AI Article Synopsis
- Many SARS-CoV-2 variants have developed mutations that impact how the virus infects and evades the immune system.
- Recent research shows that specific mutations (L452R and Y453F) in the virus's spike protein help it escape detection by a certain type of immune response known as HLA-A24-restricted cellular immunity.
- These mutations not only enhance the virus's ability to infect cells but also increase its stability and replication, highlighting a potential ongoing threat from the virus's evolution.
Article Abstract
Many SARS-CoV-2 variants with naturally acquired mutations have emerged. These mutations can affect viral properties such as infectivity and immune resistance. Although the sensitivity of naturally occurring SARS-CoV-2 variants to humoral immunity has been investigated, sensitivity to human leukocyte antigen (HLA)-restricted cellular immunity remains largely unexplored. Here, we demonstrate that two recently emerging mutations in the receptor-binding domain of the SARS-CoV-2 spike protein, L452R (in B.1.427/429 and B.1.617) and Y453F (in B.1.1.298), confer escape from HLA-A24-restricted cellular immunity. These mutations reinforce affinity toward the host entry receptor ACE2. Notably, the L452R mutation increases spike stability, viral infectivity, viral fusogenicity, and thereby promotes viral replication. These data suggest that HLA-restricted cellular immunity potentially affects the evolution of viral phenotypes and that a further threat of the SARS-CoV-2 pandemic is escape from cellular immunity.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8205251 | PMC |
| http://dx.doi.org/10.1016/j.chom.2021.06.006 | DOI Listing |
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