You are currently browsing the tag archive for the ‘SARS-CoV-2’ tag.
SARS-COV-2 Has One Big Trick – Have We Just Discovered It?
By Shlomo Maital
According to the India Times’ Economic Times: SARS-COV-2 virus has one big trick – and it may be that scientists have just figured out what it is.
“It looks like this virus has one big trick,” said Shane Crotty, a professor in the Center for Infectious Disease and Vaccine Research at the La Jolla Institute for Immunology in California. “That big trick is to avoid the initial innate immune response for a significant period of time and, in particular, avoid an early type-1 interferon response.”
According to the India Times: The work highlights the potential for interferon-based therapies to enlarge a slowly accumulating range of Covid-19 treatments. These include Gilead Sciences’ remdesivir and convalescent plasma, a component of the blood of recovered patients that may contain beneficial immune factors. These treatments provide limited benefit and are typically used in very sick, hospitalized patients. The possibility that interferon may help some people is enticing because it appears most efficacious in the early stages of infection when life-threatening respiratory failure could still be averted. Dozens of studies of interferon treatment are now recruiting Covid-19 patients.
How did the scientists figure this out? Here is the story:
When two brothers fell critically ill with Covid-19 around the same time in March, their doctors were baffled. Both were young — 29 and 31 years old — and healthy. Yet within days they couldn’t breathe on their own and, tragically, one of them died. Two weeks later, when a second pair of Covid-stricken brothers, both in their 20s, also appeared in the Netherlands, geneticists were called in to investigate. What they uncovered was a path leading from severe cases, genetic variations and gender differences to a loss of immune function that may ultimately yield a new approach to treating thousands of coronavirus patients. The common thread in the research is the lack of a substance called interferon that helps orchestrate the body’s defence against viral pathogens and can be infused to treat conditions such as infectious hepatitis. Now, increasing evidence suggests that some Covid-19 patients get very ill because of an impaired interferon response. Landmark studies published on Thursday in the journal Science showed that insufficient interferon may lurk at a dangerous turning point in SARS-CoV-2 infections.
See also:
“Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients” Science 07 Aug 2020: Vol. 369, Issue 6504, pp. 718-724
Is COVID-19 Mutating? Yes – But Not Harmfully!
By Shlomo Maital
I’ve been worrying about whether the SARS-CoV-2 virus (the piece of RNA that gives people COVID-19) is mutating. Evolution is everywhere and inexorable, and it creates animals, insects and even viruses that are well adapted to survive and meet threats. So, I wondered, is the novel coronavirus mutating, to defeat our best efforts?
The answer is no. Here are answers from Dr. Edward Holmes, an evolutionary virologist at University of Sydney, in today’s New York Times.* I present his findings as Q&A:
- “The coronavirus is mutating, and that’s fine (so far).” NYT Sept. 14, p. 11.
Do viruses really mutate?
“Viruses routinely mutate — and most of these changes are bad for the virus or even fatal, according to some studies. (A minority of mutations are neutral, and only a tiny minority beneficial.) The word “mutation” may sound ominous, but it is a humdrum fact of viral life and its implications most often aren’t nefarious for humans.”
Has COVID-19 become more virulent, more dangerous?
“ The real question is this: Has it become more virulent or more infectious than it was when it was first detected in Wuhan, central China, in December? The evidence suggests that it has not. Like the viruses that give us influenza or measles, SARS-CoV-2 has a genetic code made up of RNA, or ribonucleic acid. But RNA is highly mutable, and since SARS-CoV-2 infects us by using our body’s cells to replicate itself again and again, every time its genome is copied, an error might creep in. Most mutations are quickly lost, either by chance or because they damage some part of the virus’s main functions. Only a small proportion end up spreading widely or lasting. Mutation may be the fuel of evolution but, especially for an RNA virus, it also is just business as usual.”
How fast is COVID-19 mutating?
“RNA viruses tend to evolve rapidly — about a million times faster than human genes. Yet if SARS-CoV-2 stands out among them, it is for evolving more slowly than many: about five times less rapidly than the influenza viruses, for example. According to Nextstrain, an open-source project that tracks the evolution of pathogens in real time, and other sources, SARS-CoV-2 is accumulating an average of about two mutations per month — which means that the forms of the virus circulating today are only about 15 mutations or so different from the first version traced to the outbreak in Wuhan. To my knowledge, there is to date no evidence that SARS-CoV-2 has become more virulent or more lethal — nor, for that matter, that it has become less so.”
Even if COVID-19 has not mutated to a more dangerous form, that kills more people – has it perhaps mutated to become more infectious – in a way Nature often does, to reproduce better? Is THIS perhaps why the coronavirus has created strong second waves in many countries?
“I do not believe that the evolution of SARS-CoV-2 is what’s driving the virus’s continued spread. The coronavirus remains good at propagating itself because most of us still are susceptible to it; we are not immune, and it can still find new hosts to infect relatively easily.”
Are you sure?
“There has been much discussion over whether the D614G mutation — which affects the so-called spike protein of the virus — has made SARS-CoV-2 more infectious. The spike protein sits on the surface of the coronavirus, and it matters because it’s the part of the virus that attaches to the host’s cells. “D614G” is shorthand for a change at position 614 of the spike protein, from an aspartic acid (D) to a glycine amino acid (G). (The technical literature refers to “D614” as the earlier configuration and “G614” as the later one.) The D614G mutation, which probably initially arose in China, first appeared to become more and more frequent in the outbreak in northern Italy in February. The G614 form of the virus has since spread all over the world and has become the dominant variant. The D614G mutation does seem to have increased the infectivity of the coronavirus — at least in cells grown in laboratories, according to a recent paper by the computational biologist Bette Korber and others published in the journal Cell.”
“Apparently based partly on this and other studies, health authorities in various countries have claimed that the G614 form of the coronavirus may be 10 times more infectious than the version first detected in Wuhan. But as some epidemiologists have warned, it is difficult, not to mention unwise, to extrapolate from lab results to explain how the virus actually spreads in a real population. In the issue of Cell …. the viral epidemiologist Nathan Grubaugh and colleagues argued that the “increase in the frequency of G614 could be explained by chance and the epidemiology of the pandemic.”
Bottom line?
“For now, though, SARS-CoV-2 essentially is the same virus that emerged in December. Sure, it has mutated, but not, so far, in ways that should change how scientists think about how to tackle it — and not in ways that should worry you.”
TIMnovate 