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Home / Health / Covid-19-SARS-CoV-2 follows the rules of evolution science and technology

Covid-19-SARS-CoV-2 follows the rules of evolution science and technology

nSelection It is a powerful force. In the still controversial situation, it used the bat coronavirus and adapted it into a way that suits people. The results have spread all over the world. Now, in two separate but accidental events, it has further modified the virus, creating new variants that replace the original version.One or the other of these novel viruses is likely to soon become a major SARS̵


The knowledge of both began to spread widely in mid-December.In the UK, a group of researchers called Covid-19 GenomicsK Consortium (CØGuK) Published the genetic sequence of the mutation B.1.1.7, and nERVTAGThe team studying the threat of emerging viruses told the government that the spread of this virus is 67-75% higher than the virus that has already spread in the country. At the same time, in South Africa, Salim Abdool Kalim, a leading epidemiology scientist, introduced a variant called 501.v2 to the country on three TV channels. At that time, the variant had accounted for the province’s new covid-19 infections. 90%. Western Cape.

The UK responded on December 19, tightening the restrictions already in place. South Africa’s response was a measure taken after recording one millionth of the disease on December 28, which extended the night curfew by two hours and again banned the sale of alcohol. The response of other countries is that the crackdown is even greater than any travel between them and between the UK and South Africa.At least BHowever, in .1.1.7, this is only to close the horse shut door after the horse is tied tight. Now this variant will continue to spread in many countries/regions other than the United Kingdom and from these new sites or the United Kingdom. South Africa, Australia, the United Kingdom, Japan, and Switzerland have also reported some individual 501.v2 cases outside of South Africa.

So far, there is evidence that, despite their additional transmission capabilities, the new variants are not more dangerous than the current version of the virus on a case-by-case basis. In this case, both are following the path predicted by evolutionary biologists, leading to the long-term success of the new pathogen-this new pathogen will be more infectious (which will increase the chance of continued transmission), Instead of being more deadly (reducing it). The speed at which they spread is impressive.

The first sample B.1.1.7 Collected in southeast London on September 20. It was found in London itself the next day. A few weeks later, in early November, B.1.1.7 accounts for 28% of new infections in London. By the first week of December, this proportion had risen to 62%. It may now exceed 90%.

Variation 501.V2 has a similar history. It started in the Eastern Cape, and the earliest samples dated back to mid-October, and it has spread to other coastal provinces.

rise rapidly B.1.1.7 and 501.v2 raised several questions. One of the reasons is why these particular variants are so successful. The second is their situation. The third is whether they will resist any new vaccines that are now in place.

The first answer to these questions lies in the genome of the variant. CØGuKInvestigation B.1.1.7 shows that it is significantly different from the original version SARSCarbon monoxideV-2 17 places. In addition, some of these differences are in the spike gene, the protein that the coronavirus uses to attach to the cell’s prey. Three of the spike mutations have particularly attracted the attention of researchers.

One, n501with, Which affects the 501st link in the amino acid chain of the ear. This link is part of a structure called the receptor binding domain, which extends from link 319 to 541.It is one of the six main points of contact and helps to lock the spike to its target. The protein is called Master2 occurs on the surface membrane of certain cells lining the lung airways. The letters in the mutation name refer to the substitution of an amino acid called asparagine (“n“, is a shorthand form in biology), called tyrosine (“with“). This is important because previous laboratory work has shown that the chemical property changes caused by this substitution bind the two proteins more tightly than normal. It may be said that this particular mutation (although there is no Other mutations) shared with 501.V2.

Golden spike

B.The other two interesting spikes in 1.1.7 were mutated to 69-70del, which completely eliminated two amino acids from the chain, and P681H, It replaced proline with another amino acid histidine on chain 681. There are several reasons why the double deletion has attracted the attention of researchers. The most important reason is that it still exists in the virus mutation, which has plagued some farms. On mink skins in Denmark in November last year, people were worried about the development of the disease’s animal bank.This substitution is considered important because it is located at one end of a part of the protein called “protein” small1 /smallTwo furin cleavage sites (links 681-688) help to activate the spikes so that they can meet the target cells.Spike proteins of related coronaviruses (such as the original SARS, This might be why SARSCØV-2 is so infectious.

The South African variant 501.v2 has only three meaningful mutations, and all of them are in the receptor binding domain of the ear.apart from n501with, they are K417n with E484K (K with E Are amino acids called lysine and glutamic acid). Now, these other two links are under strict scrutiny.

For one variant, there are even three meaningful mutations. Only one will be more commonplace. Found in 17 B.Therefore, 1.1.7 constitutes a huge anomaly. Therefore, how to integrate so many changes in a virus is the second question that needs to be answered.

author CØGUnited Kingdom The paper has a suggestion. This is because, instead of accidental accumulation of changes, B.1.1.7 itself may be the result of an evolutionary process, but it occurs in a person rather than a population. They have observed that some people develop chronic covid-19 infection because their immune system is not working properly and therefore cannot clear the infection. They hypothesized that these unfortunate people might act as an incubator for the mutation of the new virus.

The theory is this. First, such patients lack natural immunity, which reduces the pressure on the virus and allows mutations to multiply, otherwise these mutations will be killed by the immune system. However, treatment of chronic covid-19 usually involves so-called convalescent plasma.This is serum collected from recovered covid patients, so it is rich in anti- SARSCØV-2. As a therapy, this method is often effective. However, the administration of such antibody mixtures will bring strong selection pressure to the now diverse virus population in patients.This one CØGUnited Kingdom The researchers believe that it may lead to the success of the mutation combination, and this combination would not be possible without this combination.It might be B.1.1.7 is one of them.

The answer to the third question is: “probably not”, that is, whether there are new variants that can resist the current vaccine. It would be a long-term coincidence if the mutations that spread without a vaccine can still protect the virus carrying them from the immune response caused by the vaccine.

However, this does not guarantee the future. The rapid emergence of these two variants shows the power of evolution. If there is a combination of mutations that can bypass the vaccine-induced immune response, it is likely that nature will find it.

Editor’s note: Some of our coverage of covid-19 is free to the following readers Economist Today, Our daily news.For more stories and pandemic trackers, please visit our center

This article appears in the “Science and Technology” section of the print edition under the heading “Theme Changes”

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