• All Disease Models Are “Wrong,” but Scientists Are Working to Fix That

    An international team of researchers has developed a new mathematical tool that could help scientists to deliver more accurate predictions of how diseases, including COVID-19, spread through towns and cities around the world. Rebecca Morrison, an assistant professor of computer science at CU Boulder, led the research. CU says that for years, she has run a repair shop of sorts for mathematical models—those strings of equations and assumptions that scientists use to better understand the world around them, from the trajectory of climate change to how chemicals burn up in an explosion.  As Morrison put it, “My work starts when models start to fail.”

  • U.S. Allows Use of Remdesivir, 1st Drug Shown to Help Virus Recovery

    U.S. regulators on Friday allowed emergency use of remdesivir, the first drug that appears to help some COVID-19 patients recover faster, a milestone in the global search for effective therapies against the coronavirus. Matthew Perrone and Marilynn Marchione write for AP that the Food and Drug Administration cleared Gilead Science’s intravenous drug for hospitalized patients with “severe disease,” such as those experiencing breathing problems requiring supplemental oxygen or ventilators. The FDA acted after preliminary results from a government-sponsored study showed that the drug, remdesivir, shortened the time to recovery by 31%, or about four days on average, for hospitalized COVID-19 patients. Those given the drug were able to leave the hospital in 11 days on average vs. 15 days for the comparison group. The drug may also help avert deaths, but that effect is not yet large enough for scientists to know for sure. The National Institutes of Health’s Dr. Anthony Fauci said Wednesday the drug would become a new standard of care for severely ill COVID-19 patients. Remdesivir, which blocks an enzyme the virus uses to copy its genetic material, has not been tested on people with milder illness. The FDA previously allowed narrow use of a malaria drug, hydroxychloroquine, for hospitalized patients who were unable to take part in ongoing studies of the medication. President Trump touted the drug as a “game changer” and repeatedly promoted it as a possible COVID-19 treatment, but no large high-quality studies have shown the drug works for that and it has significant safety concerns.

  • Hydroxychloroquine for Treatment of COVID-19 Linked to Increased Risk of Cardiac Arrhythmias

    In a brief report published today in JAMA Cardiology, a team of pharmacists and clinicians at Beth Israel Deaconess Medical Center (BIDMC) found evidence suggesting that patients who received hydroxychloroquine for COVID-19 were at increased risk of electrical changes to the heart and cardiac arrhythmias. The combination of hydroxychloroquine with azithromycin was linked to even greater changes compared to hydroxychloroquine alone. Hydroxychloroquine and azithromycin each can cause an electrical disturbance in the heart known as a QTc prolongation, indicated by a longer space between specific peaks on an electrocardiogram. QTc prolongation denotes that the heart muscle is taking milliseconds longer than normal to recharge between beats. The researchers note that the delay can cause cardiac arrhythmias, which in turn increases the likelihood of cardiac arrest, stroke, or death. “While hydroxychloroquine and azithromycin are generally well-tolerated medications, increased usage in the context of COVID-19 will likely increase the frequency of adverse drug events (ADEs),” said co-first author Nicholas J. Mercuro, PharmD, a pharmacy specialist in infectious diseases at BIDMC. Senior author Howard S. Gold, MD, an infectious disease specialist at BIDMC and an assistant professor of medicine at Harvard Medical School, said: “Based on our current knowledge, hydroxychloroquine for the treatment of COVID-19 should probably be limited to clinical trials.”

  • Epidemic Dictates an Open Exchange of Modeling Knowledge

    It has become increasingly clear that, depending on the computer model used, either we could still be in the midst of the pandemic with rising numbers of cases and deaths or we could be nearing the time to reintroduce society to normal operations. Why such disparity? Because each model works a bit differently and depending on the model used and assumptions added in, the results will change, sometimes dramatically.

