stanford Medicine. Everyone uses the bathroom theres really no avoiding it and that enhances its value as a disease-detecting device.

Prof. Gambhir believes the smart toilet may be particularly useful for monitoring people at high risk of conditions, such as prostate cancer, irritable bowel syndrome (IBS), and kidney failure, due to their genetic predispositions, for example.

His team developed a suite of gadgets that a person can fit in the bowl of an ordinary toilet. Its sort of like buying a bidet add-on that can be mounted right into your existing toilet, he says. And like a bidet, it has little extensions that carry out different purposes.

In a pilot study, 21 volunteers tested the device over several months.

The smart toilet is the perfect way to harness a source of data thats typically ignored and the user doesnt have to do anything differently.

Prof. Sanjiv Gambhir

A motion sensor activates the smart toilet to start capturing video data, which are then digitally analyzed.

One of the smart toilets algorithms can detect abnormal urine flow rate, stream time, and volume, which could be useful for flagging prostate problems in men, for example.

Another gauges the consistency of fecal matter from the images and classifies it according to the Bristol stool chart. This is a standardized system used by clinicians worldwide to diagnose problems such as constipation, gut inflammation, and a lack of dietary fiber.

The smart toilets software can also identify color changes in urine using urinalysis strips (dipstick tests). It can detect 10 different markers, including the number of white blood cells and the levels of specific proteins in the urine. These biomarkers can provide early warnings of diseases, such as kidney infections and bladder cancer.

According to an article describing the technology in Nature Biomedical Engineering, the toilets abilities are comparable to the performance of trained medical personnel.

Encrypted data from the toilet upload to a secure cloud server. In the future, this information could integrate with a healthcare providers record-keeping system for easy access by the individuals doctor.

The Stanford team envisages an app sending a text alert to the healthcare team if the device detects an urgent issue, such as blood in someones urine.

Identifying who is using the toilet will be critical in a household of several people.

The whole point is to provide precise, individualized health feedback, so we needed to make sure the toilet could discern between users, Prof. Gambhir said. To do so, we made a flush lever that reads fingerprints.

However, in case someone uses the toilet and another flushes it, or if the toilet has an auto-flush system, a camera captures what the article calls the distinctive features of their anoderm [skin tissue lining of the anus].

We know it seems weird, but as it turns out, your anal print is unique, says Prof. Gambhir.

The recognition system is fully automatic, which means that no human will see the scans.

Despite the teams best efforts to ensure user privacy and data confidentiality, the smart toilet may prove a hard sell.

A survey conducted by the researchers of 300 prospective users revealed that only 15% described themselves as very comfortable with the concept.

The researchers plans include recruiting more volunteers to test the toilet and individualizing the available tests. A patient with diabetes might want glucose levels in their urine checked, for example.

In addition to urine tests, the team would also like to build into their toilet the ability to carry out molecular analysis of stool samples.

Thats a bit trickier, but were working toward it, says Prof. Gambhir.

If successful, one advantage for the squeamish will be that they no longer have to collect their own stool samples and take them to a clinic for testing.

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'Smart toilet' recognizes users and checks for signs of disease - Medical News Today

A lot has been said and written about the Philippine-made test kitthe first in the countryfor the 2019 coronavirus disease (Covid-19).

As soon as it was announced in March that a Covid-19 test kit is being developed and manufactured in the country, all the news media platforms, columns and talk shows have been awash with stories on the subject. Its been the talk of the town.

Interviews with its creatorled by the multi-awarded Dr. Raul V. Desturahave been held left and right, seeking the story behind the diagnostic system that will help stem the spread of the virus in the country, and proud that it was made in the Philippines, plus being cheaper at P1,300 than the imported P8,000.

Actually the kit is already being used now at the Philippine General Hospital (PGH) and other major hospitals around the country that are handling Covid-19 cases after the Food and Drug Administration Philippines(FDA) approved its commercial use on April 3.

The test kit was developed in collaboration with the University of the Philippines-National Institutes of Health (UP-NIH), and funded by the Department of Science and Technology (DOST). It is manufactured by Manila HealthTek that was also supported by the DOST.

It was a just-in-time scenario for the Philippines when it badly needed test kits for Covid-19 cases.

It was a much-awaited result of research and development, which was conducted immediately when the coronavirus pandemic startled the whole world in January 2020. This completely upholds the DOST of the mantra R&D making change happen.

Despite Desturas being busy attending to interviews, they were mainly about his research on the test kit, and rarely about himself.

Who is this scientist behind the Covid-19 test kit?

As a clinician-scientist, I continuously try to narrow down the gap between basic science, medical science, biotechnology and community service by forging strong collaboration among disciplines to reach a focused goal, Destura said as quoted by the NIH UPM web site.

