Structural Details Of How SARS-CoV-2 Variants Escape Immune
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A variant of SARS-CoV-2 carry mutations that enable the virus to escape some of the immune response. New study reveals key details of how these escape mutations work. The scientists used structural biology techniques to map at high resolution how important classes of neutralizing antibodies bind to the original pandemic strain of SARS-CoV-2.

Several mutations are clustered in one site, known as the "receptor binding site," on the spike protein of the virus. Other sites on the receptor-binding domain are unaffected. Scientists say next-generation vaccines and antibody therapies should focus on other vulnerable sites.

~ How 'variants of concern' escape immune response

In the study, the researchers focused mainly on three mutations in the SARS-CoV-2 spike protein: K417N, E484K and N501Y. Alone or in combination, these mutations are found in most major SARS-CoV-2 variants. All of the mutations are found in the SARS-CoV-2 receptor binding site, which the where the virus attaches to host cells. The researchers tested representative antibodies from the major classes that target the general area in and around the receptor binding site.

They found that many of these antibodies lose their ability to effectively bind and neutralize the virus when the mutations are present. Using structural imaging techniques, the team then mapped the relevant portion of the virus at atomic-scale resolution to examine how the mutations affect sites where antibodies otherwise would bind and neutralize the virus.

~ Zeroing in on points of vulnerability

The findings suggest that while antibody responses to the SARS-CoV-2 receptor binding site can be very potent in neutralizing the original Wuhan strain, certain variants are able to escape. The study underlines the fact that the three key viral mutations do not alter other vulnerable sites on the virus. The researchers specifically showed that virus-neutralizing antibodies targeting two other areas outside the receptor binding site.

This suggests that future vaccines and antibody-based treatments could provide broader protection against SARS-CoV-2 and its variants by eliciting or utilizing antibodies against parts of the virus that lie outside the receptor binding site. The researchers note that broad protection against variants may be necessary if, as seems likely, the virus becomes endemic in the human population.

Source:
https://www.scripps.edu/news-and-events/press-room/2021/20210520-wilson-variants.html
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