Influenza A viruses balance ER stress with host protein synthesis shutoff

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Abstract
Significance: As intracellular parasites, viruses depend on the host cell machinery to produce and fold viral proteins. Because the capacity to fold proteins is limited, excessive viral translation of glycoproteins leads to ER stress. Unresolved ER stress drives host cells into apoptosis. We identify the expression of neuraminidase as the molecular source of influenza A virus–induced ER stress. The virus naturally balances it by the limitation of host protein production through the viral host shutoff protein NS1. The host cell mounts an unfolded protein response, creating additional protein folding reserves. Ultimately, the virus uses the stress-induced protein production capacities of the host cell to its own replication advantage.
Funding Information
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (182475)
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (182464)

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