My research bench to community approach is ultimately geared toward developing low-cost technologies for the control of infectious diseases in the Philippines and the generation of new knowledge to find sustainable and equitable solutions to disease of poverty, added Destura, the vice president and chairman of the Division of Medical Sciences of the National Research Council of the Philippines (NRCP).

A Presidential Lingkod Bayan 2019 Awardee, Destura is a known scientist and molecular microbiologist who is also recognized for developing local and less costly diagnostic kits for rapid detection of the most dreaded infectious diseases such as dengue, hepatitis and tuberculosis.

Notable of these is the Biotek-M, a rapid test kit for dengue that is projected to be more affordable among average Filipino families that may not be able to afford the more expensive polymerase chain reaction technology.

This new technology is hoped to advance the diagnostic capability of the hospitals for better management of the dengue disease. Biotek-M is currently being rolled out to three government hospitals.

Actually the Covid-19 test kit was based on the Biotek-M technology.

Desturas versatility is exhibited by the establishment of two world-class molecular biology laboratoriesthe Molecular Biology and Biotechnology Research Laboratory at the UP NIH and the Clinical Molecular Diagnostic Laboratory of the Medical Cityunder his leadership.

He is also a recipient of several prestigious national and international awards for his innovative research and leadership in research and clinical molecular biology.

Among the awards are the Gold Medal from the International Exhibition of Inventions of Geneva (Salon International Des Inventions Geneve), Geneva, Switzerland in April 2018; International Training and Research in Emerging Infectious Diseases Research Fellowship Award from the Center for Global Health Division of Infectious Disease and International Health, University of Virginia.

The Bill and Melinda Gates Travel Scholarship for 2005 Keystone Symposia; Outstanding Young Scientist of the Philippines in 2008; University of the Philippiness Research Productivity Award in 2011; The Outstanding Young Men of the Philippines in 2011; Gawad Agham 2015.

Outstanding Alumni in Microbiology of the University of Santo Tomas; 2015 Outstanding Alumni in Medicine of the De La Salle University; and the prestigious 2015 Dr. Jose Rizal Memorial Award in Research given by the Philippine Medical Association.

At the NRCP, Destura was named the 2015 Dr. Eusebio Y. Garcia awardee. The award is given annually to Filipino scientists in recognition of their outstanding research contributions in the fields of Molecular Biology and Molecular Pathology.

The award was founded by Dr. Eusebio Y. Garcia in 1985 to encourage more researchers to venture into this field and also to recognize the ground breaking researches made by the Filipinos in the said field.

In June 2018, immunization became a hot topic in the country because of the Dengvaxia scare. Amid the controversy, the NRCP made a categorical pronouncement on the importance of vaccines.

The NRCP statement, crafted by Destura, stated that scientific evidence has clearly demonstrated that vaccines have dramatically eradicated small pox and polio and have greatly reduced child mortality in the Philippines and in many parts of the world. The NRCP stands by the government efforts to sustain its immunization programs as we strongly urge the public to pay attention to the knowledge claim of scientists on the beneficial effects of immunization.

On March 7, while in the midst of isolation for his research work on the Covid-19 test kit, NRCP President Dr. Ramon A. Razal consulted Destura when the Department of Health raised Red Code Alert on Covid-19.

Upon Desturas expert advise and with the NRCP Governing Board approval, Razal postponed the NRCPs biggest annual event, the Scientific Conference and 87th General Assembly in Manila on March 9. The conference has an anticipated 1,200 participants from all over the country.

The decision became the Councils contribution to the national efforts to prevent the risk of further local or community transmission of Covid-19.

Destura studied Medicine at the De La Salle University Health Sciences in 1996, and went to pursue training and research fellowship in Infectious Disease at the UP-PGH from years 20012003.

He went to University of Virginia, US, for higher learning and international training in Emerging Infectious Diseases. Maria Elena A. Talingdan, S&T Media Service

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'I focus on low-cost tech to fight infectious diseases' - Business Mirror

How is Ireland doing in the fight to slow the spread of Covid-19?

After more than two weeks of lockdown with wide ranging restrictions limiting commercial and social life, the battle rages on and there are no definitive signs that a peak has been reached. The country is at a delicate and critical point in its response to the coronavirus outbreak, according to Liz Canavan the assistant general secretary at the Department of the Taoiseach. Many people have fallen ill and too many have died and while there is some optimism that the Republic may not be hit as hard by Covid-19 as Italy, Spain and the UK, it is still too early to say what may happen in the weeks ahead.

What are the numbers?

