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Env, gp160, envelope glycoprotein
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env
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HIV-1 gp160-derived peptide p18 presented by H-2Dd class I major histocompatibility complex molecules is processed by angiotensin-1 converting enzyme (ACE) prior to T cell stimulation by the peptide p18 |
PubMed
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Envelope surface glycoprotein gp120
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env
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Conformational changes in HIV-1 gp120, including an enhanced expression of the V3 loop of gp120 and of epitopes that are exposed upon CD4 binding, are consistent with the formation of a multimolecular complex between HLA class I and gp120/160 |
PubMed
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env
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Treatment of CD4+ T cells with HIV-1 gp120 significantly increases CD4 association with CD3, CD45RA, CD45RB, CD59, CD38, CD26 and HLA class I, and decreases that with CD45RC |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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Soluble HIV-1 gp41 enhancement effects on MHC class I and II antigen expression can be inhibited by soluble gp41-binding proteins of 45, 49 and 62 kD from human B cells |
PubMed
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env
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Soluble HIV-1 gp41 can selectively enhance MHC class I and II expression on human B cells, but does not increase expression of other cell surface antigens such as CD21 and CD54 (ICAM-1) |
PubMed
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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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Gag, Pr55
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gag
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HIV-1 Gag virus-like particles efficiently activate human monocyte-derived dendritic cells (MDDC) and induce MDDC maturation with an associated increase in the surface expression of CD80, CD86 and MHC classes I and II |
PubMed
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gag
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The PTAP L-domains in the p6 domain of HIV-1 Gag regulates ubiquitination of Gag which controls MHC-I presentation and gag processing in the DRiP pathway. |
PubMed
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gag
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HLA-B subjects are associated with HIV-1 disease progression with HIV-1 Gag sequence diversity |
PubMed
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gag
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HLA-B-restricted epitopes contribute to a broad Gag-specific CD8+ response that is associated with relative suppression of viremia |
PubMed
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gag
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Specific HIV-1 residues in Vpr, Gag, and Rev and HLA alleles (particularly B and C) confer susceptibility to the CTL response in HIV-1 infected patients |
PubMed
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gag
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Targeting HIV-1 Gag into the defective ribosomal product pathway enhances MHC class I antigen presentation and CD8+ T cell activation |
PubMed
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gag
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Protective HLA alleles have a true preference for HIV-1 Gag protein, while non-protective HLA alleles preferentially target HIV-1 Nef |
PubMed
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Nef, p27
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nef
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The HIV-1 Nef highly conserved valine-glycine-phenylalanine amino acid triplet (VGF) motif, which links the acidic cluster and the proline-rich motif, is important for downregulation of CXCR4 and MHC-I |
PubMed
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nef
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HLA-A2 molecules with HLA-A cytoplasmic domains are more downregulated by HIV-1 Nef than those with HLA-B domains. There is no downregulation of HLA-A2 with HLA-C cytoplasmic domains by Nef |
PubMed
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nef
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Asp327 and Tyr320 of MHC-I, Asp123 of Nef, and Arg225, Arg393, Lys396, Arg211, and Arg246 of mu 1 are involved in a crucial three-way electrostatic network, which results in the Nef-MHC-I CD-mu 1 complex formation |
PubMed
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nef
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HIV-1 Nef with A84D, Y135F, and G140R mutation impairs to its ability to downregulate MHC-I |
PubMed
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nef
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Double (W13A/V16R) and triple (W13A/V16R/M20A) substitution mutants of HIV-1 Nef fail to downregulate MHC-I |
PubMed
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nef
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HIV-1 Nef-mediated downregulation of MHC-I requires Nef motif EEEE(65)-dependent binding to the sorting protein PACS-2, which targets Nef to the paranuclear region and enables Nef PXXP(75) to bind and activate a trans-Golgi network localized Src kinase |
PubMed
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nef
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HIV-1 Nef-induced downregulation of MHC-I expression and MHC-I targeting to the trans-Golgi network (TGN) require the binding of Nef to PACS-1, a molecule that controls the TGN localization of the cellular protein furin |
PubMed
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nef
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HIV-1 Nef downregulates expression of MHC-I by blocking transport of MHC-I molecules to the cell surface through a mechanism that requires phosphoinositide 3-kinase (PI 3-kinase) activity |
PubMed
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nef
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Interaction of HIV-1 Nef with the mu subunit of AP adaptor complexes requires the recognition of tyrosine-based sorting signals, which likely facilitates the connection between MHC I and the clathrin-dependent sorting machinery |
PubMed
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nef
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A methionine residue at amino acid 20 in the alpha-helix domain is required for the ability of HIV-1 Nef to downregulate MHC-I expression but not for the downregulation of CD4 |
PubMed
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nef
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Four glutamic acids from position 62 to 65 in the SH3 domain of HIV-1 Nef bind to the cytoplasmic tail at position 320Y of MHC-I, and are required for the Nef-mediated downregulation of MHC-I from the cell surface |
PubMed
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nef
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HIV-1 Nef downregulates the expression of MHC-I at the surface of lymphoid, monocytic and epithelial cells, causing MHC-I molecules to be rapidly internalized, accumulated in endosomal vesicles and degraded |
PubMed
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nef
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Nef/Hck complex recruits and phosphorylates the tyrosine kinase ZAP-70, which binds class I PI3K to trigger MHC-I downregulation in primary CD4+ T cells |
