Variants of SARS-CoV-2 with potentially dangerous mutations are being found in the United Kingdom and other countries. We briefly explain what mutations are all about, why this time everyone was alarmed and is everything so bad

Is the new "strain" of coronavirus from the UK really dangerous? Coronavirus strain
Is the new "strain" of coronavirus from the UK really dangerous? Coronavirus strain

All viruses are constantly mutating - this is a common thing. Mutations are differences in the genetic code. One "letter" can change in it, a whole piece can disappear (this is called a deletion) or something else can happen. Sometimes the structure of a viral particle depends on this, and sometimes its "behaviour".

For example, a virus can become more or less infectious, deadly, the incubation period of the disease can be lengthened or shortened. Most mutations do not affect properties, some interfere with viruses, but others, on the contrary, are useful: they facilitate spread.

SARS-CoV-2 accumulates one to two mutations per month, which means that samples obtained today may have about 20 changes compared to the virus at the beginning of the year. Some options have a little more, while others have less.

The virus that caused a stir in the UK (it was named B.1.1.7, or VUI-202012/01) is unusual in that it seems that some of the mutations have accumulated in it very quickly. In total, 17 of them were found, eight of them - in the thorn squirrel. This protein makes SARS-CoV-2 look like a corona and is needed to enter human cells.

Scientists are wary, because the approved thorn protein vaccines "train" the immune system. In theory changes in this protein could make vaccines less effective or even useless and undermine protection for those who have had COVID-19.

"Some of these mutations, such as N501Y, are already being studied, with the suspicion that they affect the infection. [The variant found] also has a 69-70del deletion, which may have appeared due to the virus evading the immune system. observed in patients with immunodeficiency, "- explains evolutionary ecologist Samuel Alison, head of the research group at the University of Montpellier in a letter to TASS.

Whether these and other mutations really help the coronavirus remains unclear. To figure this out, you need to check the suspicious variant on cells and animals and compare it with others. It will take months.

The team of the virologist Ravindra Gupta of the University of Cambridge has already done some experiments. They examined a virus with a 69-70del deletion and another mutation, D796H ( not mentioned in the suspect report ). In laboratory conditions, the antibodies of COVID-19 patients did not adhere well to mutant viral particles, that is, it can be assumed that these mutations can deceive the immune system.

Gupta and his colleagues also "sewn" the SARS-CoV-2 spike protein into another virus - a variant with a 69-70del deletion turned out to be twice as infectious. Now they do the same thing, but simultaneously with the 69-70del deletion and the N501Y mutation. Scientists expect to receive the first results shortly after Christmas, writes Science.

But the results of laboratory experiments should be interpreted with caution. In the spring and summer, there was a lot of talk about the D614G mutation. This option quickly supplanted all others, and experiments on cells and animals indicated that it was much more contagious. But subsequent research showed that if the D614G mutation helps the coronavirus spread, then it is not as significant as expected.

VUI-202012/01 also appears to be gradually replacing others, and new cases of COVID-19 are skyrocketing in areas of the UK where it is found. Because of this, the government has imposed tier 4 restrictions, reduced holiday indulgences from five to one day, and some countries canceled flights from the United Kingdom.


Both terms are not fully established, but usually a strain is a variety of a virus with characteristic properties (phenotype), and a variant is a variety that is genetically different, but not necessarily phenotypically.

In everyday life, the word "strain" is most often used in relation to influenza viruses. Different strains of influenza virus differ in surface proteins and are recognized differently by the immune system - this is their phenotypic difference. If you call the variants of SARS-CoV-2 strains, you might think that they also "behave" differently. So far, this is just an assumption.

But what happens is not necessarily due to mutations. “At this stage, it is difficult to speak with confidence about the danger, because different factors can play a role. The B.1.1.7 branch can grow simply by coincidence, for example, after a case of superproliferation [when one patient infects many more people than average]. True, the N501Y mutation is spreading in other countries as well, ”writes Samuel Alison.

According to Alizon, it is too early to say that the VUI-202012/01 variant is easier to transmit, and even more often causes complications and leads to death. Other experts believe it will not affect the effectiveness of the vaccines either. Known mutations do not completely change the spike protein, so at least some of the antibodies will still be able to bind to it.

But VUI-202012/01 will continue to mutate. It is possible that one day he will learn to deceive a trained immune system. Ironically, vaccination can speed up this process. The more people have been ill or vaccinated, the stronger the evolutionary pressure on SARS-CoV-2: in order not to die out, the coronavirus will have to adapt.

The good news is that twenty years ago we did not have the technology to track the evolution of the virus in near real-time. The bad news is that these technologies did not appear everywhere. But the record-breaking development of vaccines against COVID-19 leaves hope that in the worst case, we will find a way out.

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