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Asp
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asp
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Antisense reading frame-derived cryptic epitopes from the gag, pol, and nef genes are inhibited by the predicted HLA-I alleles, and presented by HIV-1-infected CD8+ T-cells |
PubMed
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asp
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Antisense reading frame-derived cryptic epitopes from the env gene are inhibited by the HLA-I alleles in CD8+ T-cells |
PubMed
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Envelope surface glycoprotein gp120
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env
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The presence of HLA-C and HLA-E molecules on HIV-infected cells facilitates evasion of NK-mediated killing of anti-gp120-coated HIV-infected cells |
PubMed
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env
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HLA-C positive cells co-expressing HIV-1 gp120/gp41 fuse more rapidly and produce larger syncytia than HLA-C negative cells |
PubMed
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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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A highly conserved region of HIV-1 gp120 (amino acids 376 to 383) is recognized by an HLA-C molecule, Cw4 |
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 surface glycoprotein gp160, precursor
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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 transmembrane glycoprotein gp41
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env
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HLA-C positive cells co-expressing HIV-1 gp120/gp41 fuse more rapidly and produce larger syncytia than HLA-C negative 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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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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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 (SF2) Nef downregulates MHC-I (HLA-A/B/C); downregulation is dependent upon a proline-rich SH3 binding domain in Nef |
PubMed
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nef
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HIV-1 NL4-3 Nef downregulates HLA-A/B/C, which moderately requires the CPG-motif in Nef |
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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HIV-1 Nef clones from acute controllers display a lesser ability to downregulate CD4 and HLA class I from the cell surface, and a reduced ability to enhance virion infectivity compared to those from acute progressors |
PubMed
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nef
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HIV-1 Nef clones obtained from chronic patients infected with HIV-1 subtypes A, B, C or D show a functional hierarchy of subtype B > A/D > C for Nef-mediated HLA class I downregulation |
PubMed
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nef
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HIV-1 Nef clones, isolated from plasma of elite controllers (EC) and chronic progressors (CP), show significantly lower HLA class I downregulation activity in EC than that in CP |
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 interact with HIV-1 Nef |
PubMed
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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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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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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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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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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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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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Pr55(Gag)
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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 interact with HIV-1 Nef |
PubMed
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gag
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HIV-1 Gag peptides (Gag144-152, Gag163-171 and Gag295-304) enhance binding of KIR2DL2 to HLA-C03:04 and result in inhibition of KIR2DL2+ primary NK cells |
PubMed
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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-C/HIV-1 Gag209-218 peptide complexes bind KIR2DL2, which results in functional inhibition of primary NK cells |
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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Rev
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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
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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
|
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
|
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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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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