  • COVID-19 Treatments: Pandemic Urgency No Excuse for Ignoring Rigorous Clinical Research

    Leading biomedical ethicists are calling on the global research community to resist treating the urgency of the current COVID-19 outbreak as grounds for making exceptions to rigorous research standards in pursuit of treatments and vaccines. Crises are no excuse for lowering scientific standards, the authors of a paper, titled “Against Pandemic Research Exceptionalism,” argue.

  • Study Calls into Question Use of Malaria Drug for COVID-19

    A retrospective study of patients with COVID-19 found no evidence that the anti-malaria drug hydroxychloroquine, either with or without the antibiotic azithromycin, reduced mortality or the need for mechanical ventilation. Researchers also found that hydroxychloroquine alone was associated with increased mortality. Early excitement about the combination was based on a small French study, and President Donald Trump soon began touting the combination as a potential “game changer,” but the findings from the study, which is the largest to date to report on outcomes from treating COVID-19 patients with the anti-malaria drug and uses a database that has been used for many different studies, suggest that the hydroxychloroquine/azithromycin combination may not be as promising for treating COVID-19 as some have hoped. 

  • The Problem of Modeling

    The lessons starting to emerge from the coronavirus crisis are predominantly not epidemiological but highly general aspects of public policy, Paul Collier writes: the over-reliance on expert modelling and the mismanagement of public services. “The current epidemic is a classic application of what economists call ‘radical uncertainty’: in a world that has inevitably become too complex to be adequately captured in models, a world of both ‘known unknowns’ and ‘unknown unknowns,’ the most sensible response to the question ‘what should we do?’ is ‘I don’t know’,” he argues.

  • How to Build and Deploy Testing Systems at Unprecedented Scale

    Without a vaccine or therapeutic drugs, neither of which is guaranteed, countries thus face a future of bouncing in and out of lockdown every few months, with infection rates ebbing and flowing in response. “The result will be mounting death tolls, depressed economies and confidence-sapping uncertainty. This can, however, be partly ameliorated by extensive testing for the virus. Testing enables the government to keep tabs on the disease, reveals which social-distancing measures work, and, if those testing positive remain at home, instils confidence in the public that it is safe to go out,” the Economist argues.

  • Coronavirus Pandemic Is Paving the Way for an Increase in Superbugs

    The heroic efforts of researchers and healthcare professionals globally will eventually help us gain control of the coronavirus pandemic and there will be a decrease in the rate of new infections. The focus is still rightly on the damage this pandemic is causing, the devastating loss of life and the impact on businesses and livelihoods. But we also need to look at other prevalent crises that are affecting our healthcare systems and anticipate the impact that the COVID-19 pandemic will have on them. One of the greatest threats to healthcare systems, around the world, is antibiotic resistance. The lack of effective antibiotics and the emergence of bacteria that are resistant to the drugs we have has resulted in the antibiotic resistance crisis.

  • Coronavirus: Could the Pandemic Be Controlled Using Existing Vaccines Like MMR or BCG?

    The race is on to develop a vaccine that can protect us from the COVID-19 pandemic. An impressive 115 vaccine candidates are currently being investigated, but it is still many months before a vaccine might be approved. Sarah L Caddy writes in The Conversation that we already have hundreds of licensed vaccines for over 25 different viruses and bacteria that infect humans. We can protect ourselves against infections ranging from cholera to rabies. The common aim of all vaccines is to induce an immune response that prevents future disease. Is it possible that one of these existing vaccines could also induce protection against SARS-CoV-2, the virus causing COVID-19? Repurposing drugs is a popular strategy for treating COVID-19, as exemplified by the many trials using the Ebola drug remdesivir, or the antimalarial drug hydroxychloroquine. If an already-approved vaccine could reduce the severity of COVID-19, this would be really good news. The BCG vaccine has received recent attention for being a widely used vaccine that may help control COVID-19. A handful of studies identified an interesting association between the severity of COVID-19 in a country and how many of the population were vaccinated with BCG. The BCG vaccine apparently reduces the damage caused by COVID-19.

