Current DateSeptember 28, 2021

Covid-19: the epidemic may have been accelerated by a mutation of the virus

A mutation in the SARS-CoV-2 virus responsible for Covid-19 may have accelerated the spread of the epidemic. This is the conclusion that can be drawn from the work of the Scripps Research Department of Immunology, which supports a hypothesis already put forward at the end of April by other American scientists.

In this new study, the researchers looked into the characteristics of SARS-CoV-2 and found that through its evolution over time and through the different regions where it had spread, one could observe a mutation of its ability to be transmitted. And that where the transmission of the virus was most important, SARS-CoV-2 presented a mutation called D614G of its protein S.

A mutation observed in March 2020

However, it is this protein from the coronavirus that allows it to infect the cells of our organism – and particularly those of the nose, lungs, digestive system, and heart – through its fusion with their ACE2 receptor. It is as if our cells were carrying targets allowing these infectious agents to better strike them and, in the case of SARS-CoV-2, as if the D614G mutation of protein S of this coronavirus adjusted the fire even better.

It was in March 2020, so when the epidemic began to hit hard in Europe and particularly in Italy, that this mutation was observed with even an increase in its frequency in April. An increase in viral load found in patients with Covid-19 led scientists to this discovery. According to researchers from the Scripps Research Department of Immunology, the capacity of human cells to infect this mutated coronavirus is 9 times that of the same coronavirus before its mutation.

A mutation that followed the passage from animals to humans

This would explain, through the ability of SARS-CoV-2 to transmit more effectively, the speed at which the epidemic developed in Europe in March and April of this year. But the study analyzing this mutation of the coronavirus does not allow us to conclude on its impact on the severity of the disease affecting patients infected with the virus.

On the other hand, it sheds light on the reasons which could have led to this change. The famous protein S of the coronavirus, which allows it to infect the cells of the body through the ACE2 receptor, is, as part of a complex chemical process, activated by an enzyme called furin. However, in the developments that accompanied SARS-CoV-2 in its passage from an animal species to man, it could, according to the researchers, occur a “cleavage” limiting the action of the furin essential to the activation of the infection mechanism. And the D614G mutation of protein S of the coronavirus would have emerged to compensate for this phenomenon as part of a natural adaptation of the virus to ensure the continued transmission from host to host.

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