ArticlePLoS pathogens2017
The transcriptome of HIV-1 infected intestinal CD4+ T cells exposed to enteric bacteria.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Symptoms and Comorbidities Differ Based on Race and Weight Status in Persons with HIV in the Northern United States: a Cross-Sectional Study.Journal of racial and ethnic health disparities · 2023Trial
- Cytotoxic CD4 T Cells: Dual Agents in HIV-1 Pathogenesis and Persistence.Current HIV/AIDS reports · 2026Review
- Article
- Article
- A Two-Faced Gut Microbiome: Butyrogenic and Proinflammatory Bacteria Predominate in the Intestinal Milieu of People Living with HIV from Western Mexico.International journal of molecular sciences · 2024Article
- Integrative systems immunology uncovers molecular networks of the cell cycle that stratify COVID-19 severity.Journal of medical virology · 2023Article
- Influence of HIV infection on cognition and overall intelligence in HIV-infected individuals: advances and perspectives.Frontiers in behavioral neuroscience · 2023Review
- Identification of CD98 as a Novel Biomarker for HIV-1 Permissiveness and Latent Infection.mBio · 2022Article
- Anti-inflammatory effects of recreational marijuana in virally suppressed youth with HIV-1 are reversed by use of tobacco products in combination with marijuana.Retrovirology · 2022Article
- A Summary of the Sixth International Workshop on Microbiome in HIV Pathogenesis, Prevention, and Treatment.AIDS research and human retroviruses · 2022Article
- HIV Infection Predisposes to Increased Chances of HBV Infection: Current Understanding of the Mechanisms Favoring HBV Infection at Each Clinical Stage of HIV Infection.Frontiers in immunology · 2022Review
- Butyrate directly decreases human gut lamina propria CD4 T cell function through histone deacetylase (HDAC) inhibition and GPR43 signaling.Immunobiology · 2021Article
- Gut Innate Immunity and HIV Pathogenesis.Current HIV/AIDS reports · 2021Review
- Qualitative Differences Between the IFNα subtypes and IFNβ Influence Chronic Mucosal HIV-1 Pathogenesis.PLoS pathogens · 2020Article
- Quantifying HIV-1-Mediated Gut CD4Bio-protocol · 2020Article
- HIV infection does not alter interferon α/β receptor 2 expression on mucosal immune cells.PloS one · 2020Article
- Inflammatory and immunometabolic consequences of gut dysfunction in HIV: Parallels with IBD and implications for reservoir persistence and non-AIDS comorbidities.EBioMedicine · 2019Review
- A compartmentalized type I interferon response in the gut during chronic HIV-1 infection is associated with immunopathogenesis.AIDS (London, England) · 2018Article
- Influence of gut microbiome on mucosal immune activation and SHIV viral transmission in naive macaques.Mucosal immunology · 2018Article
- Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Global transcriptome studies can help pinpoint key cellular pathways exploited by viruses to replicate and cause pathogenesis. Previous data showed that laboratory-adapted HIV-1 triggers significant gene expression changes in CD4+ T cell lines and mitogen-activated CD4+ T cells from peripheral blood. However, HIV-1 primarily targets mucosal compartments during acute infection in vivo. Moreover, early HIV-1 infection causes extensive depletion of CD4+ T cells in the gastrointestinal tract that herald persistent inflammation due to the translocation of enteric microbes to the systemic circulation. Here, we profiled the transcriptome of primary intestinal CD4+ T cells infected ex vivo with transmitted/founder (TF) HIV-1. Infections were performed in the presence or absence of Prevotella stercorea, a gut microbe enriched in the mucosa of HIV-1-infected individuals that enhanced both TF HIV-1 replication and CD4+ T cell death ex vivo. In the absence of bacteria, HIV-1 triggered a cellular shutdown response involving the downregulation of HIV-1 reactome genes, while perturbing genes linked to OX40, PPAR and FOXO3 signaling. However, in the presence of bacteria, HIV-1 did not perturb these gene sets or pathways. Instead, HIV-1 enhanced granzyme expression and Th17 cell function, inhibited G1/S cell cycle checkpoint genes and triggered downstream cell death pathways in microbe-exposed gut CD4+ T cells. To gain insights on these differential effects, we profiled the gene expression landscape of HIV-1-uninfected gut CD4+ T cells exposed to bacteria. Microbial exposure upregulated genes involved in cellular proliferation, MAPK activation, Th17 cell differentiation and type I interferon signaling. Our findings reveal that microbial exposure influenced how HIV-1 altered the gut CD4+ T cell transcriptome, with potential consequences for HIV-1 susceptibility, cell survival and inflammation. The HIV-1- and microbe-altered pathways unraveled here may serve as a molecular blueprint to gain basic insights in mucosal HIV-1 pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.