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Clonally expanded CD4+ T cells with a unique gene signature contribute to persistence of the HIV-1 latent reservoir

ABSTRACT: Surface expression of the viral Envelope protein (Env) was used to enrich reactivated latent T cells producing HIV-RNA, and single cell RNASeq was performed to study gene expression differences between latent cells and controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE104490 | GEO | 2018/03/02

REPOSITORIES: GEO

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Clonally expanded CD4+ T cells with a unique gene signature contribute to persistence of the HIV-1 latent reservoir

Project description:Clonally expanded CD4+ T cells with a unique gene signature contribute to persistence of the HIV-1 latent reservoir

| PRJNA412829 | ENA

Distinct gene expression by expanded clones of quiescent memory CD4+ T cells harboring intact latent HIV-1 proviruses

Project description:Antiretroviral therapy controls but does not cure HIV-1 infection due to a reservoir of rare CD4 + T cells harboring latent proviruses. Little is known about the transcriptional program of latent cells. Here we report a novel strategy to enrich clones of latent cells carrying intact, replication-competent HIV-1 proviruses from blood based on their expression of unique T cell receptors. Latent cell enrichment enabled single cell transcriptomic analysis of 1,050 CD4 + T cells belonging to expanded clones harboring intact HIV-1 proviruses from 6 different individuals. The analysis revealed that most of these cells are T effector memory cells that are enriched for expression of HLA-DR, HLA-DP, CD74, CCL5, Granzymes A and K, cystatin F, LYAR and DUSP2. We conclude that expanded clones of latent cells carrying intact HIV-1 proviruses persist preferentially in a distinct CD4 + T cell population opening new possibilities for eradication.

2022-06-03 | GSE204756 | GEO

Expanded cytotoxic T-cell lymphocytes target the latent HIV reservoir.

Project description: Not available

| S-EPMC4490234 | biostudies-literature

ZIC2 ChIP-Seq in KSHV latent and lytic reactivated BCBL-1 cells

Project description:ZIC2 ChIP-Seq in KSHV latent and lytic reactivated BCBL-1 cells

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Helminth Infection Reactivates Latent γ-herpesvirus Via Cytokine Competition at a Viral Promoter

Project description:Mammals are co-infected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine gammaherpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-g (IFNg) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi's sarcoma associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNg reactivated latent murine gammaherpesvirus infection in vivo, suggesting a âtwo-signalâ model for viral reactivation. Thus chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status. All of the RNA from virus-pos cells and 50 ng of RNA from virus-neg cells was prepared for RNA-seq using ScriptSeq v2 RNA-seq library preparation kit (Epicentre). Index Primers (Epicentre) were added and samples underwent Duplex-Specific thermostable nuclease (DSN) (Evrogen) treatment to remove ribosomal RNA. Samples were pooled and sequenced on HiSeq.

2014-06-26 | E-GEOD-58116 | biostudies-arrayexpress

Helminth Infection Reactivates Latent γ-herpesvirus Via Cytokine Competition at a Viral Promoter

Project description:Mammals are co-infected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine gammaherpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-g (IFNg) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi's sarcoma associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNg reactivated latent murine gammaherpesvirus infection in vivo, suggesting a ‘two-signal’ model for viral reactivation. Thus chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status.

2014-06-26 | GSE58116 | GEO

Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation (ChIP-Seq)

Project description:We screened for small molecules that reactivated latent HIV-1 and identified benzotriazoles as latency-reducing agents. Here, we characterize the effects of HODHBt on gene expression in cultured T cells from three donors by polyA RNA-Seq and on STAT5A occupancy of the HIV-1 LTR promoter by ChIP-Seq. These and other results demonstrate that benzotriazoles block SUMOylation of phosphorylated STAT5, prolonging its transcriptional activity.

2017-01-11 | GSE84199 | GEO

Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation (RNA-Seq)

2017-01-11 | GSE84197 | GEO

Single-Cell RNA-Seq Reveals Transcriptional Heterogeneity in Latent and Reactivated HIV-infected Cells

Project description:Single-Cell RNA-Seq Reveals Transcriptional Heterogeneity in Latent and Reactivated HIV-infected Cells

| PRJNA437966 | ENA

Aminobisphosphonates reactivate the latent reservoir in people living with HIV-1

Project description:Antiretroviral therapy (ART) is not curative due to the existence of cellular reservoirs of latent HIV-1 that persist during therapy 1. Current research efforts to cure HIV-1 infection include “shock and kill” strategies to disrupt latency using small molecules or latency-reversing agents (LRAs) to induce expression of HIV-1 enabling cytotoxic immune cells to eliminate infected cells 2. However, the modest success of current LRAs urges the field to identify novel drugs with increased clinical efficacy 3,4. Aminobisphosphonates that include pamidronate, zoledronate, or alendronate, are the first-line treatment of bone-related diseases including osteoporosis and bone malignancies 5. Here, we show the use of aminobisphosphonates as a novel class of LRA: we found in ex vivo assays using primary cells from ART-suppressed people living with HIV-1 that aminobisphosphonates induce HIV-1 from latency to levels that are comparable to the T cell activator phytohemagglutinin. RNA sequencing and mechanistic data suggested that reactivation may occur through activation of the activator protein 1 signaling pathway. Stored samples from a prior clinical trial aimed at analyzing the effect of alendronate on bone mineral density, provided further of alendronate-mediated latency reversal and activation of immune effector cells.Decay of the reservoir measured by IPDA was however not detected. Our results demonstrate the novel use of aminobisphosphonates to reverse HIV-1 latency while inducing immune effector functions. This preliminary evidence merits further investigation in a controlled clinical setting possibly in combination with therapeutic vaccination.

2023-09-13 | GSE224546 | GEO

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