MNase-seq analyses for primary CD4 T cells infected with HIV (NL4-3 WT or IND116A)
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ABSTRACT:
PROVIDER: PRJNA580250 | ENA |
REPOSITORIES: ENA
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Project description:Host directed therapies against HIV-1 are thought to be critical for long term containment of the HIV-1 pandemic but remain elusive. Since HIV-1 infects and manipulates important effectors of both the innate and adaptive immune system, identifying modulations of the host cell systems in humans during HIV-1 infection may be crucial for the development of immune based therapies. Here, we quantified the changes of the proteome in human CD4+ T cells upon HIV-1 infection, both in vitro and in vivo. A SWATH-MS approach was used to measure the proteome of human primary CD4+ T cells infected with HIV-1 in vitro as well as CD4+ T cells from HIV-1 infected patients with paired samples on and off antiretroviral treatment. In the in vitro experiment, the proteome of CD4+ T cells was quantified over a time course following HIV-1 infection. 1,725 host cell proteins and 4 HIV-1 proteins were quantified, with 145 proteins changing significantly during the time course. Changes in the proteome peaked 24 hours after infection, concomitantly with significant HIV-1 protein production. In the in vivo branch of the study, CD4+ T cells from viremic patients and those with no detectable viral load after treatment were sorted and the proteomes quantified. We consistently detected 895 proteins, 172 of which were considered to be significantly different between viraemic patients and patients undergoing successful treatment. The proteome of in vitro infected CD4+ T cells was modulated on multiple functional levels, including TLR-4 signalling and the type 1 interferon signalling pathway. Perturbations in the type 1 interferon signalling pathway were recapitulated in CD4+ T cells from patients. The study shows that proteome maps generated by SWATH-MS indicate a range of functionally significant changes in the proteome of HIV infected human CD4+ T cells. Exploring these perturbations in more detail may help identify new targets for immune based interventions.
2017-02-28 | PXD005234 | Pride
Project description:Human Immunodeficiency Virus type-1 (HIV-1)-infected individuals show metabolic alterations of CD4 T cells through unclear mechanisms with undefined consequences. We analyzed the transcriptome of CD4 T cells from HIV-1 patients and revealed that elevated oxidative phosphorylation (OXPHOS) pathway is associated with poor outcomes. Inhibition of OXPHOS by the FDA-approved drug metformin, which targets mitochondrial respiratory chain complex I, suppresses HIV-1 replication in human CD4 T cells and humanized mice. In patients, HIV-1 peak viremia positively correlates with the expression of NLRX1, a mitochondrial innate immune receptor. Quantitative proteomics and metabolic analyses reveal that NLRX1 enhances OXPHOS and glycolysis during HIV-1-infection of CD4 T cells to promote viral replication. At the mechanistic level, HIV infection induces the association of NLRX1 with the mitochondrial protein, FASTKD5, to promote the expression of mitochondrial respiratory complex components. This study uncovers the OXPHOS pathway in CD4 T cells as a target for HIV-1 therapy.
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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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Project description:Sexually transmitted infections (STIs) are commonly reported among HIV-1 infected patients. The increasing prevalence of the most common STI, Chlamydia trachomatis (CT), among HIV-1 infected people suggests a role in HIV-1 infectivity. However, the mechanisms modulating the enhancement of HIV-1 infectivity during HIV-1/STIs coinfection remain elusive. The stimulation of CD4 T cells during CT infection may modulate the expression of specific genes, which in turn enhance the susceptibility and infectivity of CT-specific CD4 T cells to HIV-1 infection. After three days of CT stimulation of PBMCs followed by 3 days of HIV-1 infection, we observed a significant increase in HIV-1 p24 levels among clinically diagnosed C. trachomatis-infected patients as compared to cells from healthy donors. Similarly, ex vivo CT antigen-stimulated PBMCs from healthy donors showed enhanced susceptibility to HIV-1 as compared to unstimulated PBMCs. CT-specific CD4 T cells also harbour more HIV-1 copy numbers as compared to healthy unstimulated CD4 T cells. RNA-seq data revealed the upregulation of CCR chemokine receptors and cytokines in CD4 T cells from CT-stimulated CD4 T cells infected with HIV-1.
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Project description:CD8+ and CD4+ T cells from HIV infected patients with HIV-RNA viremia of >50 copies/ml and CD8+ and CD4+ T cells from healthy controls were isolated by negative selection (Miltenyi Biotech, Auburn, CA). Cell sorting of the CD4 and CD8 T cell subsets were performed based on surface staining of CD3+CD8+ or CD3+CD4+ and na ve CD45RA+CD27+CD127highHLA-DRlow, and CD3+CD8+ or CD3+CD4+ and memory CD45RA-CD27+CD127highHLA-DRlow. Sorted cell populations were spun down and stored as dry pellets at -80M-BM-0C. Samples analyzed by transcript levels of genes related to cytokine signaling were determined by the JAK/STAT Signaling Pathway microarray. CD8+ and CD4+ T cells from HIV infected patients with HIV-RNA viremia of >50 copies/ml and CD8+ and CD4+ T cells from healthy controls were isolated by negative selection (Miltenyi Biotech, Auburn, CA). Cell sorting of the CD4 and CD8 T cell subsets were performed based on surface staining of CD3+CD8+ or CD3+CD4+ and naM-CM-/ve CD45RA+CD27+CD127highHLA-DRlow, and CD3+CD8+ or CD3+CD4+ and memory CD45RA-CD27+CD127highHLA-DRlow. Sorted cell populations were spun down and stored as dry pellets at -80M-BM-0C. Samples analyzed by transcript levels of genes related to cytokine signaling were determined by the JAK/STAT Signaling Pathway microarray (http://www.sabiosciences.com/rt_pcr_product/HTML/PAHS-039A.html, SABiosciences Frederick, MD). Briefly, total RNA was harvested from each individual T cell subset from each patient or healthy control and contaminating DNA was digested with DNase. Messenger RNA was converted to cDNA and loaded onto PCR array plates for quantitative real-time PCR. Quantification of transcript levels was determined by normalizing to 5 housekeeping genes from each individual sample. Relative gene expression levels for each subset were averaged and compared between cell populations from the patient group and healthy controls. Because of the multiple comparisons only p values M-bM-^IM-$ 0.01 were considered significant.
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