As much of the United States braces for its Covid-19 peak in coming weeks, state and public health officials are looking ahead to prepare the country to incrementally phase out stay-at-home orders. While some experts have projected timelines for when it's safe to reopen parts of the country, former FDA Commissioner Scott Gottlieb' recently released a report that outlines explicit criteria states should meet before they flip the switch:

Covid-19 weekly webinar: What health care leaders need to know

Gottlieb's conditions emphasize the critical roles testing and surveillance play in slowing the spread of the virusthe first step to relaxing social restrictions.

Ultimately, we think a community's ability to monitor the spread of Covid-19 boils down to their ability to answer three key questions about their population: Who is immune? Who is contagious? Where is the virus still spreading?

The narrative around a community's readiness to reopen businesses largely hinges on measuring potential immunity through the availability and efficacy of antibody testing. These tests, also known as serological tests, measure the amount of antibodies (IgG and IgM) in a person's bloodeven those considered asymptomatic. Understanding the amount of antibodies in a population clarifies the full scope of community spread and reveals the virus' true transmission and fatality rates.

However, antibody testing is no a silver bullet. Stories of "reactivated" cases are reminders of how little is known about a patient's immunity after recovering from the virus. Dawn Bowdish, a professor of pathology and molecular medicine at McMaster University in Ontario told Scientific American, "We simply don't know yet what it takes to be effectively protected from this infection."

Where is it happening already?

After a small county in Colorado failed to launch a county-wide serology testing program, large-panel studies using serological tests by the National Institutes of Health and Beaumont Health Research Institute are center stage for mass Covid-19 immunity research. Findings from Beaumont's study will be particularly valuable as it is open to all 38,000 Beaumont Health employees, making it the largest study focused on the susceptibility of health care workers and their antibody responses to Covid-19. Should results prove fruitful, communities could use a variety of tactics to open up economic activity and jobs to immune individuals, such as immunity passports being considered in other countries.

What is in the way of doing more?

The short answer here is a lack of FDA-approved antibody tests. Compared to PCR tests, developing an accurate antibody test is particularly difficult because the threat of false positive is high. If the test lacks specificity, previous exposure to other viruses within the coronavirus family, like any of the four that cause the common cold, can lead to a false positive. So far, three antibody tests have EUA approval from the FDA: Cellex and Chembio's rapid tests and Ortho Clinical Diagnostics high-throughput test. At least 70 other antibody test makers have validated and are planning to market their tests in the United States under the FDA's "Policy D" for serology tests, though these tests are not FDA-approved.

While Cellex's 15-minute, rapid test has speed on its side, it is limited to processing one specimen at a time. This won't be sufficient for widespread testing until specimens can be processed on automated, high-throughput instruments.

Another underlying challenge that requires stay-at-home orders stay in effect is the lack of visibility into infectiousness. Health officials are vying for tools that will predict where outbreaks will recur and who will need care.

To complement testing, experts argue an augmented disease surveillance system is needed to give officials a national view of where patients seek care and for what symptoms. Tracking demand for Covid-19-related care can help leaders assess the infectiousness of their regions and make informed decisions about reopening while enabling public health officials to distribute resources based on near real-time data.

Where is it happening already?

The private sector is playing a big role here. Advisory Board's Andrew Rebhan spoke with Kinsa the public health company collecting up to 162,000 daily temperature readings from their internet-connected thermometers to create the U.S. Health Weather Map, which allows consumers to understand where and when an illness is spreading. Scripps and UCSF are researching whether biometric data from wearable fitness devices could predict where health care workers are about to fall ill regionally. Genomics company, DxTerity Diagnostics, launched a subscription Covid-19 testing service for employers to safely screen for, and intercept, their pre-symptomatic employees as they return to the office.

What is in the way of doing more?

Scaling and syncing disparate surveillance methods into one system will be a technical (and unlikely) feat. Feasibility aside, the prospect of sharing personal health information with any organization will always prompt a discussion about privacy. Privacy laws are likely to preclude the U.S. from considering South Korea's surveillance strategies, regardless of their efficacy. For now, public-private partnerships are the keystone to monitoring the infectiousness of the virus and proactively managing the response.

