ArticleScientific reports2026
HIV heart inflammation is mediated by HIV infected myeloid cells, HIV-tat secretion, and aberrant function of Connexin43-containing channels.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Research progress on the association between viruses and cardiac diseases.Journal of virology · 2026Review
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6 authors.
Funding
Abstract
People living with HIV (PLWH) have a 2 times higher risk of HIV-associated cardiovascular disease (HIV-CVD) compared to people without HIV, despite effective anti-retroviral therapy (ART), but the mechanism is unknown. Here, we demonstrated the presence of myeloid cells containing HIV DNA sequences (HIV+) in human ventricular heart tissues from people with HIV in the ART era. HIV+ cells show residual HIV-Tat expression that is associated with upregulation of Connexin43 (Cx43) expression, gap junctional communication, and hemichannel (HC) activity. HIV-Tat binds to the Cx43 promoter, increasing Cx43 mRNA and protein expression. Cx43 enhanced expression by HIV-Tat was localized in the intercalated disk, as well as in the lateral membrane of cardiomyocytes, resulting in Cx43-containing HC openings and release of PGE2 and ATP, as well as facilitating the secretion of inflammatory cytokines. Overall, our data demonstrated that HIV+ cells, even during ART, secrete HIV-Tat, compromising GJ and HC-mediated communication and promoting localized inflammation, which could contribute to arrhythmia.
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