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The Sars-CoV-2 virus, responsible for the Covid-19 pandemic, is a single-stranded RNA virus. It consists of around 29,900 nucleotides, which are the four bases adenine, guanine, cytosine, and uracil. Their order in the strand also encodes the information needed to synthesize their proteins. Among other things, the so-called spike protein. These are the tips that stick out of the virus ball.
What is a mutation in a virus?
The only activity of the Sars-CoV-2 virus (and also of all other viruses) is replication. To do this, the entire thread must be copied. Its approximately 30,000 bases are quite long for an RNA sequence. Therefore, there will be read and copy errors. Some letters are copied incorrectly or twice, others are skipped. Information from the cells of higher living things such as fungi, animals, and plants is stored in the cell nucleus in the form of DNA. It is twofold and there is usually a review function that removes errors. This makes possible lengths of up to 2,500,000 base pairs. Stable copy is no longer possible from around 10,000 base pairs, too many mutations would accumulate. Therefore, RNA viruses have short genomes. Corona viruses are an exception. They have a proofreading feature that guarantees a fairly stable copy of your thread. Therefore, the influenza virus or HI mutates much more frequently.
Why this particular mutation?
Most mutations have no effect on the virus. But they can help differentiate between different strains of Sars-CoV-2 and establish paternity relationships. The COG (Covid-19-Genomics Consortium) in England has examined more than 120,000 genomes of people who tested positive and found several thousand mutations. 1777 occurred in the region encoding the spike protein. So far, none have had a decisive impact on the course of the pandemic. However, researchers have now come across some notable mutations in the B.1.1.7 strain. This mutant is now VUI-202012-01 (the first variant under investigation in December 2020), as the new mutation is scientifically called. Strictly speaking, there are 17 individual mutations. 14 of them change the base order, 3 are the so-called eliminations (eliminated, failed bases). Four of them are notable.
Isn’t that a surprisingly high mutation rate we’re seeing here?
That’s so. The mutations are believed to have occurred in a chronically infected patient. It would be a virus carrier in which the virus has been fought for a long time with antibody therapy and which, therefore, has already achieved a certain genetic variability. Therefore, different mutations could also accumulate (“pile up”). Under “normal” conditions, this should take longer.
Why are these mutations noticed? What is its meaning?
In the case of this peak protein, they influence the so-called RBD (Receptor Binding Domain), where the virus attaches itself to the ACE2 receptor of the cell. The behavior of the attachment may change, which can make the virus more contagious. And it may also be that the immune system no longer recognizes it as an antigen (a substance that stimulates the immune system’s reaction). The most important mutation is N501Y, but N439K and Y453F also influence ACE2 affinity. 69-70del, is a loss mutation that occurred simultaneously with the others. It may mean that antibodies that have already been acquired no longer react to the new virus.
Why is it not possible to establish the effects on the course of the epidemic?
What mutations cause in molecular biology must be investigated in a laboratory test. At the moment, the effects can only be followed epidemiologically. British Prime Minister Boris Johnson said the new mutant was “up to 70 percent more contagious” than the old one. That was an extrapolation of what is known about the infection process in England. The mutant has spread rapidly, especially in southern England and London. We have a large number of infections and an increased presence of VUI-202012-01. This can be just a pure correlation of numbers and does not have to indicate causation. The simultaneous increase can be explained by the lack of caution on the part of Londoners (“The pubs were crowded”, it was said) and lax measures in the south of England (correlation), without having to assume that it is due to the virus (causality ).
What does the mutation mean for vaccines and immunity?
Vaccines are generally based on different strains. Unless the mutations are too deep, they should work. It can only be known exactly after laboratory tests. The relationship between the virus and the immune system (even if it is a vaccination system that stimulates the immune system) is like a rabbit-hedgehog race in which the virus is always one step ahead.
Do we have to start over now?
No, so far there is no evidence that mutations hide the virus. The 69-70del mutation caused dropouts in a specific RT-PCR test. But because the test looks for other gene segments, it still works. And if there are problems: mRNA vaccines can be more easily adapted from a molecular biological point of view than conventional vaccines. However, the production stage is not included. And maybe you would have to redo the tolerance and safety tests from scratch because serious side effects cannot be ruled out.
Will the new mutation disappear?
No, on the contrary, it will displace others, if it is really more contagious than the previous one. At the moment there is a predominant mutation (D164G) that was not the original version of the Wuhan virus, but which – as stated – changed the infectivity “moderately”. The types that can spread more quickly from one person to another have an evolutionary advantage over the others. They will prevail in the population. Unless other factors work against you.