On Tuesday, April 14th, 41 more people were reported to have died from coronavirus in the Republic taking the total number of fatalities to 406 while the number of known cases reached 11,479. Modelling data used by the National Public Health Emergency Team shows the daily growth rate has fallen from 33 per cent in the early stages of the outbreak to 9 per cent this week.

What is happening in Northern Ireland?

Ten more coronavirus-related deaths were announced in Northern Ireland on Tuesday, bringing the total number of fatalities to 134. On the same day a total of 1,967 cases had been identified in the North.

How is the Republic doing when it comes to testing?

Testing and contact tracing in real time between 24 and 48 hours is needed to fully contain the disease, experts have said. Minister for Health Simon Harris has said the mantra is to test, test, test. There have been widely reported shortages of testing kits and lab supplies and the waiting times for results, according to the Department of Health, was about seven to 10 days. But things have improved.

HSE chief executive Paul Reid said a backlog in testing had been reduced from a high point of about 35,000 people waiting for results to some 11,000. He told a briefing in Dublin on Tuesday that 25 laboratories were now being used to examine Covid-19 tests, including 20 in hospitals, the national lab in UCD, a Department of Agriculture facility and in Germany. Mr Reid said nearly 8,000 tests were completed on Saturday. That backlog will continue to be reduced and will be reduced completely by the end of this week, he said.

How does that compare with elsewhere in the world?

Mr Reid, has said that Ireland is a top-tier country although that claim has been disputed by some. Dr Sean LEstrange, a social scientist in UCD, has conducted a comparative analysis of reported testing figures. It is difficult to support the claim that Irelands testing practice for Covid-19 is in the top tier in the world, he wrote this week. Ireland is not doing badly and it is certainly not amongst the worst in the world by any stretch of the imagination. Yet compared with other similar-sized and resourced states in the European context, its performance is decidedly middling, he wrote.

How important is the testing?

If you have symptoms, it may not matter all that much. If you become sick enough to be hospitalised, you will get a fast-track result but if not, you stay at home and self-isolate until the symptoms lift. The reason testing really matters is that it is a key part of relaxing restrictions. Building a system that can turn around results, and fast, is key, according to chief medical officer Dr Tony Holohan. We need to have a contact-tracing capacity and testing capacity to give us real-time in other words same-day or following-day results, he said.

Speaking of testing, will the Leaving and Junior Certificate exams go ahead?

Last week, Taoiseach Leo Varadkar said the State exams would go ahead by hook or by crook and so they will or at least one set will. It was confirmed on Friday that the Leaving Cert would take place in late July or August. The Junior Cert, meanwhile, is set to be replaced by school-based exams which will run early in the new school year.

The changes mean tens of thousands of students who are due to progress to third level and further education are likely to commence their courses much later than originally planned. Deadlines for students to complete practicals and project work in a number of subjects such as history, geography and home economics will also be extended until late July. Students had been given a deadline of May 15th to complete this work. While the move will bring much-needed clarity to students over contingency plans for the Leaving Cert, it is likely to be a major disappointment for many students who now face an extended summer preparing for the exams.

Movement is still seriously restricted, what powers do garda have to enforce this?

At the beginning of last week, Mr Harris signed regulations granting powers of enforcement to garda. The powers were passed by the Oireachtas in late March but became active only with the Ministers signature. The regulations are based on the guidelines issued by the Government two weeks ago and anyone exercising more than 2km from their home or with people from outside their household will be in breach of the law. Anyone travelling beyond 2km for non-essential reasons will also be in breach. An offence will be committed only if a person refuses a direction from a garda to comply with the regulations. It is not the breaching of regulations that is illegal, but disobeying the gardas instructions once caught.

Will there be many arrests?

Front-line garda have been instructed to use a four-step graduated policing response in the days ahead and should give members of the public every opportunity to comply with the regulations.

Enforcement will be a last resort and only when all other avenues have been exhausted in most cases, an internal Garda document says. Before resorting to arrest, garda must go through the four-step escalation process termed Engage, Explain, Encourage, Enforce. Engage involves asking people their name and address, reason for travel and if they are aware of the restrictions. Garda may arrest anyone who refuses to give their name and address. If required they then move on to the explain stage, which involves highlighting the risks of breaking the rules. They must then encourage those in breach to stay at home to save lives. The final step, enforce, involves using Garda powers to discourage further non-compliance. This should be done only when necessary and proportionate.

How was the bank holiday weekend?

There was a very high level of compliance with restrictions on non-essential travel over the bank holiday weekend, according to Ms Canavan. A major policing operation was put in place over the Easter bank holiday with checkpoints across the country to ensure people complied with public health guidelines, over fears people would travel to holiday homes due to the fine weather.

And were there many arrests?

