ArticleAIDS (London, England)2020
Mechanistic differences underlying HIV latency in the gut and blood contribute to differential responses to latency-reversing agents.
Article in AIDS (London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Traditional Medicine Extracts ofInternational journal of molecular sciences · 2026Article
- RNA splicing patterns contribute to burst size variation among HIV-1-infected Jurkat cell clones.Journal of virology · 2025Article
- Longitudinal changes in the transcriptionally active and intact HIV reservoir after starting ART during acute infection.Journal of virology · 2025Article
- HIV and the gut: implications for HIV persistence, immune dysfunction and cure strategies.Frontiers in immunology · 2025Review
- HIV-1 latency reversal agent boosting is not limited by opioid use.JCI insight · 2024Article
- HIV transcription persists in the brain of virally suppressed people with HIV.PLoS pathogens · 2024Article
- Ethnobotanical survey and phytochemistry of medicinal plants used in the management of HIV/AIDS in Eastern Uganda.Heliyon · 2024Article
- HIV-1 latency reversal agent boosting is not limited by opioid use.medRxiv : the preprint server for health sciences · 2024Article
- Intestinal endothelial cells increase HIV infection and latency in resting and activated CD4 + T cells, particularly affecting CCR6 + CD4 + T cells.Retrovirology · 2023Article
- Controversies in the Design of Strategies for the Cure of HIV Infection.Pathogens (Basel, Switzerland) · 2023Review
- The Persistence of HIV Diversity, Transcription, and Nef Protein in Kaposi's Sarcoma Tumors during Antiretroviral Therapy.Viruses · 2022Article
- Blockade of TGF-β signaling reactivates HIV-1/SIV reservoirs and immune responses in vivo.JCI insight · 2022Article
- Novel RT-ddPCR assays for measuring the levels of subgenomic and genomic SARS-CoV-2 transcripts.Methods (San Diego, Calif.) · 2022Article
- Long-term immunologic effects of SARS-CoV-2 infection: leveraging translational research methodology to address emerging questions.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Multiply spliced HIV RNA is a predictive measure of virus production ex vivo and in vivo following reversal of HIV latency.EBioMedicine · 2021Article
- Stem cell-derived CAR T cells traffic to HIV reservoirs in macaques.JCI insight · 2021Article
- Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveWhile latently HIV-infected cells have been described in the blood, it is unclear whether a similar inducible reservoir exists in the gut, where most HIV-infected cells reside. Tissue-specific environments may contribute to differences in the mechanisms that govern latent HIV infection and amenability to reactivation. We sought to determine whether HIV-infected cells from the blood and gut differ in their responses to T-cell activation and mechanistically distinct latency reversing agents (LRAs).
designCross sectional study using samples from HIV-infected individuals (n = 11).
methodsMatched peripheral blood mononuclear cells (PBMC) and dissociated total cells from rectum ± ileum were treated ex vivo for 24 h with anti-CD3/CD28 or LRAs in the presence of antiretrovirals. HIV DNA and 'read-through', initiated, 5' elongated, completed, and multiply-spliced HIV transcripts were quantified using droplet digital PCR.
resultsT-cell activation increased levels of all HIV transcripts in PBMC and gut cells, and was the only treatment that increased multiply-spliced HIV RNA. Disulfiram increased initiated HIV transcripts in PBMC but not gut cells, while ingenol mebutate increased HIV transcription more in gut cells. Romidepsin increased HIV transcription in PBMC and gut cells, but the increase in transcription initiation was greater in PBMC.
conclusionThe gut harbors HIV-infected cells in a latent-like state that can be reversed by T-cell activation involving CD3/CD28 signaling. Histone deacetylation and protein kinase B may contribute less to HIV transcriptional initiation in the gut, whereas protein kinase C may contribute more. New LRAs or combinations are needed to induce multiply-spliced HIV and should be tested on both blood and gut.
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