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Nef stabilizes actin to prevent HIV-1 sensing by RIG-I-like receptors
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Nef stabilizes actin to prevent HIV-1 sensing by RIG-I-like receptors
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Journal Article
Nef stabilizes actin to prevent HIV-1 sensing by RIG-I-like receptors
2025
Overview
Sensing of viral pathogens by RIG-I-like receptors (RLRs) requires their priming via dephosphorylation mediated by the protein phosphatase 1 regulatory subunit 12 C (R12C), which is activated upon virus-induced actin rearrangements. Here, we show that the HIV-1 accessory protein Nef prevents R12C-mediated RLR priming, thereby suppressing viral sensing. HIV-1 variants containing single point mutations in Nef (F/R191A) that ablate its ability to bind the actin-modulating kinase PAK2 trigger increased interferon (IFN) responses in primary CD4
T cells, macrophages, and dendritic cells. Neutralization of IFN suppresses innate immune activation and enhances the replication of Nef-mutated HIV-1. We further demonstrate that HIV-1 encoding Nef F/R191A is sensed by MDA5 after proviral integration in an R12C-dependent manner. Mechanistically, PAK2 binding by Nef promotes actin repair and stabilization, thereby preventing re-localization of R12C to MDA5 and RIG-I and their subsequent dephosphorylation. Our data identify Nef as an antagonist of actin-R12C-mediated RLR priming, enabling HIV-1 to escape immune control.
Publisher
Nature Publishing Group,Nature Portfolio
Subject
/ Actin
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - virology
/ DEAD Box Protein 58 - metabolism
/ Dendritic Cells - immunology
/ HIV
/ Human immunodeficiency virus
/ Humans
/ Interferon-Induced Helicase, IFIH1 - metabolism
/ Kinases
/ Mutation
/ nef Gene Products, Human Immunodeficiency Virus - genetics
/ nef Gene Products, Human Immunodeficiency Virus - immunology
/ nef Gene Products, Human Immunodeficiency Virus - metabolism
/ p21-Activated Kinases - metabolism
/ Priming
/ Protein Phosphatase 1 - metabolism
/ Proteins
/ Sensors
/ Viruses
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