Contagious mutants
The most common mutation increases the contagiousness of the coronavirus from 2.5 to 8 times
It occurs in more than half of the studied strains of SARS-CoV-2
American molecular biologists have found that the most common mutation in the SARS-CoV-2 genome, characteristic of more than half of the studied strains of the virus, improves its ability to penetrate cells from 2.5 to 8 times. The preliminary results of their work were published by the scientists in the electronic scientific library bioRxiv (Daniloski et al., The D614G mutation in SARS-CoV-2 Spike increases transmission of multiple human cell types).
"The widespread D614G mutation significantly accelerates the transmission of the virus between a wide variety of human cell types, including cells from the lungs, liver and intestines. One of the reasons for the increased contagiousness of the virus may be that this mutation makes SARS-CoV-2 more resistant to human enzymes," the researchers write.
From the first days of the outbreak of coronavirus infection, scientists have been trying to understand in which direction and how its causative agent SARS-CoV-2 evolves. Today it is known that it accumulates mutations at about the same rate as the influenza pathogen. However, scientists do not yet know for sure how these mutations affect the contagiousness and other properties of the virus.
In particular, back in early March, Chinese biologists said that the virus could split into two subtypes – S and L, which differ from each other in the severity of symptoms and the rate of spread. Other scientists doubted this, noting that changes in the general gene pool of the virus could be caused by various random processes, and not by real differences in the contagiousness of these subtypes of SARS-CoV-2. In May, scientists from Britain and Australia showed that three varieties of the virus are circulating in the human population at once.
At the same time, as scientists from New York University (USA) under the leadership of Neville Sanjana note, about 70% of the coronavirus strains circulating today of all three subtypes have a common mutation in the S gene, which controls the production of proteins of the part of the SARS-CoV-2 envelope that is directly related to its penetration into the body.
New version of the virus
Judging by its rapid spread, this "typo" in RNA, the so-called D614G mutation, is presumably useful for the coronavirus. However, scientists did not know what exactly it changes before.
This was due to the fact that D614G almost always occurs together with another mutation, P314L, which changes the operation of the ORF1b site. It controls the production of several proteins that are critical for copying the RNA of the virus and its reproduction inside infected cells. Because of their connectedness, scientists could not determine what exactly these mutations do individually.
Sanjana and his colleagues solved this problem by creating a kind of "dummy" coronavirus. They consisted of some components of its shell and contained glowing proteins. Scientists modified part of these particles so that their spike–like protein – the molecule responsible for contact with healthy cells - contained the D614G mutation, and tracked how actively they penetrate into those tissues of the human body that are affected by the coronavirus.
Experiments have shown that this change in the RNA of the virus dramatically increased its contagiousness. In particular, the number of glowing intestinal cells increased by about 2.5 times, lung cells by five times, and liver cells by almost eight times. At the same time, it reduced by four times the probability that the immune system will begin to recognize the spike-like protein of the virus and produce antibodies to it.
In addition, scientists found out that the enzymes of the innate human immune system destroyed the shell proteins of this version of SARS-CoV-2 more slowly than in other varieties of the virus. As Sanjana and his colleagues suggest, this may accelerate the formation of new viral particles and their spread throughout the body, which may explain why the D614G mutation has become dominant in such a short time.
It should be added that the scientists' article was not reviewed by independent experts and editors of scientific journals, as is usually the case in such cases. Therefore, conclusions from it and similar articles should be treated with caution.
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