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• W2894772023 startingPage "490" @default.
• W2894772023 abstract "This study investigates the modulation of Type I IFN induction of an antiviral state by HIV. IFNs, including IFN-α, are key innate immune cytokines that activate the JAK/STAT pathway leading to the expression of IFN-stimulated genes. IFN-stimulated gene expression establishes the antiviral state, limiting viral infection in IFN-α-stimulated microenvironments. Our previous studies have shown that HIV proteins disrupt the induction of IFN-α by degradation of IFN-β promoter stimulator-1, an adaptor protein for the up-regulation and release of IFN-α into the local microenvironment via the retinoic acid-inducible gene 1-like receptor signaling pathway. However, IFN-α is still released from other sources such as plasmacytoid dendritic cells via TLR-dependent recognition of HIV. Here we report that the activation of the JAK/STAT pathway by IFN-α stimulation is disrupted by HIV proteins Vpu and Nef, which both reduce IFN-α induction of STAT1 phosphorylation. Thus, HIV would still be able to avoid antiviral protection induced by IFN-α in the local microenvironment. These findings show that HIV blocks multiple signaling points that would lead to the up-regulation of IFN-stimulated genes, allowing more effective replication in IFN-α-rich environments." @default.
• W2894772023 created "2018-10-12" @default.
• W2894772023 creator A5050785624 @default.
• W2894772023 creator A5060895017 @default.
• W2894772023 creator A5070365709 @default.
• W2894772023 date "2018-10-03" @default.
• W2894772023 modified "2023-10-12" @default.
• W2894772023 title "HIV blocks Type I IFN signaling through disruption of STAT1 phosphorylation" @default.
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• W2894772023 doi "https://doi.org/10.1177/1753425918803674" @default.
• W2894772023 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6513668" @default.
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• W2894772023 hasPublicationYear "2018" @default.
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