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Strong evolutionary constraints against amino acid changes in the P2 subdomain of sapovirus GI.1 capsid protein VP1. | LitMetric

AI Article Synopsis

  • Sapovirus (SaV) is a nonenveloped RNA virus responsible for acute gastroenteritis, primarily affecting children, and currently lacks an effective vaccine.
  • The study found that the VP1 capsid protein, which forms the virus's outer shell, has shown strong sequence conservation in the GI.1 genotype over 40 years, while the GI.2 genotype varied more widely.
  • The research highlights a unique evolutionary mechanism preserving the VP1 P2 subdomain in GI.1, providing insights that could aid in future vaccine development against SaV.

Article Abstract

Sapovirus (SaV) is a nonenveloped RNA virus that causes acute gastroenteritis in humans. Although SaV is a clinically important pathogen in children, an effective vaccine is currently unavailable. The capsid protein VP1 of SaVs forms the outer shell of the virion and is highly diverse, as often seen in the virion-surface proteins of RNA viruses, creating an obstacle for vaccine development. We here report a unique phenomenon pertaining to the variation of SaV VP1. Phylogenetic and information entropy analyses using full-length VP1 sequences from a public database consistently showed that the amino acid sequences of the VP1 protein have been highly conserved over more than 40 years in the major epidemic genotype GI.1 but not in GI.2. Structural modeling showed that even the VP1 P2 subdomain, which is arranged on the outermost shell of the virion and presumably exposed to anti-SaV antibodies, remained highly homogeneous in GI.1 but not in GI.2. These results suggest strong evolutionary constraints against amino acid changes in the P2 subdomain of the SaV GI.1 capsid and illustrate a hitherto unappreciated mechanism, i.e., preservation of the VP1 P2 subdomain, involved in SaV survival. Our findings could have important implications for the development of an anti-SaV vaccine.

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Source
http://dx.doi.org/10.1016/j.bbrc.2024.149878DOI Listing

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