CD14 is involved in control of human immunodeficiency virus type 1 expression in latently infected cells by lipopolysaccharide.

Bagasra, Omar; Wright, Samuel D.; Seshamma, Thikkavarapu; Oakes, Joseph W.; Pomerantz, Roger J.

doi:10.1073/pnas.89.14.6285

Cited by 63 publications

(31 citation statements)

References 31 publications

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“…These latter studies have been strengthened by the observation that macrophages are the major source of HIV during certain opportunistic infections (2) and that the major cellular targets for these microbial pathogens are macrophages (2,16,17). In addition, several studies have shown that the Gram-negative bacterial cell wall constituent, LPS, enhanced HIV replication in monocytoid cell lines (18,19); however, other studies have reported the induction of resistance of macrophages to HIV infection upon LPS stimulation (20)(21)(22). Such a discrepancy could have resulted from differences in methods used for macrophage propagation or in virus strains used in the experiments.…”

Section: Introductionmentioning

confidence: 91%

“…Several studies have demonstrated that the CC chemokines have little or no suppressive activity against M-tropic HIV replication in MDM (25,31,65) or monocytoid cell line (66). Other studies (18,19). In the present study, stimulation with LPS and other bacterial products (SACE and LAM) had dichotomous effects on HIV replication, depending on the virus phenotypes in question, and such outcomes resulted from a delicate balance between HIV enhancing and suppressive factors produced by the stimulated macrophages.…”

Section: Discussionmentioning

confidence: 99%

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Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Moriuchi

Moriuchi²,

Turner³

et al. 1998

J. Clin. Invest.

106

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Microbial coinfections variably influence HIV-1 infection through immune activation or direct interaction of microorganisms with HIV-1 or its target cells. In this study, we investigated whether exposure of macrophages to bacterial products impacts the susceptibility of these cells to HIV-1 of different cellular tropisms.We demonstrate that (1) macrophages exposed to bacterial cell wall components such as lipopolysaccharide (

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Section: Introductionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Moriuchi

Moriuchi²,

Turner³

et al. 1998

J. Clin. Invest.

106

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“…A recent study demonstrated that expression of CD14 was necessary for LPS-induced HIV-1 production in certain monocytic cell lines (49). Since human liver sinusoidal endothelial cells can be readily infected with HIV-1 in vitro (50), it will be important to establish whether sCD14 plays a role in LPS-induced activation of HIV-1 gene expression in virus-infected endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Cell-free pool of CD14 mediates activation of transcription factor NF-kappa B by lipopolysaccharide in human endothelial cells.

Read

Cordle

Veach

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

127

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Lipopolysaccharide (LPS), a maijor envelope component of Gram-negative bacteria, is the most frequent causative agent of septic shock and disseminated intravascular coagulation. LPS activates both CD14-positive (monocytes, macrophages, polymorphonuclear leukocytes) and CD14-negative (B-cell lines, endothelial cells) cells. CD14, a 55-kDa glycosyl-phosphatidylinositol-anchored membrane protein present on mature myeloid cells, serves as a receptor for LPS in complex with a soluble (serum-derived) LPS-binding protein (LBP). In this report, we show that human umbilical vein endothelial cells (HUVEC), which do not express measurable CD14 protein, become 3000-fold more sensitive to LPS-induced activation in the presence of serum, as measured by activation of the transcription factor NF-KB and expression of mRNA encoding tissue factor, a procoagulant molecule. This enhanced responsiveness of HUVEC is specifically mediated by the cell-free pool of CD14 (soluble CD14, sCD14) found in serum. The role of sCD14 in HUVEC activation by LPS was established by .(l) the blocking effect of monoclonal anti-CD14 antibodies which discriminate between cell-bound and sCD14,(ii) the lack of the serum-enhancing effect after immunodepletion of sCD14, and (iiW) establishing a reconstituted system in which recombinant sCD14 was sufficient to enhance the effects of LPS in the absence of serum and without a requirement for LBP. Thus, this mechanism of endothelial cell activation by LPS involves a cell-free pool of sCD14 most likely shed from CD14-positive cells of the monocytic lineage.

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“…If the hypothesis of extracellular structural mimicry is correct, then HIV-1 and GBV-C protein structures must show some degree of mutual homology. Several groups have shown neutralization of diverse isolates of HIV-1 by GBV-C E2 Abs or synthetic peptides, but have found no structural homology [9,12,[38][39].…”

Section: The Flaviviridae and Hiv-1 Homologous Mirnasmentioning

confidence: 99%

Use of Flaviviral genetic fragments as a potential prevention strategy for HIV-1 Silencing

Sheraz

Kanak

Hasan

et al. 2016

J Infect Dev Ctries

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Introduction: Coinfection with certain members of the Flaviviridae, such as Dengue Virus (DV), West Nile Virus (WNV) Yellow Fever Virus (YFV) and most importantly, GBV-C have been documented to reduce HIV-1 viral load in vivo. Numerous studies strongly support the notion that persistent coinfection with non-pathogenic virus prolongs survival in HIV-1 infected individuals. Coinfected individuals show higher CD4+ cell counts, lower HIV-1 RNA viral loads and live three times longer than clinically matched HIV-1 monoinfected patients. We have previously shown that one of the major anti-HIV defenses conferred by GBV-C coinfection is the upregulation of intracellular miRNAs in CD4+ cells that share significant mutual homologies with GBV-C and HIV-1 (>80%) genomes. Methodology: Genome-wide bioinformatics analyses were carried out to search for miRNA binding sites in mutual homologies between HIV and several members of the Flaviviridae Results: Several miRNAs shared significant mutual homology with HIV-1 genetic sequences and GBV-A, B, C, DV, WNV and YFV. These may be responsible for beneficial effects in HIV-1 infected individuals. Three highly mutual homologous miRNAs (i.e. miR-627-5, miR-369-5 and miR-548f), expressed in CD4+ cell lines, reduce HIV-1 replication by up to 90% whereas miRNAs with low mutual homologies (i.e. miR-34-1 and miR-508) impart only slight inhibition of HIV-1. Conclusion: We hypothesize that a recombinant GBV-C-based vector can be constructed which expresses several beneficial genetic motifs of the Flaviviridae without causing any side effects while stimulating a wide array of beneficial miRNAs that can more efficiently prevent HIV-1 infection.

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CD14 is involved in control of human immunodeficiency virus type 1 expression in latently infected cells by lipopolysaccharide.

Cited by 63 publications

References 31 publications

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Cell-free pool of CD14 mediates activation of transcription factor NF-kappa B by lipopolysaccharide in human endothelial cells.

Use of Flaviviral genetic fragments as a potential prevention strategy for HIV-1 Silencing

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