PubMed
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nef
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In promonocytic cells, Nef/Hck recruits the ZAP-70 homolog Syk to downregulate MHC-I |
PubMed
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nef
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Amino acid residue Y320 in the MHC-I cytoplasmic domain and residues E62-65 and P78 in HIV-1 Nef are required for interaction with the mu subunit of AP-1 |
PubMed
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nef
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Protective HLA alleles have a true preference for HIV-1 Gag protein, while non-protective HLA alleles preferentially target HIV-1 Nef |
PubMed
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nef
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MHC-I is found in the Rab7(+) vesicles and is targeted for degradation via the activity of the Nef-interacting protein, beta-COP |
PubMed
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nef
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HIV-1 group N or O Nef alleles only weakly downregulate CD4, CD28, and class I and II MHC molecules |
PubMed
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nef
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Two distinct regions of HIV-1 Nef modulate MHC-I expression on cell surface: an N-terminal alpha-helix (residues 17-26) and a proline-rich motif (residues 75-78) |
PubMed
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nef
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HIV-1 Nef alleles derived from perinatally infected children efficiently downregulate both CD4 and MHC-I in HeLa-CD4+ cells |
PubMed
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nef
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HIV-1 Nef induces drastic and moderate downregulation of CD4 and MHC-I in resting CD4(+) T lymphocytes, respectively, but markedly upregulates cell surface levels of the MHC-II invariant chain CD74 |
PubMed
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nef
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HIV-1-specific CTL clones are suppressed to kill primary CD4(+) T cells infected with a Nef-positive HIV-1 strain (NL-432) but efficiently lysed CD4(+) T cells infected with a nef-mutant NL-M20A |
PubMed
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nef
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PxxP motifs in HIV-1 Nef induce the accumulation of CCR5 in a perinuclear compartment where both molecules co-localize with MHC-1 |
PubMed
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nef
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HIV-1 Nef mutant NefAAAA, which cannot interact with the endosomal sorting protein PACS-1, increases the number of cells containing long and stable tubules, which allows the internalization of MHC-1 into the tubules from the cell surface |
PubMed
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nef
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Different levels of the modulation of MHC-1 are induced by different Nef proteins derived from HIV-1 infected adults and children |
PubMed
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nef
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HIV-1 Nef-mediated cellular phenotypes, including MHC-1 and CD4 downregulation, are differentially expressed as a function of intracellular Nef concentrations |
PubMed
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nef
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HIV-1 Nef downregulates human MHC-I more efficiently than murine MHC-I molecules in HeLa cells, and Nef does not function efficiently in murine endothelial cells |
PubMed
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nef
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HIV-1 selectively downregulates HLA-A and HLA-B but does not significantly affect HLA-C or HLA-E, which allows HIV-infected cells to avoid NK cell-mediated lysis |
PubMed
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nef
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Downregulation of MHC-I by Nef decreases the incorporation of MHC-I molecules into virions, but does not decrease virion infectivity |
PubMed
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nef
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Downregulation of major histocompatibility class I on human dendritic cells by HIV-1 Nef impairs antigen presentation to HIV-specific CD8+ T lymphocytes |
PubMed
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nef
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A dominant-negative mutant protein derived from Hck, (composed of the N-terminal region, SH2, and SH3 domains) interacts with HIV-1 Nef and inhibits Nef-induced downregulation of MHC class I |
PubMed
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nef
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Deletion of the 19 N-terminal amino acids including the myristoylation signal from HIV-1 Nef inhibits both MHC-I and CD4 downregulation while preserving most CTL, T-helper and B-cell epitopes |
PubMed
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Rev, p19
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rev
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Specific HIV-1 residues in Vpr, Gag, and Rev and HLA alleles (particularly B and C) confer susceptibility to the CTL response in HIV-1 infected patients |
PubMed
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Tat, p14
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tat
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Four mutations (C27S, K51T, R55L, and G79A) on HIV-1 Tat result in the loss of the deleterious effects of Tat on the expression of MHC I, IL-2, and CD25 genes compared with wild-type Tat in Jurkat cells |
PubMed
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tat
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HIV-1 Tat upregulates MHC class I in monocyte-derived dendritic cells and CD8(+) T cells, thereby driving T cell-mediated immune responses |
PubMed
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tat
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HIV-1 Tat represses the MHC class I gene promoter by binding to and repressing TAFII250, a component of the general transcription factor TFIID, suggesting a mechanism for HIV-1 to downregulate MHC class I expression and avoid immune surveillance |
PubMed
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Vpr, p15
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vpr
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Specific HIV-1 residues in Vpr, Gag, and Rev and HLA alleles (particularly B and C) confer susceptibility to the CTL response in HIV-1 infected patients |
PubMed
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Vpu, p16
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vpu
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HLA class I-associated immune responses have minor effects on Vpu variability, suggesting that Vpu conformation and function are preserved through many possible combinations of primary and secondary polymorphisms |
PubMed
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vpu
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Using antibodies specific to MHC class I A, B, and C molecules (clone W6/32), HIV-1 Vpu protein has been shown to downregulate the expression of MHC class I molecules on the surface of HIV-1 infected cells |
PubMed
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