  • The Next Pandemic Might Not Be Natural

    Germs have killed more people than all the wars in history, and people have been trying to make use of them throughout all those wars. In the U.S., we have seen small-scale bioterrorist attacks – the Rajneeshee poisoning of restaurants in 1986 and the Amerithrax letters that were mailed in 2001. Still, the years running up to this current coronavirus pandemic not only saw the gutting of U.S. national health institutions but also a cultural groundswell of science denial in the anti-vaccination movement. Today the United States in particular is paying for that denial in livelihoods and lives. The warnings were clear. If 9/11 was a “failure of imagination,” then history will no doubt judge the Trump administration’s response to COVID-19 as a failure of courage, compassion, and, most of all, competence.

  • Abbott Launches COVID-19 Antibody Test

    Abbott has launched its third test for coronavirus (COVID-19) and will start shipping it in the U.S. The test is a serology test – also called an antibody test – which could be a critical next step in battling this virus. Abbott says its test helps to detect the IgG antibody to SARS-CoV-2. An antibody is a protein that the body produces in the late stages of infection and may remain for up to months and possibly years after a person has recovered. Detecting these IgG antibodies will help determine if a person was previously infected with the virus that causes COVID-19. The new antibody test is to be used on Abbott’s ARCHITECT i1000SR and i2000SR laboratory instruments, which can run up to 100-200 tests an hour.

  • Super-Charging Drug Development for COVID-19

    Researchers are ramping up production of a promising drug that has proven effective in obliterating SARS-CoV in cellular cultures. The team hopes that the drug might also be effective in the fight against SARS’s close genetic cousin, the novel coronavirus (COVID-19). Northwestern University says that the team, led by Northwestern University and ShanghaiTech University, has produced the promising molecule, called valinomycin, in a cell-free system. With this approach, they increased production yields more than 5,000 times in just a few rapid design cycles, achieving higher concentrations of the molecule than achieved previously in cells.The research was published online recently in the journal Metabolic Engineering and will appear in the July 2020 print issue. 

  • Model Quantifies the Impact of Quarantine Measures on COVID-19’s Spread

    Every day for the past few weeks, charts and graphs plotting the projected apex of Covid-19 infections have been splashed across newspapers and cable news. Many of these models have been built using data from studies on previous outbreaks like SARS or MERS. Now, a team of engineers at MIT has developed a model that uses data from the Covid-19 pandemic in conjunction with a neural network to determine the efficacy of quarantine measures and better predict the spread of the virus. Mary Beth Gallagher writes in MIT News that Most models used to predict the spread of a disease follow what is known as the SEIR model, which groups people into “susceptible,” “exposed,” “infected,” and “recovered.” Dandekar and Barbastathis enhanced the SEIR model by training a neural network to capture the number of infected individuals who are under quarantine, and therefore no longer spreading the infection to others. Raj Dandekar, a Ph.D. candidate studying civil and environmental engineering, and George Barbastathis, professor of mechanical engineering, enhanced the SEIR model by training a neural network to capture the number of infected individuals who are under quarantine, and therefore no longer spreading the infection to others.

  • Virology Lab Finds Drug Originally Meant for Ebola is Effective against a Key Enzyme of Coronavirus That Causes COVID-19

    Scientists at the University of Alberta have shown that the drug remdesivir is highly effective in stopping the replication mechanism of the coronavirus that causes COVID-19, according to new research published today in the Journal of Biological Chemistry. The paper, Folio reports, follows closely on research published by the same lab in late February that demonstrated how the drug worked against the Middle East Respiratory Syndrome (MERS) virus, a related coronavirus. The paper demonstrates how remdesivir, developed in 2014 to fight the Ebola epidemic, works in detail. He likens the polymerase to the engine of the virus, responsible for synthesizing the virus’ genome.