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A frightening new strain of coronavirus, innocently named B.1.1.7, recently exploded in the south-east of England, prompting the government to tighten lockdowns in the region. While we don’t know all the details, experts are increasingly convinced that it is spread more easily than other strains. Here’s everything we know so far about this new strain.
What is that?
SARS-CoV-2 strain B.1.1.7 is a version of the virus with 23 mutations, eight of which are in the spike protein that the virus uses to bind to and enter human cells, Science Magazine reported.
Where is he from?
It was first detected on September 21 in Kent County in England, then took off and spread in November, according to the World Health Organization.
Since then, it has become the most common variant in England, accounting for more than 50% of new cases diagnosed between October and December 13 in the UK, according to the WHO.
However, some scientists now believe that the virus may have mutated in an immunocompromised person, according to Science Magazine. This is because unlike the flu, the new coronavirus can correct errors when it replicates and therefore tends to have a fairly stable genome, Live Science previously reported. However, studies have shown that people with weakened immune systems – because they take immunosuppressive drugs or are treated with chemotherapy, for example – can harbor an infectious virus for months. This, in turn, would give the virus a lot of chances to acquire mutations that would help it to replicate or escape the virus. immune system.
What do these mutations do?
We don’t know for sure. Viruses are constantly mutating, and most of these changes do not affect the degree of death or infection of the virus. In this case, some of these mutations may have occurred purely by chance and may not affect the function of the virus.
But three changes in particular worried the experts.
One, a two-amino acid deletion known as 69-70Delta, was first detected separately in a patient treated with immunosuppressants who developed COVID-19. The patient received remdesevir, convalescent plasma and neutralizing antibodies, but died months later. Although the virus did not initially have this deletion, it acquired it over months, the researchers reported in a preprinted article published on Dec. 19 in the withRiv database. (It has not been peer reviewed.) The authors suspect that it evolved to evade the immune system. Another wrinkle associated with this deletion is that it can make one of the targets of the SARS-CoV-2 PCR tests – known as the S gene – falsely negative. Some tests only look for positives in this S gene and therefore would miss the new variant. However, most PCR tests look for three distinct regions of the spike protein, so those tests won’t be affected, the WHO said.
Another mutation, known as N501Y, alters the key amino acids that make up the so-called SARS-CoV-2 receptor binding domain, where the amino acid asparagine (N) has been replaced by tyrosine (Y) in the part of the virus that attaches to the ACE2 receptor on human cells, according to the Centers for Disease Control and Prevention. A September study in the journal Cell found that this variant binds more tightly to the ACE2 receptor than other versions of the coronavirus – at least in a lab box.
Dozens of SARS-CoV-2 samples from South Africa and Australia have tested positive for this mutation, but lab tests suggest that the South African and British variants separately developed the same mutation. This suggests that it could provide an evolutionary advantage to the virus.
The third suspect mutation is P681H, which is also in the receptor binding domain of the virus. According to preliminary information published by the COVID-19 Genomics Consortium UK, this mutation is found next to the “furin cleavage site”, where the spike protein must be cleaved for the virus to enter cells, according to Science Magazine.
Does it spread more easily?
Yes. Experts now believe the new variant is between 50% and 74% more transmissible than other dominant strains, according to a study by the Center for Mathematical Modeling and Infectious Diseases (CMMID) which has not yet been peer reviewed. The WHO estimates that this would reduce 0.4 to the base reproduction number R, which dictates how many people each infected person would spread the virus to.
Based on the models of this growth, the new variant could be responsible for 90% of all new cases of COVID-19 in London and the east and south of England by mid-January, according to this study.
Is it more deadly?
We don’t know, but experts suspect that’s not the case. However, if it spreads much more easily, it means more people will be hospitalized. Once hospitals are overwhelmed, the quality of care for the sickest patients declines, which can lead to higher death rates than one would expect otherwise.
The CMMID study found that the new variant could explain an increase in hospitalizations in the south-east of England, largely due to increased spread, not necessarily because the virus is more dangerous.
Another study, also unpaired by CMMID, used a mathematical model to see whether the rapid growth of the virus in London was due to increased infectivity or its more severe nature. The latter did not match the data well, while the former did not match well.
Has the variant spread to the United States?
So far, scientists have not detected this strain anywhere in the United States, although America has not done as much genetic sequencing on viral samples as the United Kingdom. For example, by December, the United States had sequenced 51,000 viral samples from 17 million identified cases of SARS-CoV-2, According to the CDC. The UK has sequenced more than twice as many viral samples as the US, despite just over a tenth of diagnosed cases.
Dr. Stanley Perlman, immunologist and pediatric infectious disease specialist at the University of Iowa told the Center for Infectious Disease Research and Policy (CIDRAP) that he suspects the variant is already in the US. “I’d be surprised if that wasn’t the case,” he said.
Can children catch it more easily?
Several pieces of evidence in the past have suggested that children may be less susceptible to the novel coronavirus. If this new variant adheres more easily to cells, it is possible that it spreads more easily among children than before. However, more studies will be needed to see if this is the case.
There was one increased cases in children in England at the same time as this virus has increased its prevalence. This increase was not observed when the children returned to school in early fall. But schools were open while a lot of other things were closed at the time, so it is possible that schools represent one of the few chances for the virus to spread. We cannot yet say that children will catch and spread this variant more easily.
Will the vaccines work against the new virus?
Most experts believe the newly developed vaccines will still work against the new UK variant. When vaccines stimulate the immune system, the body builds an arsenal of cells to bind to many different parts of the virus. According to the CDC, mutations in a few places probably won’t be enough to make the vaccine less effective.
Since 99% of the proteins in the new variant are identical to the strain targeted by the Pfizer-BioNtech mRNA vaccine (the Moderna vaccine is very similar), it is very likely that the vaccine will work, said the CEO of BioNTech, Uğur Şahin, in a statement. Report.
It is possible that over time, a variant may emerge that will elude some of our vaccines, such as the flu shot must be updated every year. However, the new mRNA vaccines could be updated to reflect new mutations in about six weeks, Şahin told the Financial Times.
What can we do to stop this?
The new variant still spreads in the same way as the regular form of the coronavirus. This means the same things everyone has been doing to prevent the spread of the virus since March will also work for the new UK variant: washing hands, physically distancing, masks and good ventilation. Strictly adhering to these rules and avoiding unnecessary outings will help prevent its spread.
Originally posted on Live Science.
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