ArticlePLoS neglected tropical diseases2026
Pandemic-driven immune imprinting accelerates evolution of human coronavirus OC43.
Article in PLoS neglected tropical diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
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Abstract
Global pandemic interventions have reshaped host-virus dynamics, potentially altering the evolution of endemic pathogens. Here, we report accelerated genomic evolution of human coronavirus OC43 (HCoV-OC43)-a close relative of pandemic-associated coronaviruses-following recent worldwide epidemiological shifts. Bayesian analysis of longitudinal surveillance data revealed a 3.76-fold increase (8.9403 × 10 ⁻ ⁴ nucleotide substitutions/site/year, 95% HPD: 4.9075 × 10 ⁻ ⁴, 1.3053 × 10 ⁻ ³) in the spike gene substitution rate of the currently dominant genotype K post-2020. Positively selected mutations were mainly located in the spike protein, and some colocalize with antigenic epitopes. Crucially, structural modeling demonstrated that broadly neutralizing antibodies targeting conserved stem-helix (S2P6) and fusion-peptide (COV44-62/79, 76E1) epitopes of high-pathogenicity betacoronaviruses cross-bind HCoV-OC43 spike protein, establishing a mechanistic basis for immune-driven selection. These findings suggest that population-level immune imprinting may play a potential driving role in mutations within key domains of HCoV-OC43, although further validation is required. Sustained co-surveillance of co-circulating coronaviruses is imperative to anticipate emergent variants with altered pathogenicity.
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