Expression data from IFN alpha 2-treated macrophages infected with HIV
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE30536 | GEO | 2011/12/01
SECONDARY ACCESSION(S): PRJNA144657
REPOSITORIES: GEO
Similar Datasets
Project description:Temporal changes of the expression levels of the complete human transcriptome during the first 24 hours following infection of IFN-pre-treated macrophages. This approach has allowed us to identify genes involved in the IFN signaling that have an impact on HIV-1 infection of macrophages KEYWORDS: time course Purified primary macrophages were treated with 1000 IU/ml of IFNα2, for 18 hours before infection. Pre-treated macrophages were infected with the Bal strain of HIV-1 at an MOI of 1. Uninfected and untreated cells were used for control. Aliquots of cells (3x106 cells) were taken at 0,2, 4, 8, 16 and 24 hrs after infection for RNA extraction and hybridization on Affymetrix microarrays. *** No CEL file for Sample GSM757646 MDMs CTL at T0
2011-12-01 | E-GEOD-30536 | biostudies-arrayexpress
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
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
Project description:Total RNA sequencing of IFN-stimulated and HIV-1-infected macrophages
| PRJNA665220 | ENA
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. To investigate the presence of HIV on an established IFN response, MDMs were subjected to four different conditions: (1) IFN-treated only, (2) IFN-treated followed by HIV infection, (3) HIV infected only, and (4) a mock-treated and mock-infected control. Microarray gene expression analysis was performed on a total of 24 samples derived from the 4 conditions assessed at 3 time points (1, 4 and 8 days following treatment/infection) for both IFN-α2 or -ω. Initially, ISGs were identified as those that were upregulated greater than 2-fold by IFN alone (condition 1) at both Days 4 and 8. Then, the IFN-treated condition was compared to the IFN-treated followed by HIV-infection condition in order to identify those ISGs that were downregulated at least 1.5-fold by the presence of HIV at both days. Assuming that it would be counterproductive for HIV infection by itself to induce the expression of ISGs with putative anti-HIV effects, those ISGs that were upregulated greater than 2-fold in the HIV control were removed. Finally, ISGs that passed these filters and were concordant with both IFN-treatments (IFN-α2 and -ω) were identified and corresponded to the following 8 ISGs: AXL receptor tyrosine kinase (AXL), interferon-alpha inducible protein 27 (IFI27), interferon-induced protein 44 (IFI44), interferon-induced protein 44-like (IFI44L), ISG15, OAS1, OAS3 and XIAP associated factor 1 (XAF1). It should be noted that the IFN-α2 and -ω microarray experiments were performed in different batches but batch effects were not corrected since genes were identified by the filtering approach just described within each batch.
2013-01-01 | E-GEOD-41731 | biostudies-arrayexpress
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
Project description:Cannabidiol modulates type I IFN response genes and HIV infection in macrophages
| PRJNA832018 | ENA
Project description:The DNA sensor cGAS senses cytosolic DNA and catalyzes the production of the cyclicdinucleotide cGAMP, resulting in type I IFN responses. We addressed the functionality of cGAS-mediated DNA sensing in human and murine T-cells. Activated primary CD4+ T-cells expressed cGAS and responded robustly to plasmid DNA by upregulation of ISGs and release of bioactive interferon. In mouse T-cells, cGAS KO ablated sensing of plasmid DNA, and TREX1 KO enabled cells to sense short immunostimulatory DNA. Basal expression of IFIT1 and MX2 was downregulated and upregulated in cGAS KO and TREX1 KO T-cell lines, respectively, compared to parental cells. Despite their intact cGAS sensing pathway, human CD4+ T-cells failed to mount a reverse transcriptase (RT) inhibitor-sensitive immune response following HIV-1 infection. In contrast, infection of human T-cells with HSV-1 that is functionally deficient for the cGAS antagonist pUL41 (HSV-1ΔUL41N) resulted in a cGAS dependent type I IFN response. In accordance with our results in primary CD4+ T-cells, plasmid challenge or HSV-1ΔUL41N inoculation of representative T-cell lines provoked an entirely cGAS-dependent type I IFN response, including IRF3 phosphorylation and expression of ISGs. In contrast, no RT-dependent type I IFN response was detected following transduction of T cell lines with VSV-G-pseudotyped lentiviral or gammaretroviral particles. Together, T-cells are capable to raise a cGAS-dependent cell-intrinsic response to both plasmid DNA challenge or inoculation with HSV-1ΔUL41N. However, HIV-1 infection does not appear to trigger cGAS-mediated sensing of viral DNA in T-cells, possibly by revealing viral DNA of insufficient quantity, length, and/or accessibility to cGAS.
2020-05-19 | GSE150753 | GEO
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
Project description:Very little is known about the role of macrophages as immune mediators during natural HIV infection. Humanized mice are a highly valuable in vivo model to study HIV pathogenesis. Still, the presence of murine mononuclear phagocytes in these models represents a significant limitation for the study of their human counterpart. Therefore, we generated a novel humanized mouse model for the selective depletion of human myeloid cells at a time point of our choosing. These inducible human myeloid cell depletion (iHMD) mice showed specific human myeloid cell depletion with no adverse events for the animals. We used this model to demonstrate that human mononuclear phagocytes restrict HIV replication in vivo by secreting antiviral cytokines and chemokines. These in vivo data were validated by a co-culture assay, showing soluble factors are at the basics of macrophage-mediated restriction of HIV. Transcriptomic data confirmed macrophages restrict HIV replication via upregulation of antiviral cytokines and chemokines. RNA sequencing CD4+ T-cells showed cellular activation, up-regulation of HIV restriction factors and the downregulation of DNA transcription and RNA translation in the presence of macrophages. This work describes a novel role of macrophages as effector cells acting against HIV replication and disease progression.
2024-06-20 | GSE269285 | GEO