The CDC cites "very aggressive" contact tracing of those testing positive for Covid-19, and a major scale-up of personnel to take on that work, as key competencies the country must invest in to safely reopen. Former CDC Director Tom Frieden estimates upwards of 300,000 dedicated contact tracers are needed just to match the scale of contact tracing in Wuhan, China. National contact tracing efforts require laborious interviewing and investigative work from trained public health experts, but they won't be acting alone as the technology sector joins the fight.

Where is it happening already?

Massachusetts Gov. Charlie Baker (R) formed the nation's first Contact Tracing Collaboration with global non-profit, Partners In Health, to train and deploy 1,000 public health students across the state as contact tracers.

Tech giants, Apple and Google are teaming up to create a contact-tracing tool for their billions of iPhone and Android users. The ability to wirelessly exchange anonymous information via apps run by public health authorities is expected by mid-May. Covid-19 positive users can opt to upload their test results to a public health app, which will notify other users who came into close proximity over the previous several days and encourage them to isolate themselves.

What is in the way of doing more?

The U.S. has thousands of newly idled workers who could be activated for contact tracing. Nearly 7,000 PeaceCorps volunteers returned home in mid-March and there are thousands more "furloughed public employees, phone bank staff (most tracing work is done by phone), workers from health organizations, social service and nonprofit agencies, and recent graduates," Frieden wrote in a New York Times opinion piece. Expediting training for furloughed employees could reactivate part of the unemployed workforce and supplement technology-based contact tracing efforts. However, the cost and scope of such a national recruiting effort coming together in coming weeks appears unrealistic.

Advisory Board's Jackie Kimmell and Jordan Angers also note that Apple and Google's technology solution is not without limits. The bluetooth connection that contact tracing tech relies on is notoriously inconsistent and can lead to false positives. More challenging is that the technology's use is voluntary so it is only as effective as the number of people who decide to share their testing information.

Many officials are already pointing to the next phase of the new coronavirus epidemic, but without an understanding from local government about how the virus is spreading in their communitiesand how their communities are respondingthe country could be hamstrung on figuring out that "opening date" and therefore see continued micro-surges.

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We can't reopen the country without answering these 3 questions - The Daily Briefing

Everyone wants the virus that causes COVID-19 to be a one-and-done. But reports from South Korea are raising the possibility that infections can be reactivated, or that the infected, once recovered, could be infected anew.

At least 110 people in South Korea have tested positive for the pandemic virus after having been thought cured, according to reports. The World Health Organization told Reuters on Saturday the agency is working hard to get information on the cases.

Its believed the virus may have reactivated in some people, as opposed to them being re-infected all over again, or that repeat testing may simply be picking up harmless fragments of virus genetic material that can linger for weeks or months after a person recovers.

It could also come down to nothing more than faulty testing.

There are many different hypotheses

Canadian health officials are trying to verify the information from South Korea. I think there are many different hypotheses, Dr. Theresa Tam, Canadas chief public health officer, said Monday. Tam said its important to get our international partners to expand more on what is actually happening and maybe, yes, having an international collaboration in terms of looking at what happens to someone who has initially been infected.

We actually dont know if a test positive means that there is any viable virus in that particular person. Thats one of the first questions to actually answer, Tam said.

But the mystery cases illustrate just how little is known about the virus how the human body actually mounts an immunity and what actually happens in the longer term, Tam said. That could hamper the herculean efforts being poured into developing vaccines and, in the absence of a vaccine, make natural herd immunity harder to achieve.

Reports from Seoul describe people who tested negative for COVID-19 using PCR (polymerase chain reaction) testing who, some days later, tested positive again.

According to top U.S. infectious disease expert Dr. Anthony Fauci, advisor to the U.S. presidential COVID-19 task force, how long immunity lasts remains unknown. However, in an interview with the editor of the Journal of the American Medical Association, Fauci said the virus isnt changing much, and that the working assumption, although there is not 100 per cent certainty, is that if we get infected in February or March and recover, that next September, October, the person whos infected, I believe, is going to be protected.

While most people in the medical and scientific community share that thinking, wed be foolish to think we know everything about this virus, given that we have only known about its existence for about four months, cautioned Dr. Isaac Bogoch, an infectious diseases physician and scientist with the Toronto General Hospital.

