Viruses multiply rapidly and often inaccurately. Therefore, mutations (replication errors) are a commonplace occurrence. Most mutations have little to no effect on how the virus spreads or how dangerous it is. Until recently, SARS-CoV-2, the virus that causes covid-19, was not uncommon in this regard.

In mid-December 2020, a new version of the virus (known as B.1.1.7) was reported to be spreading rapidly in the UK. The first sample of the mutation was seen on September 20, in a London suburb. The second was found the next day in London itself. A few weeks later, in early November, accounted for 28% of new infections in London. Now over 90% of new infections are from this strain of the virus. It is estimated that it is 75% more efficient than the original virus. This same strain has been observed in 33 more countries.

At the same time, in South Africa, a new mutation of the virus appeared, called 501. v2, which today already accounts for about 90% of new infections in the Western Cape.

So far the evidence shows that these newer versions of the virus are not more dangerous (lethal to the host) than the prevalent versions of the virus. This finding is also consistent with our evolutionary understanding:

In order for a virus, which is dependent on a host body to multiply, to succeed long term, it must be contagious (which increases the chance of transmission to other hosts) but not more lethal (which decreases the chance of transmission). The rate of spread of SARS-CoV-2 was considered impressive. The rate of spread of the new mutation versions is much more impressive!

In the sequence analysis of B1.1.1.7 many changes in the virus proteins can be identified: 17 to be specific. Even one would have excited the researchers. 17 – That is a phenomena that is difficult to explain.

As part of all these changes, there are 3 that change the virus spike protein – – this is the protein with which the virus recognizes and binds to our cells, using the spike to gain entry into the cells. This is the same protein that is reproduced by the RNA in the Pfizer’s and Moderna’s vaccines, and against which our antibodies are formed and respond after the vaccine is given. The same antibodies that later protect us from covid-19.

The first change in the protein (N501Y), affects position 501 in the amino acid chain of the spike protein. This is one of the six main points of contact between the virus and our cell, which help bind the protein to its target (a protein called ACE-2). The chemical nature of this change explains the improved effectiveness of the infection – the change allows for a more efficient bind to the cells, leading to a more effective infection.

This mutation is also common to the South African 501.v2.

The other two mutations in the spike protein can also explain the increased level of infection. One of them was found in a virus that infected minks in Denmark in November, it caused great concern by killing 16 million minks.

The South African version, 501.v2, has three mutations, all in the spike protein.

Will one of these new mutant versions be resistant to the vaccines currently being given?

The logical answer is – “probably not”. It would be a very rare coincidence if mutations that spread in the absence of a vaccine, protect the virus from the immune response generated by that vaccine. But this is not a guarantee for the future. The emergence of these two versions shows the power of evolution. If there is a combination of mutations that can bypass the immune response caused by the vaccine, then there is a reasonable chance that nature will find it.

On the other hand, it is important to understand that the response of our immune system (whether as a result of infection or a vaccine) is polyclonal: the immune system produces a number of different antibodies, which bind in different places and in different ways to the protein. This is one of the key characteristics of our immune system: it strikes from several directions at once, making it difficult for the virus to evade it.

Finally, it is easy to test this question, and tests have indeed been performed. Preliminary data shows that antibodies taken from people who have recovered from covid-19 neutralize mutant version B1.1.1.7 very effectively.

So there are reasons for optimism. There are also reasons why scientists will devote many hours of research to the new mutant versions.





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