Coronavirus study: Stiffer ear proteins behind faster spread of variants

Coronavirus study: Stiffer ear proteins behind faster spread of variants

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A firmer ear protein may be the secret to the ability of the new COVID-19 variant to spread faster than the original strain, according to a new study.

Led by prof. Bing Chen, a professor of pediatrics at Boston Children’s Hospital, said the study investigated changes that occurred in the proteins of the D614G mutation, which is carried out by the variants from Brazil, South Africa and the United Kingdom. .

It is known that all these varieties spread more easily compared to the original strain.

According to these findings, published in the academic journal Science, the original stem’s ear protein would sometimes collapse on itself before it could bind properly to the ACE2 receptors of a human host, meaning that it would not fuse properly with the cells. But this problem seems to be fixed in the D614G mutation carrier variants. However, these nails also do not bind as well as the original variant.

“Say the original virus has 100 nails,” Chen explained in a press release. “Because of the shape stability, you may only have 50 percent functional. In the G614 variants, you may have 90% that are functional, so even though they do not bind as well, you are more likely to be infected.”

Since the news about the variants first came to light, many people have expressed concern that the existing COVID-19 vaccines may not protect against it. However, Chen and his team say it should not be a concern, as any peak-based vaccine – and the Pfizer, Moderna and Johnson & Johnson vaccines are all peak-based – are more likely to be immunized against the virus.

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