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HIV-1 indcued genes in human monocyte-derived macrophages

ABSTRACT: HIV-1 infection of monocyte-derived macrophages does not elicit a detectable type I IFN response in vitro, however, previously published data has shown that blocking STAT1 and STAT3 inhibits HIV-1 replication. Here we test to see if low levels of IFN inducible genes are detectable in human monocyte-derived macrophages that have been infected with HIV-1 in vitro.

ORGANISM(S): Homo sapiens

PROVIDER: GSE108897 | GEO | 2018/01/09

SECONDARY ACCESSION(S): PRJNA429041

REPOSITORIES: GEO

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IFN-a-induced monocyte phenotype in chronic unsuppressed HIV infection

Project description:Abstract Objectives: HIV infection dysregulates the innate immune system and alters leukocyte gene expression. The objectives were two fold: to characterize the impact of HIV infection on peripheral monocyte gene expression and to identify the predominant factor(s) responsible for altered gene expression. Design and methods: In a cross-sectional study, CD14+ monocytes were isolated from 11 HIV seronegative controls, 22 HIV seropositive subjects with low viral loads (LVL, <= 10,000 RNA copies/ml) and 22 HIV seropositive subjects with high viral loads (HVL, > 10,000 RNA/copies/ml). Total monocyte RNA was hybridized to 55K probes on high-density microarrays to obtained detailed gene expression profiles from control, LVL and HVL subjects. As potential candidates for immune disruption, we evaluated three HIV-related peripheral factors, interferon (IFN)-a, IFN-a and lipopolysaccharide (LPS) by treating HIV seronegative CD14+ monocytes for 48h and then analyzing gene expression. Plasma collected from the HIV subjects were quantified for LPS using a Pyrogene assay and for soluble (s) CD14 by ELISA. Results: In this cross-sectional study of HIV subjects (n=44), viral loads above 10,000 RNA copies/ml were associated with an activated phenotype. Characterization of the gene expression pattern by Gene Ontology reveals an ongoing immune response to viral infection including inflammation and chemotaxis. Gene expression analysis of in vitro treated HIV seronegative monocytes with IFN-a, IFN-g or LPS demonstrated that IFN-a most accurately recapitulated the HIV HVL profile. There was no detectable LPS signature even in those HIV subjects with the highest LPS and sCD14 levels. Conclusions: Monocyte gene expression in subjects with viremia is predominantly due to IFN-a, while subjects with LVL have a non-activated phenotype. In monocytes, there was no discernible expression profile linked to LPS exposure.

2009-10-09 | GSE18464 | GEO

Transcription profiling of human monocyte-derived macrophages treated with IFN alpha

Project description:To study effects of IFNalpha treatment on monocyte-derived macrophages which may influence susceptibility or resistance to HIV. Experiment Overall Design: Human monocyte-derived macrophages were stimulated with IFNalpha and analyzed for global gene expression.

2009-07-05 | E-GEOD-16755 | biostudies-arrayexpress

Transcription profiling of human monocyte-derived macrophages infected with HIV-1 or uninfected and stimulated with E. coli lipopolysaccharide

Project description:Whole genome expression profiling of HIV-1 infected and uninfected monocyte-derived macrophages

2009-01-01 | E-MEXP-1904 | biostudies-arrayexpress

HIV downregulates interferon stimulated genes in primary macrophages.

Project description:HIV is able to outpace the innate immune response, including the response mediated by interferon (IFN), to establish a productive infection. However, monocyte derived macrophages (MDMs) may be protected from HIV infection by treatment with type I IFN before virus exposure. The ability of HIV to modulate the type I IFN-mediated innate immune response when it encounters a cell that has already been exposed to IFN was investigated.

2013-01-01 | GSE41731 | GEO

Transcription profiling of human monocyte-derived macrophages infected with HIV-1 or stimulated with interferon-beta, interferon-gamma or lipopolysaccharide

Project description:Transcriptional profiling of HIV-1 infected and that of IFNbeta, IFNgamma or LPS stimulated human monocyte derived macrophages.

2009-09-01 | E-MEXP-2032 | biostudies-arrayexpress

HIV-1 indcued genes in human monocyte-derived macrophages

Project description:HIV-1 indcued genes in human monocyte-derived macrophages

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Gene expression analysis of activated monocyte-derived macrophages (aMDM) in CD44 knock out conditions

Project description:Analysis of the transcriptome of human monocyte-derived macrophages activated with IFN-gamma and LPS, in CD44 knock out conditions

2023-03-03 | GSE223391 | GEO

cART Treated monocyte derived macrophages

Project description:cART Treated monocyte derived macrophages

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IL-27 Inhibits HIV-1 Infection in Human Macrophages by Down-regulating Host Factor SPTBN1 during Monocyte to Macrophage Differentiation

Project description:The susceptibility of macrophages to HIV-1 infection is modulated during monocyte differentiation. IL-27 is an anti-HIV cytokine that also modulates monocyte activation. Here, we present new evidence that IL-27 promotes monocyte differentiation into macrophages that are non-permissive for HIV-1 infection. While IL-27 treatment does not affect expression of macrophage differentiation markers or macrophage biological functions, it confers HIV resistance by down-regulating spectrin beta non-erythrocyte 1 (SPTBN1), a required host factor for HIV-1 infection. IL-27 down-regulates SPTBN1 through a TAK-1-mediated MAPK signaling pathway. Knockdown of SPTBN1 strongly inhibits HIV-1 infection of macrophages; conversely, overexpression of SPTBN1 markedly increases HIV susceptibility of IL-27 treated macrophages. Moreover, we demonstrate that SPTBN1 associates with HIV-1 gag proteins. Collectively, our results underscore the ability of IL-27 to protect macrophages from HIV-1 infection by down-regulating SPTBN1, thus indicating that SPTBN1 is an important host target to reduce HIV-1 replication in one major element of the viral reservoir. 2 samples with different treatments were analyzed. Genes with absolute fold change >= 5 were selected.

2013-01-18 | E-GEOD-43595 | biostudies-arrayexpress

Interferon ε protects primary macrophages against HIV infection

Project description:Interferon ε (IFNε) is a unique type I IFN that is not induced by pattern-recognition response elements. IFNε is constitutively expressed in mucosal tissues including the female genital mucosa. We show here that IFNε induces an antiviral state in human macrophages that blocks HIV-1 replication. In this work, we examined effects and underlying mechanisms of IFNε in HIV infection of monocyte-derived macrophages (MDMs). We found that IFNε blocked HIV replication in macrophages. It acted on early stages of the HIV life cycle including entry and reverse transcription. It did not appear to operate through known IFN-induced HIV host restriction factors. IFNε induced immune responses in primary macrophages distinct from those induced by IFNα. Importantly, we discovered a novel protective effect of IFNε in primary macrophages against HIV by surging reactive oxygen species (ROS).

2016-10-03 | GSE83716 | GEO

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