Garda made seven arrests over the long weekend under the new legislation. An Garda Sochna said these arrests were made when people repeatedly refused to comply with directions to abide by the movement restrictions which prohibit unnecessary travel and exercise further than 2km from the home. In addition there were 144 incidents where garda enforcing the coronavirus restrictions instead made arrests under other, long-standing legislation. These incidents included arrests for public order breaches, assault, road traffic offences and drug offences. The arrests were made at house parties and street gatherings and where garda found people engaged in non-essential travel.

If I got Covid-19 can I get it again?

No one knows for certain what level of immunity those who have had and then recovered from the illness will have. We simply dont know yet what it takes to be effectively protected from this infection, Dawn Bowdish, a professor of pathology and molecular medicine in Ontario told Scientific American this week.

What we do know is that immunity to other coronaviruses, including the common cold, can start declining within weeks of infection.

Within weeks? That doesnt sound good?

No, but studies of Sars-CoV the virus that causes Sars, which shares a lot of the same elements as Covid-19 suggest that immunity peaks at around four months and offers protection for roughly two to three years. That would give time for a vaccine to be developed without those with the Covid-19 antibodies becoming reinfected.

Are more young people dying from the illness than expected?

The early narrative was that Covid-19 was an illness that largely spared young and healthy people but as it has spread across the world, it has shown itself to be more indiscriminate than many health experts initially thought. As it stands in Ireland more than 90 per cent of the victims have been over 65. While older people and those with pre-existing conditions are most at risk, it has occasionally hit young and apparently fit people including healthcare workers exposed to those with the virus. The youngest person to die so far was aged 30, the oldest was 105 years.

Why is that?

Sometimes previously undiagnosed conditions are later revealed and sometimes there are no such explanations.

What are the scientists saying?

There have been many theories circulating in medical and scientific circles. There is a school of thought which suggests that a huge dose may hit people much harder than smaller doses while another school of thought points to genetic susceptibility with some people more vulnerable to the virus than others, irrespective of their age. It is very possible that some of us could have a particular genetic make-up that makes it more likely that we will respond badly to an infection with this coronavirus, virologist Michael Skinner at Imperial College London told the Guardian newspaper this week.

A person with a high viral load has more virus particles than one with a low load, said virologist Alison Sinclair at Sussex university. We do not yet know what impact viral load has on the symptoms of a person infected with Covid-19. Whether there is a link between a high viral load and worse outcomes is going to be important to find out.

What has been happening in nursing homes in Ireland?

The number of coronavirus infection clusters in nursing homes around the country has reached 149, according to the latest detailed figures on coronavirus cases released by State officials. Nursing homes now account for one-third of the clusters of infection across the country. This is incredibly serious not only because of the vulnerability of those in such care settings. It has become clear that Covid-19 has virus loads which are three times what might be found with other respiratory viruses such as flu, including in older patients, who are more contagious than expected.

How significant is that?

It is very significant. These are the highest viral loads for any virus I know, Prof Marc Van Ranst at the Rega Institute for Medical Research in Leuven, Belgium, said this week. He said he was astonished at the number of the germs he saw from patient throat samples in his lab. Especially surprising, he said, was that elderly people harbour prodigious quantities of virus.

Not many elderly [people] are going to transmit the influenza virus to someone else. They get infected, but are not infecting others, said Prof Van Ranst not so for Covid-19. When I look at the viral loads that we find in elderly people, it is mind boggling, he said. That has been for me the big surprise with this virus. This will influence how contagious elderly people can be and perhaps is reflected in the high number of Covid-19 clusters in nursing homes, he added.

What else have we learned in recent days?

The virus is also abundant in the throats of younger patients according to viral counts reported in the science journal Nature. Nine young to middle-aged office workers near Munich, Germany, who showed mild flu-like symptoms, had their nose and throat swabbed daily and spit samples collected for viral counts. We detected Sars-CoV-2 in enormous amounts in the upper respiratory tract, said Prof Clemens Wendtner, who led the research in Germany 1,000 times more than for Sars. This was shocking news.

All nine patients showed a high rate of viral replication and shedding in their throat during their first week of infection. The virus does not need to travel to the lungs to replicate, and is abundant in the throat, making it easy to pass on. It can be spread easily by sneezing or coughing, said Prof Wendtner.

The viral loads that people encounter when someone coughs in their general direction, are so high, said Prof Van Ranst, that it makes transmission likely to happen. Compared to other respiratory viruses, this is remarkable, he added. It also meant it was easier for those with even mild symptoms to contaminate surfaces.

