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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43595 | GEO | 2013/01/18

SECONDARY ACCESSION(S): PRJNA186789

REPOSITORIES: GEO

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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

Homo sapiens

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

| PRJNA186789 | ENA

Differential expression of microRNAs in monocytes and derived macrophages in culture.

Project description:HIV-1 infection of monocytes/macrophages is modulated by several host factors. For instance, although HIV-1 successfully enters monocytes, antiviral restriction factors inhibit HIV-1 productive infection in these cells. We recently identified two microRNAs, miR-221 and miR-222, which limit HIV-1 entry during infection of monocyte-derived macrophages (MDM) by down-regulating CD4 expression. Interestingly, CD4 is also down regulated during the differentiation of monocytes into macrophages. In this study, we compared microRNA expression in monocytes and macrophages by RNAseq and found that miR-221/miR-222 are enhanced in macrophages.Taken together, these results show that both miR-221 and miR-222 act as modulators of CD4 mRNA expression throughout the monocyte/macrophage lineage, having roles in their differentiation, activation processes and modulating macrophage resistance to HIV-1.

2017-11-21 | GSE107160 | 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

Gene expression in macrophages treated with IFNalpha

Project description:To study effects of IFNalpha treatment on monocyte-derived macrophages which may influence susceptibility or resistance to HIV.

2009-06-29 | GSE16755 | GEO

Interleukin-27 is a potent inhibitor of cis HIV-1 replication in Monocyte-derived Dendritic Cells via a Type I Interferon-independent pathway

Project description:IL-27 treated DCs were shown to be highly potent inhibitors of cis HIV-1, particularly of CCR5 tropic strains. Microarray studies of IL-27 treated DCs showed no up-regulation of Type I (IFN) gene expression. Neutralization of the Type-I IFN receptor had no impact on the HIV inhibition. Lastly, IL-27 mediated inhibition was shown to act post-viral entry and prior to completion of reverse transcription. These results show for the first time that IL-27 is a potent inhibitor of cis HIV-1 infection in DCs by a Type I IFN independent mechanism.

2013-03-29 | GSE44732 | GEO

Interleukin-27 is a potent inhibitor of cis HIV-1 replication in Monocyte-derived Dendritic Cells via a Type I Interferon-independent pathway

2013-03-29 | E-GEOD-44732 | biostudies-arrayexpress

HIV-1 infected Cell Pellets and Biotinylated Cannabidiol LC-MS/MS

Project description:Previous studies have shown that cannabis use in people living with HIV-1 is associated with a lower viral load, lower circulating CD16+ monocytes, and high CD4+ T-cell count, suggesting a potential therapeutic application. HIV-1 infected U1 monocytes and primary macrophages were used to assess the effects of CBD in HIV-1 infection. Our data suggests that CBD treatment results in a significant reduction in the number of EVs released from infected cells. Additional findings suggest that this may be mediated by a reduction in viral transcription and autophagy activation. To see the effect of CBD in autophagy activation, U1 and U1 Monocyte Derived Macrophages cells were cultured and lysed. D-Biotin or Biotinylated CBD pull-down from the lysates was performed using Streptavidin-Sepharose beads, which were washed with TNE50 / TNE300 (high salt) + 0.1% NP40 buffers. The complexes were analyzed by mass spectrometry. Reactome enrichment analysis was used to assess the CBD pull-down of HIV-1 infected monocytes (U1) and HIV-1 infected MDM proteins for involvement of the autophagy pathway.

2022-04-04 | PXD027263 | Pride

HIV-1 indcued genes in human monocyte-derived macrophages

Project description: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.

2018-01-09 | GSE108897 | GEO

Circulating Monocytes in HIV-1 infected Viremic Subjects Exhibit an Anti-Apoptotic Gene Signature

Project description:Mechanisms that may allow circulating monocytes to persist as CD4 T cells diminish in HIV-1 infection have not been investigated. We have characterized steady-state gene expression signatures in circulating monocytes from HIV-infected subjects and have identified a stable anti-apoptosis gene signature comprised of 38 genes associated with p53, CD40L, TNF and MAPKinase signaling networks. The significance of this gene signature is indicated by our demonstration of cadmium chloride- or Fas ligand-induced apoptosis resistance in circulating monocytes in contrast to increasing apoptosis in CD4 T cells from the same infected subjects. As potential mechanisms in vivo, we show that monocyte CCR5 binding by HIV-1 virus or agonist chemokines serve as independent viral and host modulators resulting in increased monocyte apoptosis resistance in vitro. We also show evidence for concordance between circulating monocyte apoptosis-related gene expression in HIV-1 infection in vivo and available datasets following viral infection or envelope exposure in monocyte derived macrophages in vitro. The identification of in vivo gene expression associated with monocyte resistance to apoptosis is of relevance to AIDS pathogenesis since it would contribute to: (1) maintaining viability of infection targets and long-term reservoirs of HIV-1 infection in the monocyte/macrophage populations, and (2) protecting a cell subset critical to host survival in spite of sustained high viral replication. Keywords: two group study design 33 samples hybridized, including 13 HIV-1 Patients, 12 Healthy Controls and 4 HIV-1 Patients and 4 Controls followed 6 months later

2010-06-25 | E-GEOD-14542 | biostudies-arrayexpress

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