Early response of human monocyte-derived macrophages (MDM) to HIV-1
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE81327 | GEO | 2016/06/10
SECONDARY ACCESSION(S): PRJNA321301
REPOSITORIES: GEO
Similar Datasets
Project description:Human MDM were exposed to VSVG-pseudotyped HIV-1 NL-AD8 for 8h, 24h, and with HIV-1 + AZT for 24h MDM from 3 healthy blood donors were differentiated for 7 days, exposed or not to HIV-1 +/- AZT for 8h and 24h before being lysed. RNA was extracted, reverse-transcribed, hybridized on 2.1 ST microarrays to analyse the early transcriptomic response of MDM to infection.
2016-06-10 | E-GEOD-81327 | biostudies-arrayexpress
Project description:In this study, we used a productive HIV infection model, consisting of the CD4+ SupT1 T cell line infected with a VSV-G pseudotyped HIVeGFP-based vector, to explore the transcriptomic and m6A/m5C epitranscriptomic lansdcape upon HIV infection, and compare it to mock-treated cells at 12h, 24h, and 36h post infection.
2021-06-30 | GSE157192 | GEO
Project description:In this study, we used a productive HIV infection model, consisting of the CD4+ SupT1 T cell line infected with a VSV-G pseudotyped HIVeGFP-based vector, to explore the transcriptomic and m6A/m5C epitranscriptomic lansdcape upon HIV infection, and compare it to mock-treated cells at 12h, 24h, and 36h post infection.
2021-06-30 | GSE157190 | GEO
Project description:In this study, we used a productive HIV infection model, consisting of the CD4+ SupT1 T cell line infected with a VSV-G pseudotyped HIVeGFP-based vector, to explore the transcriptomic and m6A/m5C epitranscriptomic lansdcape upon HIV infection, and compare it to mock-treated cells at 12h, 24h, and 36h post infection.
2021-06-30 | GSE157189 | GEO
Project description:In this study, we used a productive HIV infection model, consisting of the CD4+ SupT1 T cell line infected with a VSV-G pseudotyped HIVeGFP-based vector, to explore the transcriptomic and m6A/m5C epitranscriptomic lansdcape upon HIV infection, and compare it to mock-treated cells at 12h, 24h, and 36h post infection.
2021-06-30 | GSE157187 | GEO
Project description:HIV establishes long-term latent infection in memory CD4+ T cells, but also establishes sustained long-term productive infection in macrophages, especially in the CNS. To better understand how HIV sustains infection in macrophages, we performed RNAseq analysis after infection of human-monocyte derived macrophages (MDMs) with the brain-derived HIV-1 strain YU2 and compared this with acute infection of CD4+ T cells. HIV infection in MDM and CD4+ T-cells altered many gene transcripts, but with few overlaps between these different cell types. We found interferon pathways upregulated in both MDM and CD4+ T-cells, but with different gene signatures. The interferon-stimulated gene RSAD2/Viperin was among the most upregulated genes following HIV infection in MDMs, but not in CD4+ T-cells. RSAD2/Viperin was induced early after infection with various HIV strains, was sustained over time, and remained elevated in established MDM infection even if new rounds of infection were blocked by antiretroviral treatment. Immunofluorescence microscopy revealed that RSAD2/Viperin was induced strongly in HIV infected cells, as well as in some uninfected neighboring cells, and was frequently localized at junctions between cells. Knockdown of RSAD2/Viperin following establishment of infection in MDMs reduced production of HIV transcripts and viral p24 antigen. This correlated with reduction in the number of multinucleated giant cells, and changes in the histone modifications at the HIV LTR, including loss of histone H3K7ac and H3K9me3, epigenetic marks that we have found associated with HIV in MDMs. RNA-seq transcriptomic analysis of RSAD2/Viperin knockdown during HIV infection of MDMs revealed activation of interferon alpha and gamma pathways and inactivation of Rho GTPase pathways. Taken together, these results suggest that RSAD2/Viperin supports HIV infection in macrophages through multiple mechanisms, potentially including the attenuation of the interferon response.
