Neuraminidase Activity Modulates Cellular Coinfection during Influenza A Virus Multicycle Growth
Zijian Guo1,2, Yuanyuan He1,2, Jian Xu3
1Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, Missouri, USA.
Mbio
|April 20, 2023
Summary
Influenza A virus (IAV) neuraminidase (NA) controls cellular coinfection by depleting viral receptors. Inhibiting NA increases local spread, especially when virus infectivity is low, impacting viral evolution.
Area of Science:
- Virology
- Cellular Biology
- Infectious Diseases
Background:
- Cellular coinfection by multiple virions is crucial for viral replication and spread.
- Mechanisms controlling coinfection during multicycle viral growth are not fully understood.
- Influenza A virus (IAV) populations often contain noninfectious or partially infectious particles, necessitating multiple virions for infection.
Purpose of the Study:
- To investigate virus-intrinsic factors controlling cellular coinfection by IAV.
- To identify viral components that modulate the degree of coinfection during multicycle growth.
Main Methods:
- Quantitative fluorescence microscopy to track virion spread from single infected cells.
- Genetic and pharmacological inhibition of IAV neuraminidase (NA).
Main Results:
- IAV neuraminidase (NA) is identified as a key determinant of cellular coinfection.
- NA depletes viral receptors from infected and neighboring cells, influencing coinfection.
- Inhibition of NA increases local viral spread by enhancing virion attachment to neighboring cells, particularly when viral infectious potential is low.
Conclusions:
- Virus-intrinsic factors, like NA activity, contribute to cellular multiplicity of infection.
- Optimal NA activity levels are dependent on the virus's infectious potential.
- Modulating NA activity provides a mechanism to tune coinfection frequency, with implications for virus evolution.
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