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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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 increases the levels of prostaglandin E2 (PGE2) and IL-1 in human monocytes |
PubMed
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env
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Upregulation of the human proteins CCL2, CX3CL1, IL-1beta, and CXCL10 by HIV-1 gp120 involves CB2 receptor in mesencephalic neuronal/glial culture model |
PubMed
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env
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HIV-1 gp120 induces human glial cells to release more TNF-alpha and IL-1beta than untreated cells |
PubMed
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env
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HIV-1 coat protein gp120 stimulates the release of interleukin-1beta from human neuroblastoma cells and causes cell death |
PubMed
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env
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Concomitant activation of Lyn, Pyk2, and class IA PI3K are required for gp120-induced IL-1beta production |
PubMed
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env
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HIV-1 gp120 induces IL-1beta release from macrophages in a time- and concentration-dependent manner through binding to the chemokine receptor CCR5 and coupling to G(i)alpha protein |
PubMed
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env
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Matrix metalloproteinases MMP2 and MMP9 participate in the maturation process of cleavage and activation of IL-1beta based on the intracerebroventricular injection of the HIV-1 envelope glycoprotein gp120 |
PubMed
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env
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HIV-1 gp120 stimulates monocytes to release TNF-alpha, IL-1 beta, IL-6, and granulocyte-macrophage-CSF, and this effect can be blocked with soluble CD4 |
PubMed
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env
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CD23 protein membrane expression is upregulated by HIV-1 gp120 and this upregulation induces the production of nitric oxide (NO) and IL-1beta |
PubMed
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Envelope surface glycoprotein gp160, precursor
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env
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IL-1 and TNF-alpha production are induced by the treatment of cells with HIV-1 gp160 |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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HIV-1 inhibitors T20, NVP, AZT, and raltegravir significantly attenuate HIV-1-induced IL-1B production and NLRP3 activation, suggesting that HIV-1 gp41, RT, and IN are required for pro-IL-1B expression and NLRP3 activation |
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 gp41 stimulates microglial cell production of cytokines (TNF-alpha, IL-1beta, and IL-6) and chemokines (RANTES and MIP-1alpha) |
PubMed
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Nef
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nef
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Treatment of human monocyte-derived macrophages with soluble recombinant HIV-1 Nef (rNef) upregulates the transcription of genes for several inflammatory factors, including IL-1beta, which is released upon rNef treatment |
PubMed
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nef
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IL-1beta, IL-12, and IL-15 are factors involved in the upregulation of IFN-gamma expression in coculture between Nef-pulsed iDCs and NK cells |
PubMed
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nef
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HIV-1 Nef and ALK show similar effects by increasing different cytokines/chemokines, such as IL-1beta, TNF-alpha, and RANTES, that may be relevant for HAD pathogenesis |
PubMed
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nef
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Expression of Nef from the brain-derived HIV-1 isolate YU-2 in astrocytes significantly upregulates IL-1beta expression |
PubMed
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Pr55(Gag)
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gag
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HIV-1 Gag co-localizes with bioactive IL-1B in germinal center of HIV-1 infected patients |
PubMed
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gag
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Stimulation of HIV-1 infected human adipocytes by TNF-alpha and IL-1beta increases the levels of HIV-1 Gag production |
PubMed
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Tat
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tat
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HIV-1 Tat inhibitor didehydro-Cortistatin A (dCA), an analog of a natural steroidal alkaloid, potently inhibits Tat-mediated modulation of IL-1beta, TNF-alpha and MCP-1 |
PubMed
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tat
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HIV-1 Tat upregulates IL-1beta expression in a variety of cell types, including macrophages, astrocytes, microglial cells, monocytes, and primary blood mononuclear cells (PBMCs) |
PubMed
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tat
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HIV-1 Tat- and oxovanadate-treated microglial cells synergistically induce release of TNF-alpha and IL-1beta proteins, which involves CD45 and ERK1/2 signaling pathways |
PubMed
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tat
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Specific C/EBP and NF-kappaB transcription factor binding elements within the IL-1beta promoter are involved in Tat regulation of IL-1beta production |
PubMed
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tat
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Phospholipase C/protein kinase C pathway-dependent phosphorylation of p44/42 and JNK MAP kinases is partially involved in IL-1beta induction by HIV-1 Tat |
PubMed
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tat
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Over-expression of PPARalpha or PPARgamma attenuates Tat-induced up-regulation of inflammatory mediators, such as interleukin (IL)-1beta, tumor necrosis factor-alpha, CCL2, and E-selectin |
PubMed
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tat
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Sulfated polymannuroguluronate (SPMG) significantly reverses HIV-1 Tat-induced release of pro-inflammatory cytokines such as TNF-alpha, IL-1beta, and IL-6 in THP-1 cells |
PubMed
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tat
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IL-1 stimulated NO production and iNOS mRNA expression are down-regulated by pretreatment with HIV-1 Tat-SOD fusion proteins in cultured chondrocytes |
PubMed
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tat
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HIV-1 Tat downregulates IL-1beta expression in U937 cells through the inhibition of CD26 |
PubMed
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tat
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IL-1beta, TNF-alpha, and IFN-gamma synergize with HIV-1 Tat to promote in nude mice the development of angioproliferative Kaposi's sarcoma-like lesions |
PubMed
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Vpr
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vpr
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HIV-1 Vpr activates IL-1B activity in MDMs |
PubMed
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integrase
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gag-pol
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HIV-1 inhibitors T20, NVP, AZT, and raltegravir significantly attenuate HIV-1-induced IL-1B production and NLRP3 activation, suggesting that HIV-1 gp41, RT, and IN are required for pro-IL-1B expression and NLRP3 activation |
PubMed
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retropepsin
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gag-pol
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HIV-1 protease cleaves pro-interleukin 1 beta (pro-IL-1 beta) in vitro at amino acid positions 23-24 and 98-99 |
PubMed
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reverse transcriptase
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gag-pol
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HIV-1 inhibitors T20, NVP, AZT, and raltegravir significantly attenuate HIV-1-induced IL-1B production and NLRP3 activation, suggesting that HIV-1 gp41, RT, and IN are required for pro-IL-1B expression and NLRP3 activation |
PubMed
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