ArticleThe Journal of clinical investigation2023
HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- The cell-type-specific roles of Toll-like receptors in herpes simplex virus infection and pathogenesis.Virulence · 2026Review
- The Janus face of host LncRNA in viral infections: Defender or collaborator?Communications biology · 2026Review
- Developments in genital herpes: progress in prevention and treatment.Current opinion in infectious diseases · 2026Review
- Prospects for therapeutic T-cell vaccine strategies for HIV cure.Current opinion in HIV and AIDS · 2025Review
- Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Article
- A targeted CRISPR screen identifies ETS1 as a regulator of HIV-1 latency.PLoS pathogens · 2025Article
- Immunogenicity and Protective Efficacy of an mRNA Vaccine Targeting HSV-2 UL41 in Mice.Vaccines · 2025Article
- Temporal Trends, Health Inequalities, and Risk Factors in the Global, Regional, and National Burden of Sexually Transmitted Infections Among Women of Child-Bearing Age (1990-2021): Analysis of the Global Burden of Disease Study.International journal of women's health · 2025Article
- Immunological Considerations for the Development of an Effective Herpes Vaccine.Microorganisms · 2024Review
- Evaluating anemia in HIV-infected patients using chest CT.Open medicine (Warsaw, Poland) · 2024Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Herpes simplex virus type 2 (HSV-2) coinfection is associated with increased HIV-1 viral loads and expanded tissue reservoirs, but the mechanisms are not well defined. HSV-2 recurrences result in an influx of activated CD4+ T cells to sites of viral replication and an increase in activated CD4+ T cells in peripheral blood. We hypothesized that HSV-2 induces changes in these cells that facilitate HIV-1 reactivation and replication and tested this hypothesis in human CD4+ T cells and 2D10 cells, a model of HIV-1 latency. HSV-2 promoted latency reversal in HSV-2-infected and bystander 2D10 cells. Bulk and single-cell RNA-Seq studies of activated primary human CD4+ T cells identified decreased expression of HIV-1 restriction factors and increased expression of transcripts including MALAT1 that could drive HIV replication in both the HSV-2-infected and bystander cells. Transfection of 2D10 cells with VP16, an HSV-2 protein that regulates transcription, significantly upregulated MALAT1 expression, decreased trimethylation of lysine 27 on histone H3 protein, and triggered HIV latency reversal. Knockout of MALAT1 from 2D10 cells abrogated the response to VP16 and reduced the response to HSV-2 infection. These results demonstrate that HSV-2 contributes to HIV-1 reactivation through diverse mechanisms, including upregulation of MALAT1 to release epigenetic silencing.
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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.