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Indeed, the coronavirus pandemic has wreaked havoc on research around the globe, shuttering laboratories, aborting field projects, and costing scientists months—if not years—of work. Even as labs contemplate reopening—if and when federal and local governments ease lockdown restrictions—the challenges will be enormous. Most will have to operate with just a few individuals at a time, working in shifts. All large gatherings, including lab meetings and lectures, are likely to be prohibited. And there will be stark differences in strategy between fields—and sometimes even within the same building. At the same time, many institutions are still trying to figure out how and whether to test employees for SARS-CoV-2, the coronavirus causing the current pandemic, and what to do if infections resurge.


Institutions struggle with—and differ on—the best way to restart science.

An international research team has identified the mechanism behind one of science’s most enduring mysteries: what makes the 100-year-old tuberculosis (TB) vaccine so effective at preventing newborn deaths from diseases other than TB?

The ability of Bacillus Calmette-Guérin (BCG)—one of the oldest, safest and cheapest vaccines available—to provide protection to newborns beyond its intended purpose of fighting off TB has been known since at least the 1940s, but until now no one has been able to explain why or show how it works.

In a new study, published today in Science Translational Medicine, researchers reveal how they identified a dramatic and rapid increase in neutrophils— that patrol the body and destroy invading bacterial pathogens—in mice and babies within three days of BCG vaccination.

“Vaccines have to be given a month or two before infection to provide protection,” McLellan said in the statement. “With antibody therapies, you’re directly giving somebody the protective antibodies and so, immediately after treatment, they should be protected.”

“The antibodies could also be used to treat somebody who is already sick to lessen the severity of the disease,” McLellan added.

“There is still a lot of work to do to try to bring this into the clinic,” Xavier Saelens, a molecular virologist at Ghent University in Belgium and co-author, told the Times. “If it works, llama Winter deserves a statue.”

The U.S. Department of Defense wants to test a directed energy weapon in space, one that it hopes will someday destroy ballistic missiles moments after launch. The weapon, a so-called neutral particle beam, would be boosted into space and tested from orbit in 2023.

Neutral particle beams don’t get as much attention as lasers but are attractive in their own right. The weapons work by accelerating particles without an electric charge—particularly neutrons—to speeds close to the speed of light and directing them against a target. The neutrons knock protons out of the nuclei of other particles they encounter, generating heat on the target object.

A team of researchers from Los Alamos National Laboratory, Sheffield Teaching Hospitals NHS and the Duke Human Vaccine Institute and Department of Surgery has found 14 mutations to the SARS-CoV-2 virus, one of which they suspect might be more easily spread. In the interest of speedy dissemination of findings, the group has uploaded their paper to the bioRxiv preprint server rather than waiting for peer review at another journal.

The work involved analyzing the genomes of the virus found in 6,000 infected people from around the globe. They focused most specifically on the virus genes that are responsible for producing the “spike protein,” which is the mechanism the virus uses to attach to human cells. In so doing, they found 14 mutations, but one they named D614G (also known as G614) stood out because it was found in almost all samples outside of China. It was also particularly notable because it appeared to replace a prior mutation called D614. They also noted that in the original outbreak in China, there were only D614 mutations. It was only after the virus began appearing in Europe that the G614 mutation emerged. They suggest that the fact that the G614 virus took over from the prior mutation could mean it is more easily spread.