The Nature paper confirms that for the milder form of the disease, it doesnt go as far as the lungs, but stays in the throat, said immunologist Prof Luke ONeill of Trinity College Dublin. It means it is very transmissible just by talking. You dont need to cough, he said. Also, people without symptoms, are very infectious, he added. Sars never infected the throat. Went straight to the lungs. So thats a big difference, he explained.

Are men more likely to die than women?

The short answer is yes. With the worldwide death toll closing in on 130,000 it has become clear that men are much more likely to die from coronavirus than women. Charity Global Health 50/50, which campaigns for gender equality in health, has been tracking the breakdown internationally for deaths from the virus. In every country that publishes the data, significantly more men than women have died.

In Italy, which has the highest number of deaths from the disease, men account for 58 per cent of all hospitalised cases and 72 per cent of all deaths. In Spain, men account for 59 per cent of all hospital admissions, 72 per cent of intensive care unit admissions and 65 per cent of all deaths. In China, where the virus first started, 64 per cent of fatalities have been men.

In the Republic men account for less than half (45 per cent) of all confirmed cases, but 71 per cent of deaths.

Why is that?

Irelands deputy chief medical officer Dr Ronan Glynn said there were a number of hypotheses as to why this phenomenon was happening. It is either biology or behaviour or a mixture of both, he said. In some countries significantly greater proportions of men smoke. The activity of smoking is often associated with touching your face. Royal College of Surgeons in Ireland professor of medicine Sam McConkey believes the reasons may be more general.

Its just speculation, but Im happy to speculate that men in general do not look after themselves, he said. We drink too much and we smoke too much and we do not go to the doctor. Women are much better at getting proper diagnosis and taking the proper tablets.

How long will the restrictions be in place?

As it stands the restrictions on movement and social and commercial life in the country will remain in place until May 5th but even then we are only likely to see a partial lifting of the strict regime and that is contingent on the rate of infections continuing to fall.

What does partial mean?

Senior Government officials have begun to work on plans for a phased exit from the lockdown with the priorities expected to include the reopening of more retail businesses, construction and maybe schools although that might only be for some classes and for a portion of the week only.

When the time comes for restrictions to be eased they will be lifted in reverse order with movement and retail looked at first.

Dr Cillian De Gascun, chairperson of the coronavirus expert advisory group, has warned against complacency about the dangers of Covid-19 because given the opportunity this virus will run rampant and he warned that we are not going to return to a normal state of affairs soon.

What else in being considered to bring the pandemic under control here?

Prof McConkey has said the Government was at a crossroads and was faced with two decisions on treating Covid-19. The first option would to continue efforts to flatten the curve over a period of six to nine months while the second choice is more severe and would see a short, sharp response to try to prevent the spread of the virus entirely in Ireland. This move would require a 32-county approach.

It would be challenging. It would mean restricting travel and quarantining people coming into the country, Prof McConkey said. I feel it has to be a national decision, we would have to get Northern Ireland to go with us on this journey. It would have to be an all-island approach. It needs national discussion and involve all the parties in Northern Ireland. This is the approach being adopted in countries such as South Korea and New Zealand.

Will the virus diminish as the summer approaches and temperatures climb?

That was a hope in the very early days of the crisis. While it is getting warmer, experts are no longer holding out much hope that better weather will kill off coronavirus. The flu virus goes into decline in warmer months, and is spread the same way as Covid-19, by way of small mucus droplets suspended in the air. When conditions are warmer, droplets are more likely to fall to the ground and not cause infection which is one reason flu is seasonal and dominant in winter. The other is because exposure to the cold during winter coincides with immune systems being stressed. There is no indication that any of this applies to Covid-19, Prof Kingston Mills from Trinity College told this publications Science Editor Kevin OSullivan. He said it may prove to be the case but caution had to be applied. He pointed out that Spain is a damn sight warmer, and look at what its going through.

Why are some people so infectious and what are superspreaders?

One of the questions scientists have been asking as the virus continues to spread is if some people are more infectious than others and the answer appears to be yes. There do seem to be superspreaders, a loosely defined term for people who infect a disproportionate number of others, whether as a consequence of genetics, social habits or simply being in the wrong place at the wrong time. There are also people who are infected but unlikely to spread the infection.

Two factors are at play, Martina Morris, emeritus professor of statistics and sociology at the University of Washington told the New York Times this week. There has to be a link between people in order to transmit an infection, she says. But, she adds, a link is necessary but not sufficient. The second factor is how infectious a person is. We almost never have independent data on those two things.

If you are the first person in a crowded room to get infected, and if this is an easily spread disease, you will look like a superspreader, she says. Anyone in that room could have had the same impact. You were just the first in line.

Dr Thomas Frieden, former director of the United States Centers for Disease Control and Prevention said superspreading events may involve people with symptoms that linger but who are not sick enough to stay at home. Or they could involve infected people who shed an unusual amount of virus.

