Genetic characteristics of influenza A and B viruses circulating in Russia in 2019–2023

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Relevance. Influenza viruses have a high potential for genetic change. These viruses are monitored annually around the world, including Russia, to determine the dominant genetic groups and select the strains to be included in influenza vaccines. Objectives of the study include: analysis of influenza virus circulation in Russia in 2019–2023, phylogenetic and molecular analysis of hemagglutinin (HA) sequences of influenza viruses, detection of mutations associated with drug resistance to neuraminidase (NA) inhibitors and M2-protein (M2) ion channel inhibitors. Materials and methods. Biological samples containing RNA of influenza viruses were studied: 410 A(H1N1)pdm09, 147 A(H3N2) and 167 B(Victoria). Sequencing of the HA, NA, M fragments was performed on the 3500xL Genetic Analyzer (Applied Biosytems). Data processing and analysis were carried out using DNASTAR, Nextclade, FluSurver and BioNumerics v.6.6 software. Results. Influenza A(H1N1)pdm09, A(H3N2), B(Victoria) viruses circulating in 2019-2023 were investigated. The highest variability of HA was observed in A(H3N2) viruses. All influenza A(H1N1)pdm09 viruses in the 2022–2023 season had a previously unknown mutation E224A in HA, which increases its affinity for α-2,3 sialic acids — receptors localized in the human lungs, to which the virus binds via HA. 2 and 3% of influenza A(H1N1)pdm09 viruses in 2019–2020 and 2022–2023, respectively, had the D222N mutation in the receptor-binding site of HA, which is associated with more severe disease. The oseltamivir and zanamivir resistance mutation H275Y in NA was detected in 2.3% of influenza A(H1N1)pdm09 viruses in 2022–2023. No oseltamivir and zanamivir resistance mutations in NA were detected in all tested influenza A(H3N2) and B viruses. Sequencing data revealed a mutation of adamantane resistance S31N in M2 in all studied influenza viruses A(H1N1)pdm09 and A(H3N2). Conclusions. The detection of amino acid substitutions in HA antigenic sites and resistance mutations in NA and M2 confirms the evolution of influenza viruses and the necessity for continuous genetic surveillance. The vast majority of currently circulating viruses remain sensitive to NA inhibitors.

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