ArticleCellular & molecular immunology2022
HIV-1 Vif suppresses antiviral immunity by targeting STING.
Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 61 citations in OpenAlex.
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
- Targeting KDM3B Elicits Anti-tumor Immunity by Alleviating SHP1-mediated STING Suppression in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dual Functionality of miRNAs During HIV Infection: From Viral Genome Suppression to Immune Response Modulation.Epigenomes · 2026Review
- Nanotechnology-driven STING regulation for on-demand therapy.Acta pharmaceutica Sinica. B · 2026Review
- Article
- Two orthobunyaviruses: OYAV and EBIV co-opt the AhR-CYP1A1 axis to suppress type I interferon responses.Virologica Sinica · 2026Article
- LncRNA TLR8-AS1 Restricts HIV-1 Infection and Inflammation in Macrophages by Suppressing Arachidonic Acid Metabolism Through NFAT1.Journal of inflammation research · 2026Article
- HIV-1 derived oligonucleotides induce a type I IFN/STING dependent immune suppression reversible by targeting IFNARI.PLoS pathogens · 2026Article
- Targeted demethylation of the BRD7 promoter based on CRISPR/dCas9 system inhibits the malignant progression of nasopharyngeal carcinoma.Clinical and translational medicine · 2026Article
- HIV-1 and Its Strategy for Hiding Viral cDNA from STING-Mediated Innate Immunity.International journal of molecular sciences · 2025Review
- The lignan compound matairesinol monoglucoside induces type I interferon production in HBV infection immunity by regulating STING signaling.RSC medicinal chemistry · 2025Article
- ISG20 RestrictsMicroorganisms · 2025Article
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Profiling HIV1-host protein-protein interaction networks in patient-derived exosome proteins: impact on pathophysiology and innate immune pathways.Virology journal · 2025Article
- Research trends between acquired immune deficiency syndrome and hematological malignancies: a bibliometric analysis.Discover oncology · 2025Article
- The cGAS-STING axis: a comprehensive review from immune defense to disease pathogenesis.Immunologic research · 2025Review
- Emerging role of the cGAS-STING pathway in cardiovascular diseases: biologic function, mechanisms and targeted therapy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Lumpy skin disease virus ORF142 protein inhibits type I interferon production by disrupting interactions of TBK1 and IRF3.BMC veterinary research · 2025Article
- The STING signaling pathways and bacterial infection.Apoptosis : an international journal on programmed cell death · 2025Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
Abstract
HIV-1 infection-induced cGAS-STING-TBK1-IRF3 signaling activates innate immunity to produce type I interferon (IFN). The HIV-1 nonstructural protein viral infectivity factor (Vif) is essential in HIV-1 replication, as it degrades the host restriction factor APOBEC3G. However, whether and how it regulates the host immune response remains to be determined. In this study, we found that Vif inhibited the production of type I IFN to promote immune evasion. HIV-1 infection induced the activation of the host tyrosine kinase FRK, which subsequently phosphorylated the immunoreceptor tyrosine-based inhibitory motif (ITIM) of Vif and enhanced the interaction between Vif and the cellular tyrosine phosphatase SHP-1 to inhibit type I IFN. Mechanistically, the association of Vif with SHP-1 facilitated SHP-1 recruitment to STING and inhibited the K63-linked ubiquitination of STING at Lys337 by dephosphorylating STING at Tyr162. However, the FRK inhibitor D-65495 counteracted the phosphorylation of Vif to block the immune evasion of HIV-1 and antagonize infection. These findings reveal a previously unknown mechanism through which HIV-1 evades antiviral immunity via the ITIM-containing protein to inhibit the posttranslational modification of STING. These results provide a molecular basis for the development of new therapeutic strategies to treat HIV-1 infection.
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