People have been attacking 5G masts?

There was a suspected arson attack on two large telecommunications masts in Co Donegal over the bank holiday weekend. Conspiracy theorists have linked new 5G technology to the cause of the global pandemic. The Government here and governments across the EU have all stressed there is absolutely no link between 5G and Covid-19.

What is happening on the economic front?

The coronavirus pandemic has brought the global economy to its knees and is likely to result in the worst economic downturn since the Great Depression, the International Monetary Fund (IMF) has said. In its latest world economic outlook report, it said it expects the global economy to contract sharply by 3 per cent in 2020 with the euro zone, the epicentre of the pandemic for the past month, experiencing a much sharper 7.5 per cent contraction.

Its outlook for Ireland is slightly better though still grim. It expects the economy to contract by 6.8 per cent this year, less severe than the Central Bank projection for an 8 per cent contraction. The IMF expects the Irish economy to bounce back strongly next year, expanding by 6.3 per cent, against a euro-zone average of 4.7 per cent. However, unemployment could prove trickier to ease. The IMF says the jobless rate in Ireland will rise to an average of 12 per cent in 2020, up from a low of 4.8 per cent in February, and will stay elevated at almost 8 per cent in 2021.

What are the unemployment figures in Ireland?

There are 533,000 people registered for the 350 weekly Covid-19 unemployment benefit payment which was introduced in the wake of huge job losses. The take up of a temporary wage subsidy scheme for businesses was continuing to grow, and in total 199 million has been paid out under the scheme to date.

What is being done to aid European economies?

A 500 billion deal was reached between EU finance ministers last week. It has several elements. There is the employment guarantee scheme recently invented by the European Commission. If member states put up 25 per cent collateral, they can get a slice of loans raised by the commission on the market. This would be used to subsidise companies to keep employees on the books. The scheme would be worth a maximum of 100 billion.

There are also loans from the European Investment Bank to support companies: 25 billion of extra guarantees, so it can step up lending by 200 billion.

But the biggest chunk is from the EUs bailout fund, the European Stability Mechanism, which was created to dig out states during the euro zone debt crisis. States can borrow up to 2 per cent of their GDP, with a total of 240 billion available. Usually, taking loans from the ESM comes with the requirement to balance the books known as reforms by supporters, austerity by critics.

This time, borrowing will come without these strict conditions as long as the money is solely for responding to the pandemic and relates directly or indirectly to health spending.

What else is happening?

The European Commission says the new deal should be seen in the context of various other measures, particularly the decision by the European Central Bank to throw off prior restraints to print money, by buying government bonds to keep EU countries liquid. Finance ministers and the commission have also agreed to relax the usual budget rules to give states free rein to spend and support companies, and freed up existing unused funds from the EU budget to be used to respond to the crisis.

What is the Irish Government saying about the deal?

Minister for Finance Paschal Donohoe has said the Government may need limited access to the new European Union Covid-19 rescue package to help fund the wage subsidy scheme and support companies in difficulty.

Mr Donohoe has expressed confidence that the country can create a new economy and create new services to recover and move forward, but he cautioned, we have a journey ahead of us.

The new welfare supports will be monitored and may need to be strengthened to aid the recovery as at least 200,000 workers access the wage subsidy scheme. The Minister said it was possible that Ireland would need to access funds from the European Investment Bank to help fund companies and will consider whether to access the programme to help fund wage subsidy schemes. It is hoped that Ireland will not need to use the fund from the European Stability Mechanism, he added.

What are other people saying?

Alan Ahearne, the professor of economics at NUI Galway said the rescue package was a positive outcome, but warned that the figure needed was likely to increase. Prof Aherne said that as it stands Ireland will not need to borrow from the European Stability Mechanisms new low-cost loan fund, as the European Central Bank keeps borrowing costs close to zero. He said he was cautiously optimistic the recovery would be much, much quicker than a usual recession given the welfare supports that have been put in place.

Is China over the crisis now?

No one thinks the crisis is over in any country in the world. However, the country where the first cases of the virus were recorded more than 100 days ago has made substantial progress in recent days. It reported zero new coronavirus deaths on one day last week for the first time since it started publishing daily figures in January. That is a milestone that offers grounds for some relief as the country works to stave off a second wave and struggles with ongoing outbreaks in Wuhan. The National Health Commission reported 32 new cases across China on Tuesday, all of them imported infections, bringing the number of cases involving overseas travellers to 983.

Are EU countries about to ease restrictions?