What proportion of people get immunity, to what extent do they have immunity, and how long immunity lasts are still unanswered questions, Bogoch said. When we hear about people being reinfected it obviously raises a few red flags.

Bogoch believes that the most likely explanation is that the recovered patients tested positive using PCR (polymerase chain reaction) testing, which detects viral RNA, because they still carry some residual virus in the areas being swabbed, typically the back of the nose and throat. It doesnt mean theyre contagious to others, or that the viral fragments are capable of causing disease. The test may be positive for days, even weeks after people have recovered from an infection.

Another possibility is that some people who were initially told they were positive werent positive, but then became positive. And of course, the third possibility that we really hope is unlikely is that there is either reinfection or reactivation of the virus, Bogoch said. Obviously, we hope thats an unlikely scenario. But I think it still warrants exploration.

With reactivation, the virus triggers another eruption, the way the virus that initially causes chicken pox, varicella zoster, can come back years later as shingles.

I think these are remote, but not impossible scenarios, Bogoch said. Given that the virus is so new to humans, we should at least be open-minded to other possibilities, he said.

Dr. Anand Kumar, a critical care doctor at Winnipeg Health Sciences Centre, said PCR tests have a certain sensitivity. Some viruses, like herpes, can get inside cells, go into a latent phase and then pop out again under stress. But coronavirus isnt known to be one of them.

True reinfection is possible, Kumar said. But they dont say the amount of time between the (South Koreans) being cleared and the time they became positive again.

Without seeing any kind of academic paper, the idea of people bouncing back from negative to positive would likely come down to a testing issue, added Dr. Mark Loeb, a professor of pathology and molecular medicine at McMaster University in Hamilton.

If someone has had a natural infection, its likely that they would be immune, at least in the short term, Loeb said. Its not proven, though. Were dealing with likelihoods right now. Is it likely? I think its likely. Is it certain? No.

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Can COVID-19 infect you twice? Mystery cases show how little is known about the virus - National Post

COVID-19s mortality rate has less to do with the pathology of the disease itself and more to do with common autoimmune conditions that leave patients particularly susceptible to infection.

The vast majority of deaths caused by SARS-Cov-2 have been linked to underlying illnesses like hypertension, diabetes, and cardiovascular disease. Positive cases with any one of these diseases tend to endure critical COVID-19 symptoms compared to otherwise healthy individuals.

To lighten the burden placed upon overwhelmed medical faculties experts are urging the uninfected to maintain a healthy lifestyle until COVID-19s growth curve is successfully subdued.

According to two researchers at the University of Virginia School of Medicine, those who regularly exercise decrease their odds of developing fatal reactions to SARS-Cov-2.

We cannot live in isolation forever. Regular exercise has far more health benefits than we know. The protection against this severe respiratory disease condition is just one of the many examples.

Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise

In their new paper, Dr. Zhen Yan and Hannah R.Spaulding identified an antioxidant called extracellular superoxide dismutase (EcSOD) thats naturally produced by our muscles when we commit to cardiovascular exercise.

In previously conducted studies, EcSOD seemed to improve viral clearance and enable patients to endure prolonged infection.

The longer SARS-Cov-2 replicates its genetic material inside host cells the more likely sufferers will develop acute respiratory syndrome (ARS).

The condition suppresses agents that eliminate debris inside of our lungs.

Forty percent of those that develop ARS do not survive.

EcSOD targets free radicals and protects the bodys tissue from disease and decreases oxidative stress. The antioxidant can be administered to patients who occasion aggressive manifestations of the SARS-Cov-2 pathogen, which could shorten the duration that patients are held in intensive care units as well as the number of confirmed cases that end up there in the first place.

Independent research has shown that gene therapy is a viable way to protect those with metabolic disorders and immune deficiencies.

The protective effect of endurance exercise is likely mediated by EcSOD in the cartilage tissues. In another study in mice, long-term forced treadmill running improved cartilage histology in the joint in wild type mice, the authors wrote in the new paper. The facts that EcSOD expression is promoted by endurance exercise in skeletal muscle and can be redistributed to other vital tissues to protect the target tissues against oxidative damage in various pathological processes (Fig. 2) strongly support exercise-induced EcSOD as an effective therapeutic intervention for prevention and treatment of numerous oxidative stress-related diseases.

