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

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

por Mitchell P. Ledwith, Thomas Nipper, Kaitlin A. Davis, Deniz Uresin, Zhenyu Zhang, Mariel Kleer, Denys A. Khaperskyy, Craig McCormick, Anastassia V. Komarova y Andrew Mehle

Publicado: 12 de marzo de 2025
Servidor: bioRxiv
DOI: 10.1101/2025.03.12.642847

Resumen

Summary

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 cytoplasmic NP antagonized sensing of self RNAs to counter innate immune responses. Overall, these results demonstrate that self sensing is strategically deployed by the cell to amplify the antiviral response and reveal a newly identified viral countermeasure that disrupts RIG-I activation by host RNAs.

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PREreview de Leen Arnaout y colaboradores/as

Escrito por Leen Arnaout y Claire Kuziemko

In this manuscript, Ledwith, Nipper, Davis and colleagues investigate the identity of the RNAs that activate RIG-I, a cytoplasmic sensor that triggers immune response to infection, identifying that RIG-I binds to viral RNAs, but more crucially to host RNAs that activate this antiviral state during…

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