Some EU countries are easing some restrictions or at least they will in the days ahead. In Denmark, there is what has been described as a cautious reopening, starting with daycare and primary schools opening. The Danish prime minister Mette Frederiksen has described the process as a bit like walking the tightrope. In Austria, small shops, hardware and gardening stores have been allowed to reopen under certain conditions with all retailers likely to follow from May 1st. Spain and Italy have also started to partially lift restrictions.

The European Commission has urged all EU states to co-ordinate as they begin to ease lockdown measures, warning that failure to do so could result in new spikes of the epidemic.

In a set of recommendations to be adopted this week, the commission said: It is time to develop a well co-ordinated EU exit strategy. The exit strategy should be co-ordinated between the member states, to avoid negative spillover effects.

And when will it all end allowing normality to be restored?

No one can answer that question with any confidence but it is unlikely that all restrictions will be lifted for several months and the aftershocks, in terms of public health, economic life and social activities will be felt for a lot longer than that.

While Mr Harris has raised the prospect of easing some restrictions, he warned: There isnt going to be a magic point at the start of May where life as we knew it before the coronavirus can resume. I think, being truthful, social distancing is going to remain a very big part of life not just in Ireland but the world over until we get to a vaccine or effective treatment for the coronavirus.

He said the key indicators to watch in the coming weeks would be the rate of growth of the virus, the average number of people in intensive care units and the reproductive rate of the virus, which measures how many people each infected person is likely to pass the virus on to.

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Coronavirus in Ireland: What we know so far - The Irish Times

Most antibiotic drugs approved in the past decade were similar to one another because they were all developed based on human intuition, according to Regina Barzilay, an Israeli researcher who, together with bioengineer James Collins, headed an MIT team that recently discovered a new, hyper-efficient antibiotic molecule using artificial intelligence.

Barzilays teams discovery, first published in the January edition of peer-reviewed scientific journal Cell, marks the first time in over three decades when a completely new antibiotic molecule was discovered. Called Halicin, the molecule was able to kill two of the most dangerous and durable bacteriasAcinetobacter baumannii and a bacteria from the enterobacteriaceae family. Unlike with other antibiotics, the bacteria failed to develop resistance to Halicin even after 30 consecutive days of treatment.

At the midst of what international health organisations have dubbed the post antibiotic era in which humanity is expected to fight bacteria that has become resilient to conventional treatment, MITs new discovery is nothing short of a revolution. Therefore, it may seem surprising that Barzilay, the leading scientist in the project is not a chemist, a biologist or a medical doctor, but is in fact a computer scientist. Her team focused its efforts on using computers to beat the limitations of human intuition and discover an entirely different drug, the type of which bacteria did not have a chance to familiarize themselves with yet.

According to Barzilay, what the team did was gather a vast range of molecules and test the effect each of them had on delaying the growth of pathogens. The methodology we developed allowed the AI to process the connection between the chemical response and the delay in activity, so that it could predict the effect of new molecules it is exposed to, she said. The system developed by her team scans through a multitude of existing research on known chemical compounds in search of molecules with a potential to function as new antibiotics.

Since 1987, every new antibiotic drug was based on already discovered families of molecular structures that have been used extensively. This becomes a problem as bacteria evolves quickly, developing ever growing resilience against these structures. Since the discovery of penicillin, the first antibiotic compound, early in the previous century, more and more bacteria and viruses have developed resilience and the result is extremely hard to fight superbugs.

The often cited 2016 ONeill report, commissioned by the British government and soon adopted by the United Nations, estimated that, barring a significant leap in addressing antimicrobial resistance, by 2050, 10 million people will die from superbugs every year, costing global economy an accumulated $100 trillion in terms of lost global production. In November, the U.S. Centers for Disease Control and Prevention (CDC) announced the the post antibiotic era has arrived.

As if this werent bad enough, in todays pharmaceutical industry, it is not financially viable to develop new antibiotics. Developing a drug, passing it through regulatory processes, and marketing it, takes an average of 10 years and $1 billion. Despite the public health benefit of introducing new drugs, hospitals and health maintenance organizations (HMOs) are wary to use new and expensive antibiotics, given the readily available cheap options and only do so as a last resort, for short periods of time. This means developing remedies for chronic medical conditions are simply more profitable and this is what both the human and fiscal capital of the industry are focused on.

To exemplify how broken the pharmaceutical market is, one needs to look no further than San Francisco-headquartered late-stage biopharmaceutical company Achaogen Inc. In April 2019, just several months after gaining regulatory approval for a new antibiotic drug it developed, Achaogen, founded in 2002, filed for bankruptcy. Instead of helping the company thrive, the approval brought Achaogens stock down and its sales amounted to a mere $1 million, negligible compared to the required investment.

