MilliporeSigma and The Jenner Institute report that the Institute has begun preparations for the large-scale production of its COVID-19 vaccine candidate, ChAdOx1 nCoV-19. With patients enrolled for clinical trials for this vaccine, rapid development of the large-scale manufacturing process is a critical step in quickly and safely delivering it from the lab to patients, according to Udit Batra, CEO, MilliporeSigma.

“We have brought the future of vaccine manufacturing to the present,” said Batra. “This is an important step in treating COVID-19 and other diseases that impact global public health. This work marks a milestone in the vaccine manufacturing development journey, as clinical testing continues to advance.”

Tapping into MilliporeSigma’s previous work provided a head start for plans to scale up the manufacture of Jenner’s COVID-19 vaccine candidate, added Batra. Developing the manufacturing process itself would normally take at least six months to a year, but in just two months’ time, MilliporeSigma supported the Jenner team and their collaborators to evaluate the existing manufacturing platform for use with the new vaccine candidate, and improved critical process steps, he continued.

This is very surreal. A study was done to assess the safety of common drugs, and COVID, and whether taking them leads to severe symptoms. There has been concern as these drugs increase ACE2 receptors coronavirus binds to. So someone had the bright idea of going through over 12,000 digital patients records to come up with the conclusion the drugs are safe to take and they do not cause worse symptoms. No animal studies, no clinical trials, and this was actually published.

“For the study, the researchers identified patients in the NYU Langone Health electronic health record with COVID-19 test results. For each identified patient with COVID-19 test results, the team discretely extracted medical history needed for the analysis, which compared treated and untreated patients.”

First you do a mouse study at least to review how coronavirus behaves in mice who are given the drugs, and compare it to mice not given the drugs. If science has been reduced to just going over records and coming to a conclusion, with no experimentation I have officially lost my mind.

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Despite concerns expressed by some experts, common high blood pressure drugs did not increase the risk of contracting COVID-19 — or of developing severe disease — in a study of 12,594 patients.

Published online May 1 in the New England Journal of Medicine, the study was launched in response to a March 17 joint statement issued by the American Heart Association, the American College of Cardiology, and the Heart Failure Society of America. It urgently called for research to answer a question raised by past studies: do high blood pressure (antihypertensive) drugs worsen COVID-19 patient outcomes?

Led by researchers from NYU Grossman School of Medicine, the study found no links between treatment with four drug classes — angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, or calcium channel blockers — and increased likelihood of a positive test for COVID-19.

The Max Delbrück Center for Molecular Medicine is devoted to biomedical research with the aim of understanding the molecular basis of health and disease and translating findings as quickly as possible into clinical applications. Better prevention, diagnosis and treatment of diseases are the ultimate goals.

Cytokine storms may affect the severity of COVID-19 cases by lowering T cell counts, according to a new study published in Frontiers in Immunology. Researchers studying coronavirus cases in China found that sick patients had a significantly low number of T cells, a type of white blood cell that plays a crucial role in immune response, and that T cell counts were negatively correlated with case severity.

Interestingly, they also found a high concentration of cytokines, a protein that normally helps fight off infection. Too many cytokines can trigger an excessive inflammatory response known as a cytokine storm, which causes the proteins to attack healthy cells. The study suggests that coronavirus does not attack T cells directly, but rather triggers the cytokine release, which then drives the depletion and exhaustion of T cells.

The findings offer clues on how to target treatment for COVID-19, which has become a worldwide pandemic and a widespread threat to human health in the past few months. “We should pay more attention to T cell counts and their function, rather than respiratory function of patients,” says author Dr. Yongwen Chen of Third Military Medical University in China, adding that “more urgent, early intervention may be required in patients with low T lymphocyte counts.”

“just last year, the National Institute for Allergy and Infectious Diseases, the organization led by Dr. Fauci, funded scientists at the Wuhan Institute of Virology and other institutions for work on gain-of-function research on bat coronaviruses.

In 2019, with the backing of NIAID, the National Institutes of Health committed $3.7 million over six years for research that included some gain-of-function work. The program followed another $3.7 million, 5-year project for collecting and studying bat coronaviruses, which ended in 2019, bringing the total to $7.4 million.”

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Biomedical research ultimately helps protect public health, Fauci argued. The Wuhan lab that received U.S. taxpayer money is suspected of playing a role in starting the Covid-19 pandemic.

With the curve finally flattening in the US, the ramping up of anti-viral and vaccine trials against SARS-CoV-2—the virus that causes Covid-19—and the launch of antibody tests to screen for previous infection, it seems like science is rapidly moving towards the end game. How exactly the Covid-19 pandemic will finally bugger off into history is still anyone’s guess, but virologists and public health experts generally agree that immunity is key—either through widespread safe and effective vaccination, or when enough of our population has recovered from infections and gained herd immunity.

Well. That’s the hand-waving, shruggie emoji, “eh who knows” short answer.

Like most processes in biology, immunity to SARS-CoV-2 is complex and mysterious, with results that could rapidly diverge into many possible futures. It’s partly why estimates of how long Covid-19 sticks around to wreak havoc can vary enormously, from months to years to…well, seasonal and forever, similar to the flu.

Dr. Jason Williams discusses his decision to administer follistatin gene therapy, a myostatin inhibitor, to himself in 2015.

Visit Integrated Health Systems to learn more about follistatin gene therapy.

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