Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Faure, Éric; Lécine, Patrick; Lipcey, Carol; Champion, Serge; Imbert, Jean

doi:10.1111/j.1432-1033.1997.00568.x

Cited by 7 publications

(9 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data indicate that even though some interactions by soluble factors (e.g., cytokines) can occur, close proximity or contact of cells is required for full induction. These results are consistent with other investigations demonstrating that conditioned medium from M and other cell types did not induce viral replication in U1 and ACH2 cells to the same magnitude as that obtained by cell-cell contact (20,27). The inductive effect required the presence of viable M , since we found that paraformaldehyde-fixed M did not induce viral replication.…”

Section: Discussionsupporting

confidence: 82%

“…Several studies have demonstrated that coculture of latently infected cells with M and other cell types induced the nuclear localization of NF-B (20,(25)(26)(27)(28). To determine the kinetics of the activation of NF-B by coculture, nuclear proteins were isolated from cocultures of U1 or ACH2 and M at 0, 3, 6, and 24 h, and the amounts of NF-B p50 and p65 in the nuclear extracts were determined by ELISA.…”

Section: Induction Of Nf-bmentioning

confidence: 99%

“…Thus, the activation of HIV-1 replication by coculture required cell-cell contact. The activation of HIV-1 replication was preceded by the activation of NF-B and cytokine secretion (27). It is probable that the activation of NF-B by coculture could involve the induction of transcription factors such as C/EBP and other cellular factors (28).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms for Macrophage-Mediated HIV-1 Induction

Devadas

Hardegen

Wahl

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

Viral latency is a long-term pathogenic condition in patients infected with HIV-1. Low but sustained virus replication in chronically infected cells can be activated by stimulation with proinflammatory cytokines such as TNF-α, IL-1 β, or other host factors. However, the precise mechanism by which cellular activation induces latently infected cells to produce virions has remained unclear. In the present report, we present evidence that activation of HIV-1 replication in latently infected U1 or ACH2 cells by human macrophages is mediated by a rapid nuclear localization of NF-κB p50/p65 dimer with concomitant increased expression of proinflammatory cytokines. Multiplexed RT-PCR amplification of mRNA isolated from cocultures of macrophages and U1 and ACH2 cells showed significant induction of IL-1β, IL-6, IL-8, TNF-α, and TGF-β expression within 3 h of coincubation. Fixation of macrophages, U-1, or ACH2 cells with paraformaldehyde before coculture completely abrogated the induction of NF-κB subunits and HIV-1 replication, suggesting that cooperative interaction between the two cell types is an essential process for cellular activation. Pretreatment of macrophage-U1 or macrophage-ACH2 cocultures with neutralizing anti-TNF-α Ab down-regulated the replication of HIV-1. In addition, pretreatment of macrophage-U1 or macrophage-ACH2 cocultures with the NF-κB inhibitor (E)3-[(4-methylphenyl)sulfonyl]-2-propenenitrile (BAY 11-7082) prevented the induction of cytokine expression, indicating a pivotal role of NF-κB-mediated signaling in the reactivation of HIV-1 in latently infected cells by macrophages. These results provide a mechanism by which macrophages induce HIV-1 replication in latently infected cells.

show abstract

Section: Discussionsupporting

confidence: 82%

Section: Induction Of Nf-bmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms for Macrophage-Mediated HIV-1 Induction

Devadas

Hardegen

Wahl

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…In addition, establishment of HIV-1 infection and induction of proviral expression in monocytes/macrophages require endogenous C/EBP factors (27,28). Although NF-B has been shown to be involved in endothelial cell-induced activation of HIV-1 transcription in infected cells (20,52), the role of C/EBP␤ in macrophageendothelial cell interactions is not known.…”

mentioning

confidence: 99%

“…One potential mechanism by which endothelial cells create a microenvironment that is favorable for HIV-1 replication is by inducing transcription factors such as NF-B or C/EBP␤ in macrophages through either direct cell contact or soluble factors (20). In this study, we specifically address the role of C/EBP␤ in the regulation of HIV-1 expression in response to endothelial cell-derived signals.…”

mentioning

confidence: 99%

Endothelial Cells Enhance Human Immunodeficiency Virus Type 1 Replication in Macrophages through a C/EBP-Dependent Mechanism

