ArticleJournal of medical virology2025
The Compensatory Effect of S375F on S371F Is Vital for Maintaining the Infectivity of SARS-CoV-2 Omicron Variants.
Article in Journal of medical virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- A cocktail of SARS-CoV-2 S stem helix domain and receptor binding domain human monoclonal antibodies prevents the emergence of viral escape mutants.Microbiology spectrum · 2026Article
- Stringent selection drives convergence toward omicron-like SARS-CoV-2 receptor-binding motifs.Nature communications · 2026Article
- Targeting asparagine and cysteine in SARS-CoV-2 variants and human pro-inflammatory mediators to alleviate COVID-19 severity; a cross-section and in-silico study.Scientific reports · 2025Article
- A cocktail of SARS-CoV-2 spike stem helix domain and receptor binding domain human monoclonal antibodies prevent the emerge of viral escape mutants.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The emergence of Omicron variants dramatically changed the transmission rate and infection characteristics compared to previously prevalent strains, primarily due to spike protein mutations. However, the impact of individual mutations remained unclear. Here, we used virus-like particle (VLP) pseudotyped to investigate the functional contributions by 12 common mutations in the spike protein. We found that the S371F mutation in the receptor binding domain (RBD) of spike protein led to a 5- and 10-fold decrease of ACE2 utilization efficiency and viral infectivity, respectively, accompanied by a 5- to 11-fold reduction of neutralization sensitivity to monoclonal antibodies. However, the S375F mutation in the RBD had a compensatory effect, rescuing the infectivity of the S371F Omicron variant. Based on molecular dynamics simulations, we proposed a "tug of war" model to explain this compensation phenomenon. These results provide a comprehensive and dynamic perspective on the evolution of this important pandemic virus.
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Registered trials
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