ArticleJournal of virology2026
Inhibition of type I interferon signaling is a conserved function of gamma-herpesvirus-encoded microRNAs.
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Herpesviruses encode multiple factors that disarm innate immune signaling to evade host anti-viral responses. Several viral microRNAs expressed by Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) disrupt the induction of type I interferons (IFN) and/or the subsequent signaling events activated through type I IFN receptors. Here, we aimed to determine whether non-human primate (NHP) γ-herpesviruses (rhesus lymphocryptovirus [rLCV], rhesus rhadinovirus [RRV], and Japanese macaque rhadinovirus [JMRV]), closely related to EBV and KSHV, use similar microRNA (miRNA)-mediated strategies to regulate IFN responses. Through functional screens, we identified multiple viral miRNAs that attenuated type I IFN-mediated activation of an IFN-stimulated response element reporter and diminished expression of interferon-stimulated genes (ISGs). Infection of primary cells with miRNA-deficient rLCVs resulted in augmented expression of ISGs. Abrogation of EBV BART miRNA homologs from rLCV, in particular, led to heightened sensitivity of latently infected cells to exogenous type I IFN. Through sequence analysis and reporter assays, we show that targets of these viral miRNAs include transcripts encoding the type I IFN receptors (IFNAR1, IFNAR2) and core components of JAK/STAT signaling pathways (JAK1, IRF9). Taken together, these data demonstrate that suppression of type I IFN responses is a conserved function for NHP γ-herpesvirus miRNAs and provide important mechanistic insight into how these viral miRNAs regulate type I IFN signaling pathways.IMPORTANCEGamma-herpesviruses establish life-long infections in their hosts. Evading anti-viral responses is a key component of long-term viral persistence. In this work, we show that small noncoding RNAs expressed by multiple non-human primate γ-herpesviruses regulate anti-viral responses by directly targeting components of the type I interferon (IFN) signaling pathway.
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