Shortly thereafter, in January 2020, Melinta Therapeutics Inc. also went bankrupt, after failing to monetize on four drugs. These two boutique companies joined five big pharmaceutical companies that have shut down all of their antibiotic research between 2017 and 2018, bringing the World Health Organization (WHO) to issue a statement earlier this year warning that declining private investment and lack of innovation in the development of new antibiotics are undermining efforts to combat drug-resistant infections. The vast majority of the 60 products currently in development, WHO wrote, bring little benefit over existing treatments and very few target the most critical resistant bacteria.

Barzilays team is attempting to bridge this gap between the needs of the general population and the financial needs of commercial companies. The coronavirus crisis shows how desperately we need innovative solutions, Barzilay said. We have to be quick in developing a treatment and one way to do that is to look at existing drugs or a combination of such, she said.

The team used 2,335 different compounds to teach its AI system to make predictions. Each compound was tested on different bacteria to examine the reaction. Once it studied existing drugs, the computer went on to scan massive new databases of moleculesincluding a wide range of drugs and synthetic and natural materialsto detect any compound that could slow down the growth of Escherichia coli (E. Coli). Since only a small portion of the databases the system studied was of antibiotic compounds, the AI system did not develop any prejudice or bias as to how an antibiotic molecule looks like. All it did was scan for molecules that had non-traditional operating mechanisms that allow them to fight infections that have developed resilience to many existing drugs.

Among the molecules it scanned, the system identified 120 promising molecules. Barzilay and the rest of the team then manually filtered out any molecule that resembled existing antibiotics or was known to be poisonous, leaving them with 23 molecules to test. One of the molecules was Halicin, which stood out because its operating mechanismoverlooked by chemists up to this point targeted the bacterias metabolism.

Barzilay, 50, was born in Chisinau, Moldova and immigrated to Israel with her parents at the age of 20. She studied computer science at

Ben- Gurion University of the Negev (BGU) and moved to New York in

1998 for a PhD at Columbia University. She then moved on to a post doctoral fellowship at Cornell University, finally landing in 2003 at MIT, where she is a professor in the computer science department.

Over the years, Barzilay focused on research related to natural language processing, until, in 2016, she was offered to join a research by the chemical engineering department of the U.S. Defense Advanced Research Projects Agency (DARPA). Barzilay said she was curious to get into this field and spent the first two years learning about the most effective ways to design molecules without even thinking about the pharmaceutical industry, that was not using AI for chemical discovery.

Over the years, some pharma companies managed to harness AI tools developed at MIT for various discoveries, but this was not enough, Barzilay said. My problem was that I was not privy to the whole process, she explained. We would give them the tool, the companies would use it, but I did not know what happened with it. That is why she searched for an in-house collaboration in the university that would bring it full circle. This is how the connection with Collins, who is a pioneer in synthetic biology, was made, resulting in the discovery of Halicin.

Machine learning can completely transform the field of chemical discovery, Barzilay said. The current pandemic illustrates how crucial finding the right medicine in time is and it is hard to believe that coronavirus will be the last pandemic, so we have to create mechanisms for designing new molecules on demand, she said.

Over the past month, as almost everyone was confined to their homes and MITs facilities stood empty, Barzilay and Collins team has been hard at work to discover a cure for Covid-19. One of the reasons we were able to conduct the antibiotic experiment so easily was because we had someone in-house that could test different compounds on human cells to see which of them get infected and which do not, Barzilay said. The problem with Covid-19, she said, was that the scans could not be done at MIT as safely handling the virus required special highly secure quarantine facilities and that there wasnt enough accessible data to train the system.

In the last week, however, fragments of information were released by various sources, Barzilay said. Her team combined these fragments with what is known of the 50 drugs that are currently being tested for

Covid-19 and of SARS (Severe acute respiratory syndrome), another of Covid-19s family of viruses to surface in 2004. We developed several methodologies to combine these different groups of information and created a model that is searching for a molecule that has the potential to fight the virus, Barzilay said.

Read the original:

Hitting the Reset Button on Antibiotics - CTech

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Read this article:

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

Ann Sheehy, College of the Holy Cross

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

comments

Read the original post:

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

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

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

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

Related: 10 deadly diseases that hopped across species

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

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

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

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

Originally published on Live Science.

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See the rest here:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

With reporting by Elizabeth Pennisi.

See original here:

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

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

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

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

Original post:

The Rise of Micro and Nanoflow In Proteomics - Technology Networks

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Meanwhile, Cuomo advocates for turning our surroundings into comedy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

"I also respect people have a personal choice.

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

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

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

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

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

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

Read the original post:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Hygiene advice

Medical advice

Mask and glove usage

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Read more from the original source:

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

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

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

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

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

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

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

See the rest here:

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