A frightening new strain of coronavirus, innocently called B.1.1.7, recently exploded in southeastern England, prompting the government to restrict blockages in the region. Although we do not know all the details, experts are increasingly confident that it is more easily transmitted than other strains. Here is everything we know so far about this new variety.
What is it?
The 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 and enter human cells, Science Magazine reported.
Where did it come from?
It was first detected on September 21 in Kent County, 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 United Kingdom, according to the WHO.
However, some scientists now believe that the virus may have mutated in an immunocompromised person, according to the journal Science. That’s because, unlike the flu, the new coronavirus can correct errors when it replicates and therefore tends to have a very stable genome, Live Science reported earlier. However, studies have shown that people with weakened immune systems – because they are taking immunosuppressive drugs or being treated with chemotherapy, for example – can harbor infectious viruses for months. This, in turn, would give the virus many chances to acquire mutations that help it to replicate or prevent 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 the degree of mortality or infection of the virus. In that case, some of these mutations may have come about by chance and may not affect the virus’s function.
But three mutations in particular worried experts.
One, a deletion of two amino acids known as 69-70Delta, was first detected separately in a patient undergoing immunosuppressants who developed COVID-19. The patient received remdesevir, convalescent plasma and neutralizing antibodies, but died months later. Although the virus initially did not have this exclusion, it acquired it over months, the researchers reported in a pre-printed article published on December 19 in the medRiv database. (It has not been peer-reviewed.) The authors suspect that it evolved to escape the immune system. Another aspect associated with this exclusion is that it can cause one of the targets of the SARS-CoV-2 PCR tests – known as the S gene – to be falsely negative. Some tests look only for positives in this S gene and, therefore, would miss the new variant. Most CRP tests, however, look for three distinct regions of the peak protein, so those tests will not 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 binds to ACE2 receptor in human cells, according to the Centers for Disease Control and Prevention. A September study in the journal Cell found that this variant binds more strongly to the ACE2 receptor than other versions of the coronavirus – at least on a laboratory plate.
Dozens of samples of SARS-CoV-2 from South Africa and Australia tested positive for this mutation, but laboratory tests suggest that the South African and United Kingdom variants developed the same mutation separately. This suggests that it may provide an evolutionary advantage for the virus.
The third suspected mutation is P681H, which is also in the receptor-binding domain of the virus. According to preliminary information posted by the COVID-19 Genomics Consortium UK, this mutation is close to the “furin cleavage site”, which is where the peak protein must be cleaved for the virus to enter cells, according to the journal Science.
Does it spread more easily?
Yes. Experts now think the new variant is between 50% and 74% more transmissible than other dominant strains, according to a study by Center for Mathematical Modeling and Infectious Diseases (CMMID) that has not yet been peer-reviewed. The WHO estimates that this would add 0.4 to the basic reproductive number R, which determines how many people each infected person would spread the virus to.
Based on models of this growth, the new variant could account for 90% of all new cases of COVID-19 in London and the east and south of England by mid-January, the study concluded.
Is it more deadly?
We don’t know, but experts suspect not. However, if it spreads much more easily, it means that more people will be hospitalized. As hospitals become overburdened, the quality of care for the most ill patients falls, which can lead to higher mortality rates than would be expected.
The CMMID study found that the new variant could explain an increase in hospitalizations in southeastern England, largely due to increased spread, not necessarily because the virus is more dangerous.
Another study, also not peer-reviewed by CMMID, used a mathematical model to see if the rapid growth of the virus in London was due to increased infectivity or because it was more severe. The latter did not fit well with the data, while the former fit well.
Did the variant spread to the US?
So far, scientists have not detected this strain anywhere in the United States, although the United States has not done as much genetic sequencing on viral samples as the United Kingdom. For example, in December, the U.S. sequenced 51,000 viral samples from 17 million identified cases of SARS-CoV-2, According to the CDC. The United Kingdom sequenced more than twice as many viral samples as the United States, despite having just over one tenth of the diagnosed cases.
Dr. Stanley Perlman, immunologist and pediatric infectious disease specialist at the University of Iowa told the Center for Infectious Diseases Research and Policy (CIDRAP) that he suspects the variant is already in the US “I would be surprised if it wasn’t,” he said.
Can children catch more easily?
Several lines of evidence in the past have suggested that children may be less susceptible to the new coronavirus. If this new variant adheres more easily to the cells, there is a chance that it will spread more easily among children than before. However, further studies are needed to see if this is the case.
There was a increase in cases in children in England at the same time that this virus increased its prevalence. This increase was not seen when the children returned to school in the early autumn. But schools were opened while many other things were closed at this time, so it is possible that schools represented one of the few chances of the virus spreading. We cannot yet say that children will catch and spread this variant more readily.
Will vaccines work against the new virus?
Most experts believe that 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 attach to many different parts of the virus. Mutations in a handful of spots are unlikely to be enough to make the vaccine less effective, according to the CDC.
Given that 99% of the proteins in the new variant are identical to the target strain of the Pfizer-BioNtech mRNA vaccine (the Modern vaccine is very similar), the vaccine is highly likely to work, said BioNTech CEO Uğur echahin in a news briefing .
It is possible that, over time, a variant will emerge that avoids some of our vaccines, similar to the way the flu vaccine needs to be updated each year. However, new mRNA vaccines can 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 common form of the coronavirus. This means that the same things that everyone has been doing to prevent the virus from spreading since March will also work for the new variant in the UK: washing your hands, getting away from body, masks and good ventilation. Strictly adhering to these rules and avoiding unnecessary tours will help prevent their spread.
Originally published on Live Science.