Productively HIV-1 infected and bystander primary human CD4+ T-cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1036599 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26701813_1.fastq.gz | Fastqsanger.gz | |||
| SRR26701813_2.fastq.gz | Fastqsanger.gz | |||
| SRR26701814_1.fastq.gz | Fastqsanger.gz | |||
| SRR26701814_2.fastq.gz | Fastqsanger.gz | |||
| SRR26701815_1.fastq.gz | Fastqsanger.gz |
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Project description:CD4+ T-cells are the main target of HIV-1 and several host factors can positively or negatively modulate HIV-1 infection of these cells. MiRNAs aresmall regulatory RNAs that are involved in the regulation of basic cellular functions. They are also increasingly recognized as host factors regulatingHIV-1 infection, replication and persistence. In order to identify miRNAs involved in HIV-1 infection of CD4+ T-cells, we performed globaltranscriptomic analyses of productively infected and HIV-1 exposed but non infected bystander CD4+ T-cells and compared their MIRNA profiles with uninfected cells. Theseanalyses were performed in CD4+T-cells isolated from 3 different healthy blood donors. Both miRNA and mRNA expression profiles were compared. Our results show that bystander and uninfected CD4+ T-cells do not display important differences in their miRNA expression profiles even though their respectivemRNA expression profiles were markedly different. In contrast, both mRNA and miRNA expressionprofiles from productively infected CD4+ T-cells were significantly different from those of uninfected cells. Overall, these results suggest that HIV-1infection impacts the miRNA expression profile of primary CD4+ T-cells.
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Project description:CD4+ T-cells are the main target of HIV-1 and several host factors can positively or negatively modulate HIV-1 infection of these cells. MiRNAs aresmall regulatory RNAs that are involved in the regulation of basic cellular functions. They are also increasingly recognized as host factors regulatingHIV-1 infection, replication and persistence. In order to identify miRNAs involved in HIV-1 infection of CD4+ T-cells, we performed globaltranscriptomic analyses of productively infected and HIV-1 exposed but non infected bystander CD4+ T-cells and compared their MIRNA profiles with uninfected cells. Theseanalyses were performed in CD4+T-cells isolated from 3 different healthy blood donors. Both miRNA and mRNA expression profiles were compared. Our results show that bystander and uninfected CD4+ T-cells do not display important differences in their miRNA expression profiles even though their respectivemRNA expression profiles were markedly different. In contrast, both mRNA and miRNA expressionprofiles from productively infected CD4+ T-cells were significantly different from those of uninfected cells. Overall, these results suggest that HIV-1infection impacts the miRNA expression profile of primary CD4+ T-cells.
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Project description:Macrophages are heterogeneous immune cells with distinct origins, phenotypes, functions and tissue localization. Their susceptibility to HIV-1 is subject to variations from permissiveness to resistance, owing in part to regulatory microRNAs. Here, we used RNAseq to examine the expression of >400 microRNAs in productively infected and bystander cells of HIV-1-exposed macrophage cultures. Two micro-RNAs up regulated in bystander macrophages, miR-221 and miR-222, were identified as negative regulators of CD4 expression and CD4-mediated HIV-1 entry. Both microRNAs were enhanced by TNF-α, an inhibitor of CD4 expression. MiR-221/miR-222 inhibitors recovered HIV-1 entry in TNF-α-treated macrophages by enhancing CD4 expression, and increased HIV-1 replication and spread in macrophages by countering TNF-α-enhanced miR-221/miR-222 expression in bystander cells. In line with these findings, HIV-1-resistant intestinal myeloid cells express higher levels of miR-221 than peripheral blood monocytes. Thus, miR-221/miR-222 act as effectors of the antiviral host response activated during macrophage infection that restrict HIV-1 entry.
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Project description:mRNA expression profiles in productively HIV-1 infected and bystander primary human CD4+ T-cells
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Project description:miRNA expression profiles in productively HIV-1 infected and bystander primary human CD4+ T-cells
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Project description:Kuo H, Ahmad R, Lee GQ, Chen H, Ouyang Z, Szucs MJ, Kim D, Tsibris A, Chun T, Battivelli E, Verdin E, Rosenberg ES, Carr SA, Yu XG, Lichterfeld M. Immunity 2018. HIV-1 infection of CD4 T cells leads to cytopathic effects and cell demise, which is counterintuitive to the observation that certain HIV-1-infected cells possess a remarkable long-term stability and can persist for decades in infected individuals treated with suppressive antiretroviral therapy (ART). Using quantitative mass spectrometry-based proteomics, we show that HIV-1 infection can activate cellular survival programs that are governed by BIRC5, a molecular inhibitor of cell apoptosis that is frequently over-expressed in malignant cells. BIRC5 and its upstream regulator OX40 are upregulated in productively and latently infected CD4 T cells, and are functionally involved in maintaining their integrity and viability. Moreover, OX40-expressing CD4 T cells from ART-treated patients are strongly enriched for sequence-intact HIV-1, and pharmaceutical inhibition of BIRC5 results in a selective decrease of HIV-1-infected cells in vitro. Together, these findings suggest that BIRC5 supports long-term survival of HIV-1-infected cells and offer new perspectives for clinical strategies to reduce persisting viral reservoirs.
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