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

Lee, Eileen S.; Zhou, Huiyu; Henderson, Andrew J.

doi:10.1128/jvi.75.20.9703-9712.2001

Cited by 18 publications

(21 citation statements)

References 63 publications

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“…To examine the binding of nuclear extracts from infected cells to the labeled NF-B probe, 5 l of lysate (mock, rSV5, rSV5⌬SH, or rSV5⌬SHϩMuV-SH infected), the NF-B probe (about 40,000 cpm), 2 l of 10ϫ EMSA buffer (25 mM HEPES, pH 7.5, 60 mM NaCl, 9% glycerol, 1 mM EDTA, 7.5 mM DTT, 50 mM MgCl 2 ), 2 l of poly(dI-dC) (1 g/l), and water up to 20 l were incubated together at room temperature for 30 min. As controls, unlabeled NF-B oligomers and nonspecific competitor AP-1 primers (AP1 5Ј, 5Ј-GGG GAA GCT TTG ACT CA-3Ј) (25) were added to nuclear lysates from mock-, rSV5-, rSV5⌬SH-, or rSV5⌬SHϩMuV-SH-infected cells. Nuclear extracts and labeled oligomer mix-…”

Section: Methodsmentioning

confidence: 99%

Function of Small Hydrophobic Proteins of Paramyxovirus

Wilson¹,

Fuentes²,

Wang

et al. 2006

J Virol

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110

108

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Section: Methodsmentioning

confidence: 99%

Function of Small Hydrophobic Proteins of Paramyxovirus

Wilson¹,

Fuentes²,

Wang

et al. 2006

J Virol

Self Cite

110

108

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“…Members of this family include C/EBP , C/EBP (also termed LAP, NF-IL6 , IL-6DBP, AGP/EBP), C/EBP , C/EBP (NF-IL6) and C/EBP (Mueller et al, 1990). Interestingly, regulatory sequences of HIV-1, which are located within the LTR, harbor three C/EBP sites that bind C/EBP (Tesmer et al, 1993) (Fig 2) and these sites are essential to initiate virus replication in cells of the monocyte/macrophage lineage (Henderson et al, 1995) and in endothelial cells as recently described (Lee et al, 2001). PKA and transcription factors of the ATF/CREB family may be critical for HIV-1 expression and regulation.…”

Section: 22mentioning

confidence: 95%

Emerging Roles of Prostaglandins in HIV-1 Transcription

Dumais¹,

Côté²,

Ducharme³

2011

HIV and AIDS - Updates on Biology, Immunology, Epidemiology and Treatment Strategies

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“…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%

“…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). NF-B plays a critical role in the activation of HIV-1 gene expression by cytokines and other stimuli, but the pathways that regulate the switch from latency to the infectious phase have not been elucidated.…”

mentioning

confidence: 99%

Mechanisms for Macrophage-Mediated HIV-1 Induction

Devadas

Hardegen

Wahl

et al. 2004

The Journal of Immunology

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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.

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

Cited by 18 publications

References 63 publications

Function of Small Hydrophobic Proteins of Paramyxovirus

Function of Small Hydrophobic Proteins of Paramyxovirus

Emerging Roles of Prostaglandins in HIV-1 Transcription

Mechanisms for Macrophage-Mediated HIV-1 Induction

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