Two U.S. officials told NBC News that coronavirus patient information, as well as vaccine research, is sought after by hackers, including those working for China.
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— white blood cells 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.”
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.
If this is viable, this will cut the cost of healthcare dramatically, and improve billions of lives over the centuries.
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“Magufuli, who holds a doctorate in chemistry, said the testers had randomly obtained several non-human samples on animals and fruits which included a sheep, a goat and a pawpaw and the results came out positive. The samples were given human names and ages and were submitted to the country’s National Referral Laboratory to test for coronavirus without the lab technicians knowing the true identity of the samples.”
Tanzania president John Magufuli is under mounting pressure from concerns around coronavirus.
Broad-spectrum antivirals are desirable, particularly in the context of emerging zoonotic infections for which specific interventions do not yet exist. Sheahan et al. tested the potential of a ribonucleoside analog previously shown to be active against other RNA viruses such as influenza and Ebola virus to combat coronaviruses. This drug was effective in cell lines and primary human airway epithelial cultures against multiple coronaviruses including SARS-CoV-2. Mouse models of SARS and MERS demonstrated that early treatment reduced viral replication and damage to the lungs. Mechanistically, this drug is incorporated into the viral RNA, inducing mutations and eventually leading to error catastrophe in the virus. In this manner, inducing catastrophe could help avoid catastrophe by stemming the next pandemic.
Coronaviruses (CoVs) traffic frequently between species resulting in novel disease outbreaks, most recently exemplified by the newly emerged SARS-CoV-2, the causative agent of COVID-19. Here, we show that the ribonucleoside analog β-d-N4-hydroxycytidine (NHC; EIDD-1931) has broad-spectrum antiviral activity against SARS-CoV-2, MERS-CoV, SARS-CoV, and related zoonotic group 2b or 2c bat-CoVs, as well as increased potency against a CoV bearing resistance mutations to the nucleoside analog inhibitor remdesivir. In mice infected with SARS-CoV or MERS-CoV, both prophylactic and therapeutic administration of EIDD-2801, an orally bioavailable NHC prodrug (β-d-N4-hydroxycytidine-5′-isopropyl ester), improved pulmonary function and reduced virus titer and body weight loss. Decreased MERS-CoV yields in vitro and in vivo were associated with increased transition mutation frequency in viral, but not host cell RNA, supporting a mechanism of lethal mutagenesis in CoV.
Coronavirus disease 2019 (COVID-19) presents with a broad clinical spectrum, varying from asymptomatic infection to severe pneumonitis, leading to acute respiratory distress syndrome (ARDS) and death(Guan, et al 2020). Accumulating evidence suggests that in severe COVID-19, an acute hyperinflammatory syndrome characterised by fever, hypoxia and increased serum inflammatory markers, occurring 5–10 days from the first symptoms, is the major driver of morbidity and death(Zhou, et al 2020b). Hyperinflammation is not specific to COVID-19. Similar syndromes were previously described in respiratory disease associated with other coronaviruses, including the severe acute respiratory syndrome-coronavirus (SARS-CoV) in 2003 and Middle East respiratory syndrome-coronavirus (MERS-CoV) in 2012(Castilletti, et al 2005, Tseng, et al 2005).
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