Envelope surface glycoprotein gp120
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env
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HIV-1 CN54, JRFL, and Ada Env (gp120) upregulates IL-6, CCL2, CCL4, CXCL8, and IL-1b through TLR4 and CCR5 induction in monocyte derived macrophages and hepatic stellate cells because treatment with an anti-TLR4 antibody mitigated the response |
PubMed
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env
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HIV-1 JRFL Env (gp120) upregulates IL8 in ARPE-19 cells |
PubMed
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env
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HIV-1 ADA infection decreases production of CXCL8 (IL8), CCL2 (MCP-1), and IL6 at a basal level or after Fc receptor, complement receptor 3, or bacterial stimulation in primary human macrophages |
PubMed
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env
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HIV-1 IIIB Env (gp120) upregulates production of TNF (TNF-a), IL-17A, CCL2 (MCP1), CCL5 (RANTES), IL6, IL10, CXCL8 (IL8), CXCL1 (GRO-a), and CCL1 (I309) in stimulated monocyte derived macrophages |
PubMed
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env
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Interleukin 8 (IL-8) gene expression is enhanced in monocytes treated with HIV-1 gp120 |
PubMed
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env
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Curcumin, a potent and safe anti-inflammatory compound, inhibits HIV-1 gp120-mediated upregulation of the proinflammatory cytokines TNF-alpha and IL-6, and the chemokines IL-8, RANTES, and IP-10 in primary human genital epithelial cells |
PubMed
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env
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HIV-1 gp120 upregulates the expression of interleukin 8 (IL8) in human B cells |
PubMed
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env
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HIV-1 gp120 upregulates the expression of IL-6 and IL-8 via the p38 signaling pathway and the PI3K/Akt signaling pathway in astrocytes |
PubMed
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env
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The binding of soluble HIV-1 gp120 to TLR2 or TLR4 results in upregulation of the TNF-alpha and IL-8 production through NF-kappaB activation |
PubMed
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env
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HIV-1 gp120-mediated increases in IL-8 production in astrocytes are mediated through the NF-KappaB pathway |
PubMed
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env
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In endometrial epithelium-derived cells, gp120 from CCR5-tropic HIV-1 increases the release of monocytes/chemokines-attracting chemokines (IL-8 and GRO) and proinflammatory cytokines (TNF-beta and IL-1alpha) |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates CXCL8 (IL-8) and CCR5 expression, leading to inhibition of HIV-1 infection in cells |
PubMed
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env
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Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism |
PubMed
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env
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Exposure of TZM-bl 2 cells to CA (p24) for 1h prior to HIV gp41 decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) |
PubMed
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env
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Exposure of human T cells to HIV gp41 increases extracellular CXCL8 (IL-8) levels but to a lesser extent than CA (p24) and gp41 |
PubMed
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env
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A synthetic peptide corresponding to the immunosuppressive domain (amino acids 574-592) of HIV-1 gp41 inhibits activation of PBMCs and upregulates the expression of IL-8 in peptide-treated PBMCs |
PubMed
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env
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The interaction between HIV-1 gp41 fusion peptide and lymphocyte membrane is blocked by interleukin-8 and abolished by pre-treating the cells with heparin sulfate (HS) |
PubMed
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Nef
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nef
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HIV-1 Nef induces IL6 and CXCL8 (IL8) expression in a PIK3-PKC dependent, AKT independent manner |
PubMed
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nef
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HIV-1 Nef induces IL6 and IL8 expression through the NF-kappaB pathway |
PubMed
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nef
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HIV-1 Nef treatment induces IL6 and IL8 production in SVGA cells and primary human fetal astrocytes |
PubMed
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nef
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HIV-1 Tat and Nef combination treatment induces release of both IL-6 and IL-8 in human mesenchymal stem cells |
PubMed
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nef
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HIV-1 Nef expression by immature human and macaque dendritic cells (DCs) upregulates IL-6, IL-12, TNF-alpha, CXCL8, CCL3, and CCL4 release, but without upregulating co-stimulatory and other molecules characteristic of mature DCs |
PubMed
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Pr55(Gag)
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gag
