Influenza virus antagonizes self sensing by RIG-I to enhance viral replication
Ledwith, M. P.; Nipper, T.; Davis, K. A.; Uresin, D.; Komarova, A. V.; Mehle, A.
10.1101/2025.03.12.642847 bioRxivShow 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 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.
Matching journals
The top 4 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- A conserved long-range RNA interaction in SARS-CoV-2 recruits ADAR1 to enhance virus proliferation 98%
- Global remodeling of ADP-ribosylation by PARP1 suppresses influenza A virus infection 97%
- Revealing the host antiviral protein ZAP-S as an inhibitor of SARS-CoV-2 programmed ribosomal frameshifting 97%
Similar papers in this journal
Similar papers in this journal
- Structural and functional analysis of the Nipah virus polymerase complex 96%
- SPIDR: a highly multiplexed method for mapping RNA-protein interactions uncovers a potential mechanism for selective translational suppression upon cellular stress 96%
- Regulation of interferon signaling by transposon exonization 96%
Similar papers in this journal
- Viral-mediated ubiquitination impacts interactions of host proteins with viral RNA and promotes viral RNA processing 97%
- Superinfection with intact HIV-1 results in conditional replication of defective proviruses and nonsuppressible viremia in people living with HIV-1 96%
- FOXO1 promotes HIV Latency by suppressing ER stress in T cells 96%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.