Human Immunodeficiency Virus Type 1 (HIV‐1) Plasma Virus Load and Markers of Immune Activation among HIV‐Infected Female Sex Workers with Sexually Transmitted Diseases in Abidjan, Côte d'Ivoire

Nkengasong, John N.; Kestens, Luc; Ghys, Peter D.; Koblavi-Dème, Stéphania; Bilé, Ebi; Kalou, Mireille; Ya, Leonard Kouadio; Traoré-Ettiègne, Virginie; Maurice, Chantal; Laga, Marie; Wiktor, Stefan Z.; Greenberg, Alan E.

doi:10.1086/319855

Cited by 30 publications

(25 citation statements)

References 15 publications

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“…It has been reported that with respect to the effects of individual STDs on HIV load, only genital ulcers and gonococcal infection are associated with higher viral load. Chlamydia, which is very close to GC in terms of infectious properties, does not enhance HIV load (64). We did not examine the specificity of GC to HIV infection of DCs.…”

Section: Discussionmentioning

confidence: 95%

Neisseria gonorrhoeaeEnhances Infection of Dendritic Cells by HIV Type 1

Zhang

Báfica

et al. 2005

The Journal of Immunology

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Clinical studies indicate that Neisseria gonorrhoeae (gonococci (GC)) has the capacity to enhance HIV type 1 (HIV-1) infection. We studied whether GC enhances HIV infection of activated dendritic cells (DCs). The results show that GC can dramatically enhance HIV replication in human DCs during coinfection. The GC component responsible for HIV infection enhancement may be peptidoglycan, which activates TLR2. TLR2 involvement is suggested by bacterial lipoprotein, a TLR2-specific inducer, which stimulates a strong enhancement of HIV infection by human DCs. Moreover, participation of TLR2 is further implicated because GC is unable to stimulate expression of HIV in DCs of TLR2-deficient HIV-1-transgenic mice. These results provide one potential mechanism through which GC infection increases HIV replication in patients infected with both GC and HIV.

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Section: Discussionmentioning

confidence: 95%

Neisseria gonorrhoeaeEnhances Infection of Dendritic Cells by HIV Type 1

Zhang

Báfica

et al. 2005

The Journal of Immunology

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“…Staining and analysis were performed in phosphate-buffered saline (PBS) with 1% fetal calf serum (FCS). For intracellular perforin analyses, after surface-marker labeling, cells were fixed and permeabilized with PermeaFix (Ortho Diagnostic Systems, Raritan, NJ) before intracellular staining with antiperforin monoclonal antibody (27)(28)(29)(30)(31)(32)(33)(34)(35); BD PharMingen). Isotype-matched controls were used for both surface and intracellular staining.…”

Section: Flow Cytometrymentioning

confidence: 99%

IL-8 responsiveness defines a subset of CD8 T cells poised to kill

Hess

Means

Autissier

et al. 2004

Blood

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CD8 T cells play a key role in host defense against intracellular pathogens. Efficient migration of these cells into sites of infection is therefore intimately linked to their effector function. The molecular mechanisms that control CD8 T-cell trafficking into sites of infection and inflammation are not well understood, but the chemokine/chemokine receptor system is thought to orchestrate this process. Here we systematically examined the chemokine receptor profile expressed on human CD8 T cells. Surprisingly, we found that CXC chemokine receptor 1 (CXCR1), the predominant neutrophil chemokine receptor, defined a novel interleukin-8/CXC ligand 8 (IL-8/CXCL8)-responsive CD8 Tcell subset that was enriched in perforin, granzyme B, and interferon-␥ (IFN␥), and had high cytotoxic potential. CXCR1 expression was down-regulated by antigen stimulation both in vitro and in vivo, suggesting antigen-dependent shaping of the migratory characteristics of CD8 T cells. On virus-specific CD8 T cells from persons with a history of Epstein-Barr virus (EBV) and influenza infection, CXCR1 expression was restricted to terminally differentiated effector memory cells. In HIV-1 infection, CXCR1-expressing HIV-1-specific CD8 T cells were present only in persons who were able to control HIV-1 replication during structured treatment interruptions. Thus, CXCR1 identifies a subset of CD8 T cells poised for immediate cytotoxicity and early recruitment into sites of innate immune system activation. IntroductionA central feature of the adaptive immune response is the generation of antigen-specific effector and memory T cells. Naive T cells are induced to proliferate (clonal expansion) and differentiate upon encounter with cognate antigen presented by dendritic cells in secondary lymphoid structures. 1,2 Activation and subsequent differentiation lead to the formation of several CD8 T-cell memory subsets with different functional and migratory properties, classified as central memory, effector memory, and terminally differentiated effector memory cell subsets. 3,4 Terminally differentiated effector memory CD8 T cells express high levels of perforin, granzyme A and B, and Fas ligand; are highly cytotoxic; and home to sites of infection and inflammation. Effector memory CD8 T cells are thought to allow for a recall response in the tissue, as these cells survey nonlymphoid organs in search of cognate antigen and, while able to produce interferon-␥ (IFN␥) upon antigen recognition, are only moderately cytotoxic. In contrast, central memory cells recirculate between the blood and the lymphoid compartment and are thought to provide a pool of antigen-experienced cells with a high proliferative capacity but a lower activation threshold than naive cells, thus allowing for a more rapid generation of effector cells during a recall response. 3,5,6 Distinct migratory properties are a determining factor in T-cell subset function. Homing characteristics are thought to be controlled by the expression pattern of adhesion molecules and chemokine receptors acquired...

