Influenza virus antagonizes self sensing by RIG-I to enhance viral replication.

ABSTRACT: Innate immune sensors must finely distinguish pathogens from the host to mount a response only during infection. RIG-I is cytoplasmic sensor that surveils for foreign RNAs. When activated, RIG-I triggers a broad antiviral response that is a major regulator of RNA virus infection. Here were show that RIG-I not only bound viral RNAs, but was activated by host RNAs to amplify the antiviral state. These were primarily non-coding RNAs transcribed by RNA polymerase III. They were benign under normal conditions but became immunogenic during influenza virus infection where they signaled via RIG-I to suppress viral replication. This same class of RNAs was bound by influenza virus nucleoprotein (NP), which normally functions to encapsidate the viral genome. NP interacted with RIG-I and antagonized s

SUBMITTER: Ledwith MP 

PROVIDER: S-EPMC11952396 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature