ArticleMucosal immunology2024
Translocating bacteria in SIV infection are not stochastic and preferentially express cytosine methyltransferases.
Article in Mucosal immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Systemic Evaluation of Administered FITC-Dextran or Evans Blue Dye to Determine Intestinal Barrier Permeability in Nonhuman Primates.Pathogens & immunity · 2026Article
- Trends and hotspots in research of virus and gastrointestinal mucosal immunity: a bibliometric analysis of four decades.Virology journal · 2025Article
- Mechanisms of HIV-immunologic non-responses and research trends based on gut microbiota.Frontiers in immunology · 2024Review
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Authors and funding
17 authors.
Funding
Abstract
Microbial translocation is a significant contributor to chronic inflammation in people living with HIV (PLWH) and is associated with increased mortality and morbidity in individuals treated for long periods with antiretrovirals. The use of therapeutics to treat microbial translocation has yielded mixed effects, in part, because the species and mechanisms contributing to translocation in HIV remain incompletely characterized. To characterize translocating bacteria, we cultured translocators from chronically SIV-infected rhesus macaques. Proteomic profiling of these bacteria identified cytosine-specific methyltransferases as a common feature and therefore, a potential driver of translocation. Treatment of translocating bacteria with the cytosine methyltransferase inhibitor decitabine significantly impaired growth for several species in vitro. In rhesus macaques, oral treatment with decitabine led to some transient decreases in translocator taxa in the gut microbiome. These data provide mechanistic insight into bacterial translocation in lentiviral infection and explore a novel therapeutic intervention that may improve the prognosis of PLWH.
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