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MVA-gag induces a significant release of cytokines such as IL-2R, IL-6, IL-8, TNF-alpha, IFN-gamma, MCP-1, MIP-1alpha, MIP-1beta, and RANTES by the infected monocyte-derived dendritic cells in comparison with uninfected cells |
PubMed
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Tat
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tat
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HIV-1 Tat upregulates CXCL8 mRNA and protein expression in CRT-MG human astroglioma cells |
PubMed
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tat
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HIV-1 Tat upregulates (CXCL8) IL8 protein expression in human monocytes and monocyte-derived dendritic cells in a TLR4-CD14-MD2 dependent manner |
PubMed
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tat
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HIV-1 Tat and Nef combination treatment induces release of both IL-6 and IL-8 in human mesenchymal stem cells |
PubMed
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tat
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HIV-1 Tat-induced upregulation of IL-8 in a time-dependent manner involves NF-kappaB and AP-1 transcription factors, activation of the p38 MAPK beta subunit, and PI3K/Akt pathway in astrocytes |
PubMed
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tat
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HIV-1 Tat upregulates IL-8 expression in astrocytes, monocytes, monocyte derived macrophages, Jurkat T-cells, HeLa cells, and human brain endothelial cells, an effect that likely contributes to the immune dysregulation observed during HIV-1 infection |
PubMed
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tat
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HIV-1 Tat downregulates the expression of adiponectin protein and upregulates the expression of IL-6, IL-8, and MCP-1 proteins in human SGBS preadipocytes |
PubMed
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tat
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HIV-1 Tat protein upregulates expression of IL-6 and IL-8 in human breast cancer cells by an NF-kappaB-dependent pathway |
PubMed
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tat
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HIV-1 Tat upregulates IL-8 and VEGF production and release from polymorphonuclear leukocytes (PMNL), indicating that PMNL recruitment by Tat is linked to angiogenesis |
PubMed
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tat
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HIV-1 Tat upregulation of IL-8 is linked to the cell cycle and involves NF-kappa B, RelA, c-rel, and CREB-binding protein |
PubMed
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tat
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Upregulation of IL-8 by HIV-1 Tat is implicated in the pathogenesis of Kaposi's sarcoma |
PubMed
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tat
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HIV-1 Tat downregulates IL-8 expression in the Raji B-cell line, however in the presence of PMA+PHA Tat induced IL-8 expression |
PubMed
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tat
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Upregulation of IL-8 by HIV-1 Tat in astrocytes is inhibited by the MEK1/2 inhibitor UO126, indicating a role for MEK1/2 in Tat-mediated chemokine induction |
PubMed
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Vpr
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vpr
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Treatment of human primary astrocytes with HIV-1 Vpr upregulates secretion of IL6, CXCL8 (IL8), MCP-1, and MIF and downregulates secretion of serpin E1, a serine proteinase inhibitor (known as PAI-1) |
PubMed
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vpr
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HIV-1 Vpr downregulates the expression of IL8 in human monocyte-derived dendritic cells |
PubMed
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vpr
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HIV-1 Vpr induced upregulation of CXCL8 (IL8) involves PI3K/Akt mediated activation of NFKB1 (NF-kappa-B) in astrocytes |
PubMed
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vpr
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HIV-1 Vpr-mediated upregulation of CXCL8 (IL8) involves NFKB1 (NF-kappa-B) |
PubMed
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vpr
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HIV-1 Vpr enhances the secretion of CXCL8 (IL8) from human fetal astrocytes |
PubMed
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vpr
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HIV-1 Vpr upregulates the expression of CXCL8 (IL8) mRNA in human fetal astrocytes |
PubMed
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vpr
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HIV-1 Vpr upregulates the expression fo CXCL8 (IL8) mRNA in SVGA in a dose-dependent manner |
PubMed
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vpr
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HIV-1 Vpr upregulates the expression of CXCL8 (IL8) mRNA in SVGA astrocytes in a time dependent fashion |
PubMed
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vpr
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HIV-1 Vpr enhances the secretion of CXCL8 (IL8) from SVGA astrocytes in a time dependent fashion |
PubMed
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vpr
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HIV-1 involves the JUN (AP-1) transcription factor in the induction of CXCL8 (IL8) in astrocytes |
PubMed
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vpr
