ArticleNature communications2022
Prevalence and mechanisms of evolutionary contingency in human influenza H3N2 neuraminidase.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Genetic characterization of influenza A viruses circulating in Hong Kong, China, 2023: the first influenza epidemic after the lifting of 2.5 years of COVID-19 non-pharmaceutical interventions.Emerging microbes & infections · 2025Article
- The Ongoing Epidemics of Seasonal Influenza A(H3N2) in Hangzhou, China, and Its Viral Genetic Diversity.Viruses · 2025Article
- Co-evolution of immunity and seasonal influenza viruses.Nature reviews. Microbiology · 2023Review
- Leveraging vaccination-induced protective antibodies to define conserved epitopes on influenza N2 neuraminidase.Immunity · 2023Article
- Phylogenetic identification of influenza virus candidates for seasonal vaccines.Science advances · 2023Article
- Mutational fitness landscape of human influenza H3N2 neuraminidase.Cell reports · 2023Article
- Prevalence and mechanisms of evolutionary contingency in human influenza H3N2 neuraminidase.Nature communications · 2022Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Neuraminidase (NA) of human influenza H3N2 virus has evolved rapidly and been accumulating mutations for more than half-century. However, biophysical constraints that govern the evolutionary trajectories of NA remain largely elusive. Here, we show that among 70 natural mutations that are present in the NA of a recent human H3N2 strain, >10% are deleterious for an ancestral strain. By mapping the permissive mutations using combinatorial mutagenesis and next-generation sequencing, an extensive epistatic network is revealed. Biophysical and structural analyses further demonstrate that certain epistatic interactions can be explained by non-additive stability effect, which in turn modulates membrane trafficking and enzymatic activity of NA. Additionally, our results suggest that other biophysical mechanisms also contribute to epistasis in NA evolution. Overall, these findings not only provide mechanistic insights into the evolution of human influenza NA and elucidate its sequence-structure-function relationship, but also have important implications for the development of next-generation influenza vaccines.
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Registered trials
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