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Envelope surface glycoprotein gp120
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env
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Cytokines induced in vitro by HIV-1 gp120 in normal peripheral blood mononuclear cells (PBMC) include interferon-alpha (IFN-alpha) and IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), IL-6, IL-10, IL-1 alpha and IL-1 beta |
PubMed
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env
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HIV-1 gp120-mediated inhibition of IFN-alpha production involves CD4 and BDCA2 in plasmacytoid dendritic cells |
PubMed
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env
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HIV-1 gp120 inhibits CpG-A-induced secretion of IFN-alpha and IFN-beta proteins in PBMCs |
PubMed
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env
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TLR-9-induced IFN-alpha production is inhibited by both monomeric and trimeric HIV-1 gp120 in plasmacytoid dendritic cells (pDC) |
PubMed
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env
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Interferon-alpha- and interferon-gamma-induced sialoadhesin-expressing monocytes adsorb HIV-1 through interaction with the sialic acid residues on the viral envelope glycoprotein gp120 |
PubMed
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env
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Treatment of cells with IFN reduces HIV-1 gp120 incorporation, as well as HIV-1 envelope-mediated incorporation of ICAM-1, into virions resulting in viruses that exhibit a significantly decreased ability to become bound to CD4+ target cells |
PubMed
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env
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Sulfate containing galactolipids such as sulfatides on responder cells may be part of the HIV-1 gp120-membrane complex that initiates the induction of interferon (IFN) |
PubMed
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env
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Interaction of HIV-1 gp120 with cell-associated CD4 leads to the induction of IFN alpha; preincubation of cells with anti-CD4 or the presence of soluble CD4 during incubation inhibits IFN alpha induction |
PubMed
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env
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HIV-1 gp41 or gp120 synthetic peptides induce the production of interleukin (IL)-1 and tumor necrosis factor (TNF); in contrast, gp41 or gp120 synthetic peptides are able to depress the production of interferon (IFN)-alpha, IFN-gamma, and IL-2 |
PubMed
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env
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HIV-1 gp120-specific cell mediated cytotoxicity (CMC) is enhanced by IL-2 or the combination of IL-2 and IFN-alpha |
PubMed
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Envelope surface glycoprotein gp160, precursor
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env
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IFN-alpha treated effector clones (gp120+CD8+ HPB-ALL/HIV) simultaneously downregulate CD8 expression and upregulate expression of both major histocompatibility antigen complex class I (MHC-I) and HIV-1 gp120/gp160 |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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HIV-1 gp41 selectively enhances MHC class I, ICAM-1, IFN-alpha, IFN-beta, and IFN-omega expression in H9 cells |
PubMed
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Nef
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nef
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HIV-1 isolate R3A Nef mutants G2, WL58, RR106, LL165, E160NNSLL165, and DD175 fail to induce release of IFN-alpha in pDCs, suggesting that the Nef function responsible for CD4 downregulation is crucial for pDCs stimulation by R3A |
PubMed
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nef
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A highly pathogenic HIV-1 isolate R3A induces release of IFN-alpha in a Nef-dependent manner in plasmacytoid dendritic cells (pDCs) |
PubMed
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Pr55(Gag)
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gag
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HIV-1 Gag virus-like particles induce production of IFN-alpha in human monocyte-derived dendritic cells, which upregulates expression of APOBEC3G/F and increases incorporation of APOBEC3G/F into nascent virions |
PubMed
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gag
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Interferon alpha inhibits the release of HIV-1 Gag/capsid proteins from infected cells by inducing changes in posttranslational modifications of Gag proteins |
PubMed
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Tat
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tat
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HIV-1 Tat inhibits CpG-A-induced secretion of IFN-alpha and IFN-beta proteins in PBMCs |
PubMed
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tat
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HIV-1 Tat upregulates IFN-alpha secretion by macrophages, an effect that augments MIP-1alpha and MIP-1beta secretion and induces immunosuppression of uninfected T cells |
PubMed
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tat
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IFN treatment significantly reduces HIV-1 mRNA levels from a Tat defective provirus, suggesting Tat can overcome the inhibitory effects of IFN on HIV-1 replication |
PubMed
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tat
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HIV-1 Tat enhances translation of the interferon-inducible enzymes 2-5A synthetase and dsRNA-dependent protein kinase, suggesting interaction of Tat with interferons during HIV-1 replication |
PubMed
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Vif
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vif
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IFN-alpha enhances APOBEC3G expression and inhibits suppression of APOBEC3G by HIV-1 Vif |
PubMed
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Vpr
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vpr
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Synthetic HIV-1 Vpr substantially inhibits type I IFN-alpha production by pDCs without inducing apoptosis in pDCs |
PubMed
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Vpu
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vpu
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IFNalpha/ribavirin treatment in vivo induces APOBEC3G, APOBEC3F, and BST-2 expression and results in hyper-mutations in viral genome and A11G/S61A mutations in HIV-1 Vpu. These two mutations in Vpu enhances the interaction between BST-2 and Vpu |
PubMed
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vpu
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IFNalpha induces retention of viral particles on the surface of fibroblasts, T cells, or primary lymphocytes infected with HIV-1 lacking the Vpu protein. HIV-1 Vpu counteracts the IFNalpha-induced retention of virus particles |
PubMed
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reverse transcriptase
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gag-pol
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Infection of IFN-alpha-treated primary macrophages, dendritic cells, and activated PBLs by HIV-2 and SIVmac is inhibited more potently than HIV-1 and the differential inhibition by IFN-alpha is caused by defects of vDNA accumulation by RT activity |
PubMed
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gag-pol
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IFN-alpha interferes with the initiation of HIV-1 reverse transcription resulting in a significant reduction in the relative levels of HIV-1 proviral DNA |
PubMed
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