Additionally, after administering EcSOD, mice suffering from renal failure began to endure less kidney damage over time.

We often say that exercise is medicine. EcSOD set a perfect example that we can learn from the biological process of exercise to advance medicine, Yan concluded.

Although COVID-19 seldomly results in medical intervention, fatal manifestations of the disease are almost always avoidable.

Poor diet and sedentary lifestyles are responsible for the majority of the fatal outcomes documented in the US, Italy and Wuhan, China.

Given the prevalence of diseases caused by poor lifestyle choices, The CDC reports that 20% to 40% of hospitalized COVID-19 cases will lead to ARS.

All you hear now is either social distancing or ventilator as if all we can do is either avoiding exposure or relying on a ventilator to survive if we get infected, Yan said in a press statement. The flip side of the story is that approximately 80% of confirmed COVID-19 patients have mild symptoms with no need of respiratory support.

Be sure to read the full paper published in the journal Redox Biology.

Excerpt from:

Scientists find doing this simple activity every day can help fend off dying of COVID-19 - Ladders

Darryl / stock.adobe.com

Coronaviruses, so named for their knobby surface projections that create a crown-like appearance,1-3 were first identified in the 1930s but are thought to have originated more than 10,000 years ago.4,5 They and their associated illnesses have been observed in cattle, horses, cats, dogs, swine, rabbits, rodents and bats, among others.6,7

In humans, seven coronavirus strains have been identified, as have their bat and rodent reservoirs, and their intermediate hosts, including cattle, camels and civets.8-16 Most of these strains cause nothing more than the common cold in people, but threesevere acute respiratory syndrome (SARS),17 Middle East respiratory syndrome (MERS)18 and SARS-CoV-2have proven more daunting.

As the professionals with the most thorough understanding of One Health, veterinarians around the world have been working hard on COVID-19 diagnostic, prevention and treatment measures. Heres a look at some of the work being done.

At Cornell University College of Veterinary Medicine, a group of researchers have shunted their work to focus on SARS-CoV-2. Virology professor and coronavirus expert Gary Whittaker, PhD, who has done extensive research on MERS, is investigating the SARS-CoV- 2 spike protein and its mechanisms for fusing with the host cell.19 He hopes to apply his findings to drug and vaccine development. The team also includes investigators who are working on diagnostic tests for SARS-CoV-2.

Researchers at Louisiana State University School of Veterinary Medicine are working to develop a COVID-19 vaccine, slated to begin animal trials soon. The group, which includes investigators who study bovine coronaviruses, is collaborating with researchers at Tulane University, one of the first facilities to obtain samples of SARS-CoV-2 from the Centers for Disease Control and Prevention.

The coronavirus that afflicts cats and causes deadly feline infectious peritonitis (FIP) has long been a subject of research at the University of California, Davis, School of Veterinary Medicine. Investigators at the school have used an antiviral drug shown to block virus replication in monkeys and mice as a springboard for developing a protocol to treat FIP in cats experimentally infected with feline enteric coronavirus.20

"Its the virus-infected cells that are producing all of these nasty cytokines that are causing this inflammation, explains Niels Pedersen, DVM, PhD, who has been studying feline coronavirus for the past five decades, so if you can stop the replication cold in its tracks, you're going to immediately stop the cytokines from being produced."

Treatment has been largely successful in feline studies, which gives Pedersen hope for the nearly identical remdesivir, now in clinical trials for the treatment of SARS-CoV-2. If it can be done in cats, why can't it be done in humans?" he says.

The concept of drug repurposing might also be applied to the parasiticide ivermectin, an FDA-approved anti-parasitic agent for animals and humans that, in recent years, has been shown to have antiviral activity in vitro by interfering with virus replication.21-25 In vitro studies have demonstrated that ivermectin interferes with replication of many viruses, including human immunodeficiency virus 1,22 West Nile virus,23 dengue virus,22,24 Venezuelan encephalitis virus,25 simian virus,22,26 pseudorabies27 and influenza.21

A recent study,28 published in the journal Antiviral Research, demonstrates that ivermectin impedes SARS-CoV-2 in vitro.* Previous reports on similar coronaviruses describe the role of specific proteins in viral transport into the host nucleus, suggesting that ivermectins nuclear transport inhibitory activity may be effective against SARS-CoV-2.

