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Updated: Jun 12, 2025
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Measuring Influenza Neutralizing Antibody Responses to AH3N2 Viruses in Human Sera by Microneutralization Assays Using MDCK-SIAT1 Cells
Published on: November 22, 2017
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Antigenic drift and subtype interference shape A(H3N2) epidemic dynamics in the United States
Amanda C Perofsky1,2, John Huddleston3, Chelsea L Hansen1,2
1Fogarty International Center, National Institutes of Health, Bethesda, United States.
Elife
|September 25, 2024
Summary
Influenza A(H3N2) virus evolution, measured by genetic distance in surface proteins, predicts epidemic size and intensity. Subtype interference from influenza A(H1N1) also significantly impacts A(H3N2) epidemics.
Area of Science:
- Virology
- Epidemiology
- Evolutionary Biology
Background:
- Influenza viruses constantly evolve antigenic variants through mutations in hemagglutinin (HA) and neuraminidase (NA) surface proteins.
- Antigenic drift contributes to reinfection but its role in annual epidemic variability remains unclear.
Purpose of the Study:
- To link influenza A(H3N2) virus evolution to regional epidemic dynamics in the United States from 1997-2019.
- To identify evolutionary predictors of A(H3N2) epidemic characteristics.
Main Methods:
- Integrated phenotypic measures of HA antigenic drift with sequence-based measures of HA and NA fitness.
- Inferred antigenic and genetic distances between viruses across successive seasons.
- Estimated epidemic magnitude, severity, timing, transmission, age-specific patterns, and subtype dominance.
Main Results:
- Genetic distance in HA and NA epitopes strongly predicted A(H3N2) epidemiology.
- Increased seasonal epitope distance correlated with larger, more intense epidemics, higher transmission, and greater A(H3N2) dominance.
- Influenza A(H1N1) incidence impacted A(H3N2) epidemics more than viral evolution, suggesting subtype interference.
Conclusions:
- Genetic distance of influenza A(H3N2) surface proteins is a key evolutionary predictor of epidemic dynamics.
- Subtype interference, likely via cross-immunity, plays a major role in influenza A virus infection dynamics.
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