Fast-spreading UK Coronavirus version: answered all your questions


A fearsome new strain of coronovirus, spontaneously named B.1.1.7, has recently exploded in southeast England, helping the government to block the region. Although we do not know all the details, experts believe that it is transmitted more easily than other strains. Everything about the tension of this novel is known so far.

What is this?

Science magazine reported that the B.1.1.7 strain of SARS-CoV-2 is a variant of the virus with a 23 mutation, eight of which are in the spike protein that the virus uses to bind and enter human cells.

Where it came from?

According to the World Health Organization, it was first detected on 21 September in Kent County in England.

Since then, it has become the most common variant in England, representing more than 50% of new cases diagnosed between October and December 13 in the UK, according to WHO.

However, some scientists now believe that the virus may have mutated into a person who, according to Science magazine, was defenseless. This is because, unlike the flu, the novel coronovirus can fix mistakes when it repeats, and therefore has a fairly stable genome, Live Science previously reported. However, studies have shown that people who have weakened the immune system – because they are taking immunological drugs or being treated with chemotherapy, for example – can irritate infectious viruses for months. This, in turn, will give the virus multiple opportunities to receive mutations that will help replicate or eject the immune system.

What do these mutations do?

we are not 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 occur purely by coincidence and may not affect the function of the virus.

But three mutations, in particular, have worried experts.

One, a two-amino-acid deletion known as 69–70 delita, was first detected separately in a patient being treated with immunosuppressants developing COVID-19. The patient received remdisevir, proto-fluid and neutralizing antibodies, but died months later. Although the virus did not initially have the deletion, it acquired it in months, the researchers reported in a preprint article to be published in the Medrive database on 19 December. (This has not been peer reviewed.) The authors suspect that it evolved to evoke 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 test negative. Some tests only seek positivity in this S gene and will therefore miss the new variant. Most PCR assays look for three distinct regions of the spike protein, so those assays will not be affected, WHO said.

Another mutation, known as N501Y, replaces the major amino acids that make up the so-called receptor-binding domain of SARS-CoV-2, where the amino acid asparagine (N) combines with trosrosine (Y) According to the Centers for Disease Control and Prevention, the virus that arrives at the ACE2 receptor on human cells. A September study in the journal Cell found that this variant binds the ACE2 receptor more tightly than other versions of coronovirus – at least in a lab dish.

Dozens of SARS-CoV-2 samples from South Africa and Australia have tested positive for this mutation, but laboratory tests show that the same mutation has developed in different forms in South African and UK. This suggests that it may provide an evolutionary advantage to 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, according to Science magazine, this mutation sits next to the “furin cleavage site”, which allows the virus to cleave the spike protein to enter cells needed.

Does it spread more easily?

Yes. Experts now believe that the new variant is 50% to 74% more effective, 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 it will deal with the original breeding number R by 0.4, which determines how many people each infected person will spread the virus to.

Based on the model of that increase, the new version may account 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 do not know, but experts suspect it is not. However, if it spreads more easily, it means more people will be hospitalized. Once hospitals are overwhelmed, the quality of care for the sickest patients drops, which may otherwise increase the death rate.

The CMMID study found that the new variant could explain indigestion in hospitals in southeastern England, largely due to the outbreak, not necessarily the virus being more dangerous.

Another study, also not peer-reviewed by CMMID, used mathematical models to see whether the rapid growth of the virus in London was caused by infectious growth, or was due to more severe. The latter did not fit the data well, whereas the former fit well.

Has the variant spread in the US?

So far, scientists have not detected this strain anywhere in the US, although the US has not done nearly as much genetic sequencing on viral samples as it has in the UK. For example, as of December, the US sequenced 51,000 viral samples out of the 17 million cases of SARS-CoV-2 identified, according to the CDC. Despite slightly more than a tenth of diagnosed cases, the UK has sequenced more than two viral samples as the US.

A pathologist and pediatric infectious disease specialist at the University of Iowa, Drs. Stanley Pearlman told the Center for Infectious Diseases Research and Policy (CIDRAP) that he suspected the variant already existed in the US. ‘ said.

Can children easily catch it?

Several lines of evidence in the past have suggested that children may be less susceptible to novel coronaviruses. If this new version sticks to cells more easily, there is a chance that it can spread more easily among children than before. However, further study will need to see what is the matter.

In England, there has been an increase in cases of children at the same time, as the virus has increased its prevalence. When children were first returned to schools in the early fall, this was not seen. But while schools were open at this time, many other things were closed at this time, so it is likely that the schools represented a relatively low probability virus. We cannot yet say that children will catch and stretch this version more easily.

Will vaccines work against new viruses?

Most experts believe the newly developed vaccines will still work against the novel UK version. When vaccines stimulate the immune system, the body creates an arsenal of cells to bind many different parts of the virus. According to the CDC, mutations in a handful of locations will probably not be sufficient to make the vaccine less effective.

Given that 99% of the protein on the new version is similar to the strain of the Pfizer-BioNtech mRNA vaccine target (the modern vaccine is very similar), it is highly likely that the vaccine will work, BioNTech Uğur Şahin said in a news briefing.

It is possible that a variant may emerge over time that will evacuate some of our vaccines, similar to how flu vaccines should be updated every year. However, the new mRNA vaccines can be updated to reflect the new mutation in about six weeks, toldahin told the Financial Times.

What can we do to stop this?

The new version still spreads similarly to the normal form of coronovirus. This means that since March everyone has been doing the same thing to stop the spread of the virus, it will also work for the new UK version: hand washing, physical distance, mask and good ventilation. Strictly following those rules and avoiding unnecessary outings will help prevent its spread.

Originally published on Live Science.

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