Cells infected with SARS-CoV-2 were treated two hours post infection with a single dose of ivermectin at serial dilutions. At 24 hours, the addition of 5 M ivermectin produced a 99.8% reduction in cell-associated viral RNA, which increased to 99.98% at 48 hours; this equated to an approximately 5,000-fold reduction of viral RNA compared with control samples. No cell toxicity was observed at this concentration.

The studys Australian investigators, from Monash University and the Peter Doherty Institute for Infection and Immunity, hypothesize that ivermectin inhibits the IMP/1-mediated nuclear import of viral proteins, but they hope to confirm this mechanism in the case of SARS-CoV-2. The identification of the specific SARS-CoV-2 and/or host component(s) impacted is an important focus their future work.

This research sets the stage for development of an effective antiviral drug that, if given to patients early in infection, could reduce SARS-CoV-2 viral load, block disease progression and limit person-to-person transmission.

The answers to the COVID-19 pandemic will be shaped like medications and vaccines. And surely, they will be colored by extensive data established by the veterinary community.

*Editors note: The FDA has issued a public warning stating that people should not self-medicate with ivermectin in an effort to treat or prevent COVID-19. The warning reads, in part: FDA is concerned about the health of consumers who may self-medicate by taking ivermectin products intended for animals, thinking they can be a substitute for ivermectin intended for humans. People should never take animal drugs, as the FDA has only evaluated their safety and effectiveness in the particular animal species for which they are labeled. These animal drugs can cause serious harm in people. People should not take any form of ivermectin unless it has been prescribed to them by a licensed health care provider and is obtained through a legitimate source. For the full FDA letter, click here.

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Veterinary medicine at the forefront in the fight against COVID-19 - dvm360

XconomyNational

If Peter Marks had a magic wand to perfect the sophisticated process that takes a new vaccine from idea to reality, the US could have a way to prevent some people from COVID-19 infection in nine months to one year.

In the real world, the journey to a vaccine OKd under emergency guidelines is more likely to take 12 to 18 months, said Marks, who runs the FDAs Center for Biologics Evaluation and Research, on a Friday teleconference hosted by the Commonwealth Fund and the Alliance for Health Policy Teleconference for Media and Policymakers.

Marks said factors that will play a role in FDAs issuance of an emergency use authorizationnot an approvalwill include the level of coronavirus circulating, how well the vaccine works, and how safe it appears. Some of the data to back up safety and efficacy claims are likely to come from less traditional sources, such as adaptive trials, or those designed to allow changes along the way in response to early results, and real-world evidence.

Facilitating the development of a vaccine for COVID-19 is an agency priority now and for the foreseeable future since the US will likely see a second wave or even third wave [of infections] if we dont get it right and get it right quickly, he said.

The agency aims to ensure vaccine makers move forward the candidates with the most potential, he said.

What that will really mean from the FDA perspective is working with the various sponsors of the vaccines to most efficiently look at their preclinical data, understand as much as we can about the characteristics of these vaccines, (and) help people develop plans that are most efficient at understanding whether their candidates will get to the level of protection that would really warrant carrying them forward, because, frankly, vaccine candidates that have very low efficacy or not tremendous efficacy, in this particular case, could just distract from capacity for more robust candidates to come forward, he said.

Marks described the careful calculus of ensuring that any vaccine distributed is safe and effective while removing roadblocks to the fastest possible authorization and distribution.

We may not have the long-term data that we normally might like, so we may be putting real-world evidence into practice in this case by vaccinating relatively larger populations of individualsit may be individuals at higher risk for things like thisthen gathering data in the real world, he said.

Choosing which candidates to advance is an especially necessary and high-stakes effort in the face of a pandemic, Marks said.

My unique perspective on this is that its time to really mobilize as best we can in our animal modeling to try and compare things, to the extent that we can, and try and sort things out before we get to humans, knowing its never perfect to make that transition There is an opportunity cost to taking any candidate forward, and so you want to take your best candidates forward because, by definition, they will occupy capacity over one another, he said.