2024-08-27 | GSE253073 | GEO
Project description:Histone profiling of monocyte-derived macrophages (MDM)
| PRJNA925919 | ENA
Project description:Macrophages are a major target for human immunodeficiency virus type 1 (HIV-1) infection. However, macrophages are largely heterogeneous and may exhibit differences in permissiveness to HIV-1 infection. This study highlights the interplay of macrophage heterogeneity in HIV-1 pathogenesis. We show that monocyte-derived macrophages (MDM) could be divided into two distinct subsets: CD14+Siglec-1hiCD4+ (non-adherent MDM), and CD14+Siglec-1LoCD4- (adherent MDM). The CD14+Siglec-1hiCD4+MDM subset represented the smaller proportion in the macrophage pool, and varied among different donors. Fractionation and subsequent exposure of the two MDM subsets to HIV-1 revealed opposite outcomes in terms of HIV-1 capture and infection. Although the CD14+Siglec-1hiCD4+MDM captured significantly more HIV-1, infection was significantly higher in the CD14+Siglec-1LoCD4-MDM subset. Thus, CD14+Siglec-1hiCD4+MDM were less permissive to infection. Depletion of CD14+Siglec-1hiCD4+MDM or a decrease in their percentage, resulted in increased infection of MDM, suggestive of a capacity of these cells to capture and sequester HIV-1 in an environment that hinders its infectivity. Increased expression of innate restriction factors and cytokine genes were observed in the non-adherent CD14+Siglec-1hiCD4+MDM, both before and after HIV-1 infection, compared to the adherent CD14+Siglec-1LoCD4-MDM. The differential expression of gene expression profiles in the two macrophage subsets may provide an explanation for the differences observed in HIV-1 infectivity.
2018-02-22 | GSE103666 | GEO
Project description:HIV-associated neurocognitive disorders (HAND) affect 15-55% of HIV-positive patients, with no therapy. HIV-infected monocyte-derived macrophages (MDM) invade the brain of these individuals, promoting neurotoxicity. We demonstrated increased expression of cathepsin B (CATB), a lysosomal protease, in monocytes and post-mortem brain tissues of women with HAND. Increased CATB release from HIV-infected MDM leads to neurotoxicity, and its secretion is associated with NF-κB activation, oxidative stress, and lysosomal exocytosis. Cannabinoid receptor 2 (CB2R) agonist, JWH-133, was shown to decrease HIV-1 replication, CATB secretion, and neurotoxicity from HIV-infected MDM but the mechanisms are not entirely understood. We hypothesized that HIV-1 infection upregulates the expression of proteins associated with oxidative stress and that a CB2R agonist could reverse these effects. To test our hypothesis MDM were isolated from healthy women donors (n=3), infected with HIV-1ADA, and treated with JWH-133. After 13 days post-infection cell lysates were labeled by Tandem Mass Tags (TMT) and analyzed by LC/MS/MS quantitative proteomics bioinformatics. While HIV-1 infection upregulated CATB, NF-κB signaling, Nrf2-mediated oxidative stress response, and lysosomal exocytosis, JWH-133 treatment downregulated their expression. Our results suggest that JWH-133 is a potential alternative therapy against HIV-1 induced neurotoxicity and warrant in vivo studies to test its potential against HAND.
2024-06-22 | PXD048464 | Pride
Project description:Purpose: The goals of this study are to investigate the differentially expressed miRNAs between ALV-J-infected primary monocyte-derived macrophages (MDM) and uninfected control by Illumina deep sequencing. Methods:Total RNA from two ALV-J-infected MDM (designated: J3h_1, J3h_2, J36h_1 and J36h_2) and two uninfected MDM samples (designated: NC3h_1, NC3h_2, NC36h_1 and NC36h_2) was isolated by TRIzol following the manufacturer’s instruction at 3 h post infection (hpi) and 36 hpi. RNA samples of two individuals within each group were pooled with equal amounts, and then were subjected to Illumina deep sequencing by Illumina Hiseq 2000. Results: compared to the uninfected MDM, we identified 13 significant up-regulated miRNAs and 2 significant down-regulated miRNAs in ALV-J infected MDM at 3 hpi, and 6 significant up-regulated miRNAs and 2 significant down-regulated miRNAs in ALV-J infected MDM at 36 hpi. Conclusions: Our results suggest that DE miRNAs involved in the immune response induced by ALV-J infection in MDM at 3 hpi. In addition, only 25 miRNAs-target DEGs were identified in MDM with ALV-J infection at 36 hpi, and these target DEGs can’t be significantly enriched in any GO terms and KEGG pathway..
2017-08-29 | GSE103206 | GEO