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“…Symptomatic Ng infection is associated with increased detection of viral-derived nucleic acids from genital secretions of men and women (11)(12)(13), and this effect was reversed upon successful Ng treatment. Concurrent Ng infection is associated with an increase in HIV-1 viremia (14,15), decreases in HIV-1 target lymphocyte [cluster of differentiation 4-positive (CD4 + ) T-cell] counts (14), and a decrease in effector [cluster of differentiation 8-positive (CD8 + ) T-cell] lymphocyte responses (16). Because of the impact of Ng on HIV-1 shedding, coinfection is associated with a two-to fivefold increase in male-to-female transmission rates (3).…”

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confidence: 99%

Neisseria gonorrhoeae-derived heptose elicits an innate immune response and drives HIV-1 expression

Malott¹,

Keller

Gaudet³

et al. 2013

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

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Clinical and epidemiological synergy exists between the globally important sexually transmitted infections, gonorrhea and HIV. Neisseria gonorrhoeae , which causes gonorrhea, is particularly adept at driving HIV-1 expression, but the molecular determinants of this relationship remain undefined. N. gonorrhoeae liberates a soluble factor that potently induces expression from the HIV-1 LTR in coinfected cluster of differentiation 4-positive (CD4 + ) T lymphocytes, but this factor is not a previously described innate effector. A genome-wide mutagenesis approach was undertaken to reveal which component(s) of N. gonorrhoeae induce HIV-1 expression in CD4 + T lymphocytes. A mutation in the ADP-heptose biosynthesis gene, hldA , rendered the bacteria unable to induce HIV-1 expression. The hldA mutant has a truncated lipooligosaccharide structure, contains lipid A in its outer membrane, and remains bioactive in a TLR4 reporter-based assay but did not induce HIV-1 expression. Mass spectrometry analysis of extensively fractionated N. gonorrhoeae- derived supernatants revealed that the LTR-inducing fraction contained a compound having a mass consistent with heptose-monophosphate (HMP). Heptose is a carbohydrate common in microbes but is absent from the mammalian glycome. Although ADP-heptose biosynthesis is common among Gram-negative bacteria, and heptose is a core component of most lipopolysaccharides, N. gonorrhoeae is peculiar in that it effectively liberates HMP during growth. This N. gonorrhoeae- derived HMP activates CD4 + T cells to invoke an NF-κB–dependent transcriptional response that drives HIV-1 expression and viral production. Our study thereby shows that heptose is a microbial-specific product that is sensed as an innate immune agonist and unveils the molecular link between N. gonorrhoeae and HIV-1.

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Human Immunodeficiency Virus Type 1 (HIV‐1) Plasma Virus Load and Markers of Immune Activation among HIV‐Infected Female Sex Workers with Sexually Transmitted Diseases in Abidjan, Côte d'Ivoire

Cited by 30 publications

References 15 publications

Neisseria gonorrhoeaeEnhances Infection of Dendritic Cells by HIV Type 1

Neisseria gonorrhoeaeEnhances Infection of Dendritic Cells by HIV Type 1

IL-8 responsiveness defines a subset of CD8 T cells poised to kill

Neisseria gonorrhoeae-derived heptose elicits an innate immune response and drives HIV-1 expression

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