Esther Krofah, who heads the Milken Institutes FasterCures center, said drug companies appear to be operating with a similar timeline in mind, given some recent announcements about plans to ramp up manufacturing of their vaccine candidates in the event they prove safe and efficacious.

In recent weeks Johnson & Johnson (NYSE: JNJ) announced it had selected a lead vaccine candidate to advance against the novel coronavirus, and committed to boosting its manufacturing capacity to be able to make more than one billion doses of such a vaccine. The company anticipates human tests of its candidate to start at the latest by September, and said it expects batches could be ready for use under emergency guidelines in early 2021.

Thats a substantially accelerated timeframe in comparison to the typical vaccine development process, the company noted. Krofah says Milken is tracking 86 active vaccine projects, including six clinical trials; two dozen more are slated to enter the clinic in summer or early fall.

LJ Tan, chief strategy officer at the Immunization Action Coalition, emphasized the speed at which COVID-19 vaccine development is occurring compared to typical timelines for new vaccine innovation.

Tan previously spent about 16 years in leadership roles at the American Medical Association, most recently as director of medicine and public health and as director of infectious disease, immunology, and molecular medicine for more than a decade.

Traditional vaccine development, through all its phases, can take 10, 15, sometimes 20 years, and can cost at least $800 million dollars or even more, Tan said. When you build in all the costs to build the manufacturing facility, the equipment, the quality control that goes into this, the figure can go way over $1 billion to bring a vaccine from development all the way through to market.

Moderna (NASDAQ: MRNA), whose vaccine candidate was the first to start human testing in the US, said Thursday that it anticipated the start of a Phase 2 study this quarter, if safety data from the National Institutes of Health-led Phase 1 trial supports continuation. The Cambridge, MA-based biotech also announced that the US Biomedical Advanced Research and Development Authority (BARDA) had agreed to award it up to $483 million to fund the vaccines development through FDA review and ramp up its manufacturing to allow it to be produced at scale this year.

The company said it plans to add as many as 150 new employees by 2021.

Some vaccine candidates are being advanced in multiple geographies. This week Inovio Pharmaceuticals (NASDAQ: INO) announced a $6.9 million award from the Coalition for Epidemic Preparedness to move its vaccine into a Phase 1/2 trial in South Korea. Working with International Vaccine Institute and the Korea National Institute of Health, the trial will parallel Inovios ongoing Phase 1 in the US, which started April 6.

Remember, ultimately, were not talking about just vaccinating a few hundred thousand individuals, were taking about vaccinating a few hundred million people in this country alone and a few billion people globally, so one really would like to try to get it right to the extent they can, obviously working at a very rapid pace, Marks said.

Image: iStock/Nastco

Sarah de Crescenzo is an Xconomy editor based in San Diego. You can reach her at sdecrescenzo@xconomy.com.

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COVID-19 Vax Efforts Aim to Balance Speed, Efficacy in Race to Market - Xconomy

A woman hangs face masks out to dry before distributing them for free in a neighborhood in Tangerang, on the outskirts of Jakarta, on 9 April.

By Dyna Rochmyaningsih Apr. 18, 2020 , 3:35 PM

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

Scientists in Indonesia are exasperated at the countrys response to the COVID-19 pandemic, calling it shambolic and secretive, with a lack of coordination between the national and provincial governments. They also complain that officials have sometimes snubbed their efforts to help.

We have missed many opportunities in the past. What we need now is strong leadership to tackle the pandemic, says Nurul Nadia, a public health expert at the Center for Indonesias Strategic Development Initiatives. She and others say the country needs a clear national strategy for lockdowns and a dramatic increase in testing capacity if it is to control whatat least by official numbersis a comparatively small outbreak.

As of 18 April, Indonesia had 6248 confirmed COVID-19 cases, including 535 deaths. Nearly half of the known burden is in the capital, Jakarta, but all 34 provinces now report cases.

Epidemiologists say the number of actual cases is much higher. According to an estimate by Timothy Russel and colleagues at the London School of Hygiene & Tropical Medicine, published last month, only 5.4% of all symptomatic cases are reported in Indonesia, which means the country likely has well over 100,000 cases by now. One sign that COVID-19 is widespread is that mortality is spiking: Reuters reported last week that Jakarta had 4400 funerals in March, 40% more than in any other month since January 2018.