Lee

Zhou

Henderson

2001

J Virol

View full text Add to dashboard Cite

Fluid Shear Stress Activation of IκB Kinase Is Integrin-dependent

Bhullar¹,

Li²,

Miao³

et al. 1998

Journal of Biological Chemistry

132

View full text Add to dashboard Cite

Vascular endothelial cells (ECs),1 serving as a barrier between the circulating blood and the vessel wall, are constantly exposed to fluid shear stress. The focal nature of atherosclerotic lesions in the arterial tree demonstrates the critical role of flow conditions in atherogenesis. In vitro experiments using flow channels with cultured ECs have shown that shear stress activates the platelet derived-growth factor gene (1), a potent mitogen for vascular smooth muscle cells. The shear stress activation of the platelet derived-growth factor gene is through the action of the transcription factor NF-B on the shear stressresponsive element GAGACC (2, 3). In addition, electrophoresis mobility shift assay showed that nuclear extracts isolated from ECs exposed to shear stress increase their binding to oligonucleotides containing the B enhancer element (4), and a luciferase reporter driven by the B enhancer element was shown to be shear-inducible (5). However, the signal transduction pathway leading to the activation of NF-B in ECs in response to shear stress is still unclear.The transcription factor NF-B was first identified as a protein that binds to a specific DNA site in the intronic enhancer of the immunoglobulin light chain gene (6). It is composed of homo-or heterodimers of members of the Rel family of transcription factors that control the expression of numerous genes involved in the immune and inflammatory responses, cell adhesion, and growth control (see Refs. 7 and 8 for review). NF-B can be activated by many types of extracellular stimuli, including tumor necrosis factor (TNF), interleukin-1, bacterial endotoxin lipopolysaccharide, viral infection, viral proteins, antigen receptor cross-linking of T and B cells, calcium ionophores, phorbol esters, UV radiation, free radicals, hypoxia, etc. (see Ref. 9 for review). In almost all cell types, NF-B is sequestered in the cytoplasm through tight association with the inhibitory IB proteins, including IB-␣ and IB-␤. Activation of NF-B by a variety of stimuli is dependent upon the phosphorylation and subsequent degradation of the IB proteins; this allows the translocation of NF-B into the nucleus to activate various target genes. Phosphorylation of IB proteins occurs at specific residues, Ser-32 and Ser-36 of IB-␣ and Ser-19 and Ser-23 of IB-␤ (10 -13). Following phosphorylation, IB proteins are ubiquitinated and then degraded by a proteasome-dependent pathway (10 -17). The IB kinase (IKK) complex was recently purified and is composed of several subunits (18 -21). Two of the subunits, 85 and 87 kDa in size, were termed IKK␣ and IKK␤, respectively. These two proteins (with 52% homology) contain an N-terminal catalytic kinase domain and several putative protein interaction motifs, including a leucine zipper and a helix-loop-helix domain at their C termini (18,19).Integrins are a family of Ͼ20 different transmembrane heterodimers composed of ␣-and ␤-subunits that are associated noncovalently. All integrins consist of a large extracellular domain, a transmembrane region,...

show abstract

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Cited by 7 publications

References 38 publications

Mechanisms for Macrophage-Mediated HIV-1 Induction

Mechanisms for Macrophage-Mediated HIV-1 Induction

Endothelial Cells Enhance Human Immunodeficiency Virus Type 1 Replication in Macrophages through a C/EBP-Dependent Mechanism

Fluid Shear Stress Activation of IκB Kinase Is Integrin-dependent

Contact Info

Product

Resources

About