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HIV-1 Vpr involves the CEBPD (C/EBP-delta) transcription factor in the induction of CXCL8 (IL8) in astrocytes |
PubMed
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vpr
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Vpr-mediated upregulation of CXCL8 (IL8) involves MAPK8 (JnK-MAPK) in astrocytes |
PubMed
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vpr
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Vpr-mediated upregulation of CXCL8 (IL8) in astrocytes involves p38-MAPK11 (beta isoform of p38-MAPK) |
PubMed
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vpr
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HIV-1 Vpr regulates interleukin 8 (CXCL8 (IL8)) expression, with reports showing both up- and downregulation of CXCL8 (IL8) |
PubMed
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capsid
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gag
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CXCL8-induced upregulation of HIV-1 p24 levels and 2-LTR circles is inhibited by CXCR1 or CXCR2 neutralization in HIV-1-infected monocytes-derived macrophages |
PubMed
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gag
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The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates CXCL8 (IL-8) and CCR5 expression, leading to inhibition of HIV-1 infection in cells |
PubMed
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gag
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Treatment with chemokine CXCL8 significantly upregulates HIV-1 CA (p24) levels in supernatants of both HIV-1-infected monocytes-derived macrophages as well as microglia in a dose-dependent manner |
PubMed
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gag
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Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism |
PubMed
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gag
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Simultaneous exposure of TZM-bl2 cells with HIV CA(p24) and MA (p17) decreases MA (p17)- induced production of CXCL8 (IL-8) in a dose-dependent manner |
PubMed
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gag
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Exposure of TZM-bl 2 cells to CA(p24) for 1h prior to HIV gp41 or MA (p17) decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) |
PubMed
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gag
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Exposure of human T cells to HIV CA (p24) increases extracellular CXCL8 (IL-8) levels in a dose dependent manner and to a greater extent than gp41 but to a lesser extent than MA (p17) exposures. |
PubMed
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gag
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PLA-p24-loaded human monocyte-derived dendritic cells enhance the secretion of MIP-1beta, IL-6, IL-8, and TNF-alpha in comparison with PLA-loaded cells alone |
PubMed
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integrase
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gag-pol
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The formation of 2-long terminal repeat circles, a measure of viral genome integration, is higher in CXCL8-treated, HIV-1-infected monocytes-derived macrophages and microglia, suggesting the interaction between HIV-1 IN and CXCL8 |
PubMed
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gag-pol
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IL-8 decreases HIV-1 reverse transcription and viral integration during the early infection, suggesting the interaction between HIV-1 IN and IL-8 |
PubMed
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matrix
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gag
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Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism |
PubMed
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gag
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Simultaneous exposure of TZM-bl2 cells with HIV CA(p24) and MA (p17) decreases MA (p17)- induced production of CXCL8 (IL-8) in a dose-dependent manner |
PubMed
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gag
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Exposure of TZM-bl 2 cells to CA(p24) for 1h prior to HIV MA(p17) decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) |
PubMed
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gag
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Exposure of human T cells to HIV MA (p17) increases extracellular CXCL8 (IL-8) levels in a dose dependent manner and to a greater extent than CA (p24) and gp41. |
PubMed
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gag
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The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates IL-8 and CCR5 expression, leading to inhibition of HIV-1 infection in cells |
PubMed
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gag
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Surface plasmon resonance analysis reveals that HIV-1 p17 binds IL-8 |
PubMed
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nucleocapsid
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gag
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HIV-1 NC upregulates IL8 in HEK 293T cells |
PubMed
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reverse transcriptase
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gag-pol
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IL-8 decreases HIV-1 reverse transcription and viral integration during the early infection, suggesting the interaction between HIV-1 RT and IL-8 |
PubMed
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