Thousands of migrant workers left Jakarta and returned to their hometowns in March, when the disease began to surge in the city, potentially spreading the virus around the country. Scientists have warned about another exodus just before 23 May, when Muslims celebrate Eid al-Fitr, a holiday marking the end of the Ramadan. A survey by the Indonesian Institute of Sciences (LIPI), in collaboration with academic researchers, found that 68% of respondents on Java hope to visit family then, some of them on other islands. There will be a surge of positive cases and deaths if we dont limit mobility soon, says Henry Surendra, an epidemiologist at the Eijkman-Oxford Clinical Research Unit in Jakarta. I am afraid that many areas will end up like Jakarta, Nadia says.

The Indonesian government, worried about paralyzing the economy, has long downplayed the danger of the pandemic. In early March, Achmad Yurianto, the director-general for disease control at Indonesias Ministry of Health, told Science he doesnt care what scientists say about the pandemic because they are not important if their information only creates panic. Health minister Terawan Agus Putranto suggested in February that prayer helped keep COVID-19 out of the country.

The Ministry of Health has authorized large-scale social restrictions or partial lockdowns for cities and provinces, providing they can show an escalating number of deaths and extensive local transmission. They must also demonstrate that theyre able to meet residents basic needs during the lockdown. But Nadia says many governors lack the epidemiological support to do such analyses. Should we wait for widespread infection and seeing people die first? she asks. If so, the concept of prevention wont work. So far, the health ministry has approved lockdown proposals from 10 cities, but compliance is low.

Meanwhile, testinga huge challenge in a country of more than 267 million, scattered over some 6000 islandshas been lagging. So far Indonesia has tested fewer than 40,000 people. Wide-scale testing may come too late for cities with a major outbreak, but if combined with isolation of patients and quarantining of their contacts, it could still help contain the virus in places where it has just arrived, says Panji Hadisoemarto, an epidemiologist at the University of Padjajaran in Bandung, West Java. Better late than never.

The government has assigned 132 referral hospitals around the country to take nose and throat swabs from suspected cases. But many lack the protective equipment to take samples safely. As a result, patients must sometimes be driven to hospitals many hours away. And the hospitals dont run the tests themselves; the samples are sent to one of 32 designated test labs, causing further delays.

Seeking to increase testing capacity, the Indonesian Biomedical Association (PBMI) has identified 106 laboratories in 25 provinces that meet the World Health Organizations technical requirements to test for COVID-19. Their findings, presented in early April, were quickly welcomed by Indonesias national COVID-19 Task Force, says Fenny Dwivanny, a molecular biologist at the Bandung Institute of Technology. That same day, health minister Terawan Agus Putranto issued a letter allowing qualified labs to do the tests.

There will be a surge of positive cases and deaths if we dont limit mobility soon.

But on 15 April, Yurianto told the press that the health ministry will authorize only 78 labs to scale up testing. We are dealing with a very deadly virus. We cant just do the PCR tests in any lab, he says.

Labs, even in the capital, also face a shortage of swabs, reagents, and protective gear, says Ahmad Utomo, a molecular biologist and senior advisor at PBMI. Utomo is encouraged, however, that the Ministry of State-Owned Enterprises is installing 18 PCR machines and 2 RNA extractorsrobots that can isolate viral RNA faster and more safely than humans canin hospitals run by the ministry in 12 provinces. (The ministry did not respond to a query from Science about details of its testing plans.

The Indonesian Young Scientists Forum (YSF) has also urged the health ministry to involve Indonesian scientists in sequencing the genomes of SARS-CoV-2 isolates from the country. So far, health ministry researchers have submitted only four partial sequences from Indonesia submitted to GISAID, the online database where scientists from around the world deposit their sequences. YSF scientists met officials at the ministry on 17 April to discuss collaboration, but no definitive decisions were taken, says Berry Juliandi, a biologist at Bogor Agricultural University and YSF spokesperson.

Despite their frustration, many scientists are eager to work with the government, says Utomo. Just show us the way and have a friendly attitude, he says. Open the doors for us.

Read the rest here:

'Open the doors for us.' Indonesian scientists say government snubs offers to help fight coronavirus - Science Magazine

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