By Nancy Lapid

(Reuters) – The following is a roundup of some of the latest scientific studies on the novel coronavirus and efforts to find treatments and vaccines for COVID-19, the illness caused by the virus.

Physical inactivity tied to higher COVID-19 risks

Patients with COVID-19 who have been consistently physically inactive have a significantly higher risk of severe outcomes than patients who were getting at least some exercise or regularly met physical activity guidelines prior to the illness, researchers found. Among the 48,440 patients in their study, 14.4% were consistently inactive in the two years before their COVID-19 diagnosis, 79.1% had some activity, and 6.4% consistently met recommended physical activity guidelines of at least 150 minutes per week. Compared with those who consistently met activity guidelines, people who were consistently inactive were more than twice as likely to be hospitalized and to die from the virus, according to a report in the British Journal of Sports Medicine. Consistently inactive patients also had worse outcomes than patients who got some exercise without meeting the guideline-recommended minimum. “It is well known that immune function improves with regular physical activity, and those who are regularly active have a lower incidence, intensity of symptoms and death from viral infections,” said coauthor Dr. Robert Sallis of the Kaiser Permanente Fontana Medical Center in California. “Regular physical activity is associated with improvements in lung capacity and cardiovascular and muscular functioning that may serve to lessen the negative impacts of COVID-19 if it is contracted,” he added.

New trial attempts to re-infect COVID-19 survivors

British scientists on Monday launched a trial that will deliberately re-expose COVID-19 survivors to the coronavirus to examine their immune responses and see if they become re-infected. The information from the so-called challenge trial “will allow us to design better vaccines and treatments, and also to understand if people are protected after having COVID, and for how long,” said study leader Helen McShane of the University of Oxford. The first stage of the trial will seek to establish the lowest dose of the coronavirus needed in order for it to start replicating in about 50% of the volunteers, while producing few to no symptoms. A second phase will infect different volunteers with that standard dose. Everyone will quarantine for at least 17 days, and anyone who develops symptoms will receive a monoclonal antibody treatment manufactured by Regeneron Pharmaceuticals Inc. Researchers leading a separate UK study are administering the virus to volunteers who were not previously infected. “These challenge studies… will significantly improve our understanding of the dynamics of virus infection and of the immune response, as well as provide valuable information to help with the on-going design of vaccines and the development of anti-viral therapies,” Lawrence Young, a virologist at Warwick Medical School in the UK, said in a statement.

Low interferon levels drive weak response to the virus

People who become critically ill with COVID-19 appear to have lower-than-average levels of inflammatory proteins called interferons, and a new study helps explain why low interferon levels would matter. Researchers identified 65 genes that are triggered into action by interferons – including some that inhibit the ability of the virus to enter cells and others that suppress manufacture of the virus’ genetic material or inhibit its ability to assemble itself – part of the virus replication process. Eight of the “interferon-stimulated genes” act not only against the SARS-CoV-2 virus that causes COVID-19 but also against the SARS-CoV-1 virus that caused the 2003 SARS outbreak, the researchers reported in Molecular Cell. “The interferon response to SARS-CoV-2 infection relies on a limited subset of … genes that govern a diverse set of cellular functions,” the researchers said. “We wanted to gain a better understanding of the cellular response to SARS-CoV-2, including what drives a strong or weak response to infection,” coauthor Sumit Chanda of Sanford Burnham Prebys in La Jolla, California said in a statement. “We’ve gained new insights into how the virus exploits the human cells it invades, but we are still searching for its Achilles heel.”

(Reporting by Nancy Lapid, Lisa Rapaport and Alistair Smout; Editing by Bill Berkrot)