ArticleVirology2015
Short chain fatty acids potently induce latent HIV-1 in T-cells by activating P-TEFb and multiple histone modifications.
Article in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
The trial behind it
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
33 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- Protein acylation in inflammatory diseases: from mechanisms to therapeutic strategies.Cell communication and signaling : CCS · 2025Review
- Dual role for microbial short-chain fatty acids in modifying SIV disease trajectory following anti-α4β7 antibody administration.Annals of medicine · 2024Article
- Article
- Protein modification by short-chain fatty acid metabolites in sepsis: a comprehensive review.Frontiers in immunology · 2023Review
- Medicinal Chemistry of Anti-HIV-1 Latency Chemotherapeutics: Biotargets, Binding Modes and Structure-Activity Relationship Investigation.Molecules (Basel, Switzerland) · 2022Review
- Lactate drives cellular DNA repair capacity: Role of lactate and related short-chain fatty acids in cervical cancer chemoresistance and viral infection.Frontiers in cell and developmental biology · 2022Review
- A Reliable Primary Cell Model for HIV Latency: The QUECEL (Quiescent Effector Cell Latency) Method.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Butyrate directly decreases human gut lamina propria CD4 T cell function through histone deacetylase (HDAC) inhibition and GPR43 signaling.Immunobiology · 2021Article
- Redefining the Histone Deacetylase Inhibitor Pharmacophore: High Potency with No Zinc Cofactor Interaction.ACS medicinal chemistry letters · 2021Article
- Review
- Commensal bacteria in the upper respiratory tract regulate susceptibility to infection.Current opinion in immunology · 2020Review
- Herpesvirus-bacteria synergistic interaction in periodontitis.Periodontology 2000 · 2020Review
- Current trends and new developments in HIV research and periodontal diseases.Periodontology 2000 · 2020Review
- Gut Microbiome, Short-Chain Fatty Acids, and Mucosa Injury in Young Adults with Human Immunodeficiency Virus Infection.Digestive diseases and sciences · 2019Article
- Nanotechnology approaches to eradicating HIV reservoirs.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2019Review
- Hybrid nanocarriers incorporating mechanistically distinct drugs for lymphatic CD4Science advances · 2019Article
- Diversity of vaginal microbiota in sub-Saharan Africa and its effects on HIV transmission and prevention.American journal of obstetrics and gynecology · 2019Review
- Infectious Threats, the Intestinal Barrier, and Its Trojan Horse: Dysbiosis.Frontiers in microbiology · 2019Review
- Altered Immunity and Microbial Dysbiosis in Aged Individuals With Long-Term Controlled HIV Infection.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
HIV patients with severe periodontitis have high levels of residual virus in their saliva and plasma despite effective therapy (HAART). Multiple short chain fatty acids (SCFAs) from periodontal pathogens reactivate HIV-1 in both Jurkat and primary T-cell models of latency. SCFAs not only activate positive transcription elongation factor b (P-TEFb), which is an essential cellular cofactor for Tat, but can also reverse chromatin blocks by inducing histone modifications. SCFAs simultaneously increase histone acetylation by inhibiting class-1/2 histone deacetylases (HDACs) and decrease repressive histone tri-methylation at the proviral LTR by downregulating expression of the class-3 HDAC sirtuin-1 (SIRT1), and the histone methyltransferases enhancer of Zeste homolog 2 (EZH2) and suppressor of variegation 3-9 homolog 1 (SUV39H1). Our findings provide a mechanistic link between periodontal disease and enhanced HIV-1 replication, and suggest that treatment of periodontal disease, or blocking the activities of SCFAs, will have a therapeutic benefit for HIV patients.
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What OpenQuestion holds
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.