A new frightening strain of coronavirus, harmlessly named B.1.1.7, recently exploded across southeast England, prompting the government to tighten blockades in the region. Although we do not know all the details, experts are increasingly sure that it is easier to transmit than other strains. Here is everything we know so far about this new genus.
Strain B.1.1.7 SARS-CoV-2 is a version of the virus with 23 mutations, eight of which are in the spike protein that the virus uses to bind and enter human cells, Reported by the journal Science.
Where did it come from?
It was first discovered on September 21 in the county of Kent in England, and then took off and expanded in November, according to the World Health Organization.
It has since 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 a person who is immune-compromised, according to Science Magazine. This is because, unlike the flu, the new coronavirus can correct errors when it replicates and thus tends to have a fairly stable genome, Live Science previously reported. However, studies have shown that people who have a weakened immune system – because they take immunosuppressants or, for example, are being treated with chemotherapy – can have an infected virus for months. This, in turn, would give the virus a good chance of acquiring mutations that help it replicate or avoid immune system.
What do these mutations do?
We don’t know for sure. Viruses mutate all the time and most of these changes do not affect how deadly or contagious the virus is. In this case, some of these mutations may have occurred purely by accident and may not affect the function of the virus.
But the three mutations have particularly worried experts.
One, two deletions of amino acids known as 69-70Delta, were first detected 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 for months, the researchers reported in a preprint article published on December 19. medRiv database. (Not reviewed.) The authors suspect it evolved to evade the immune system. Another wrinkle associated with this deletion is that it can make one of the targets of SARS-CoV-2 PCR tests – known as the S gene – false negative. Some tests only look for positive data in this S gene and would therefore miss a new variant. Most PCR tests, however, require three separate areas of protein classes, so those tests will not be affected, the WHO said.
Another mutation, known as N501Y, alters key amino acids that make up the so-called SARS-CoV-2 receptor binding domain, where the amino acid asparagine (N) is 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. 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 laboratory vessel.
Dozens of SARS-CoV-2 samples from South Africa and Australia have been shown to be positive for this mutation, but laboratory tests suggest that the South African and UK variants developed the same mutation separately. This suggests that it may provide an evolutionary advantage to the virus.
The third suspected mutation is P681H, which is also in the domain of virus receptor binding. According to preliminary information he published COVID-19 Genomics Consortium UK, this mutation is located next to the “furin cleavage site”, where the spike protein must be cleaved for the virus to enter the cells, according to Science Magazine.
Is it easier to spread?
Yes. Experts now think the new variant is between 50% and 74% more transmissible than other dominant strains, according to the study Center for Mathematical Modeling and Infectious Diseases (CMMID) which has not been reviewed yet. The WHO estimates that this would refer to 0.4 to the basic reproductive number R, which dictates to how many people an infected person would spread the virus.
Based on that growth model, the new variant could be responsible for 90% of all new COVID-19 cases in London and East and South England by mid-January, the study found.
Is it more deadly?
We don’t know, but experts suspect it isn’t. However, if it spreads much more easily, it means more people will be hospitalized. Once hospitals prevail, the quality of care for the sickest patients declines, which can lead to higher mortality rates than would otherwise be expected.
The CMMID study found that the new variant could explain the increase in the number of hospitalizations in the south-east of England, mainly due to increased spread, not necessarily because the virus is more dangerous.
In another study, which was also not reviewed by CMMID, a mathematical model was used to determine whether the rapid growth of the virus in London was due to increased infectivity or more severe. The latter did not fit well into the data, while the former fit nicely.
Has the variant spread to the United States?
So far, scientists have not discovered this strain anywhere in the US, although America has not done nearly as much genetic sequencing on viral samples as the UK. For example, in December, the U.S. sequenced 51,000 virus samples from 17 million identified cases of SARS-CoV-2, According to the CDC. The UK sequenced more than twice as many virus samples as the US, although it had just over a dozen diagnosed cases.
Dr. Stanley Perlman, immunologist and pediatric infectious disease specialist from the University of Iowa told the Center for Infectious Diseases Research and Policy (CIDRAP) to suspect that the variant is already in the U.S., “I would be surprised if it wasn’t,” 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 new coronavirus. If this new variant is more easily glued to the cells, there is a chance that it may spread more easily among children than before. However, further studies will be needed to determine if this is the case.
Was an increase in the number of cases in children in England at the same time as this virus has increased its prevalence. This phenomenon was not seen when the children first returned to school in early autumn. But schools were open while many other things were closed at the time, so it is possible that schools represented one of the relatively rare chances that the virus had to spread. We still cannot say that children will find it easier to catch and spread this variant.
Will vaccines work against the new virus?
Most experts think the newly developed vaccines will continue to work against the new UK version. When vaccines stimulate the immune system, the body builds an arsenal of cells to bind to many different parts of the virus. Mutations on a handful of spots are unlikely to be enough to make the vaccine less effective, according to the CDC.
Given that 99% of the protein in the new variant is identical to the strain targeted by the Pfizer-BioNtech mRNA vaccine (Moderna is very similar), it is very likely that the vaccine will work, said BioNTech CEO Uğur Şahin briefing.
It is possible that over time, a variant may emerge that will avoid some of our vaccines, similar to how the flu vaccine needs to 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 continues to spread in the same way as the common form of coronavirus. This means that the same things that everyone has been doing to prevent the spread of the virus since March will work for the new UK version: hand washing, physical removal, masks and good ventilation. Strict adherence to these rules and avoiding unnecessary outings will help prevent its spread.
Originally posted on Live Science.