Evidence map›Paper›PMID 24501407›Full record

ArticleJournal of virology2014

Short-chain fatty acids from periodontal pathogens suppress histone deacetylases, EZH2, and SUV39H1 to promote Kaposi's sarcoma-associated herpesvirus replication.

Xiaolan Yu, Abdel-Malek Shahir, Jingfeng Sha, Zhimin Feng, Betty Eapen, Stanley Nithianantham, Biswajit Das, Jonathan Karn, Aaron Weinberg, Nabil F Bissada and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

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  18. Hypoxia and HIF-1α promote lyticJournal of virology · 2023
    Article
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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Xiaolan YuDepartment of Biological Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Abdel-Malek Shahir
Jingfeng Sha
Zhimin Feng
Betty Eapen
Stanley Nithianantham
Biswajit Das
Jonathan Karn
Aaron Weinberg
Nabil F Bissada
Fengchun Ye
Case Western Reserve University · USHubei University · CN

Funding

Epigenetic regulation of viral infection and replication by periodontal bacteriaR56DE023912 · NIDCR · CASE WESTERN RESERVE UNIVERSITY · PI YE, FENGCHUN · 2013 to 2014
$964k
NIDCR NIH HHS 1R56 DE023912-01NIDCR NIH HHS R56 DE023912
6 · The paper itself

Abstract

unlabelledPeriodontal pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum produce five different short-chain fatty acids (SCFAs) as metabolic by-products. We detect significantly higher levels of SCFAs in the saliva of patients with severe periodontal disease. The different SCFAs stimulate lytic gene expression of Kaposi's sarcoma-associated herpesvirus (KSHV) dose dependently and synergistically. SCFAs inhibit class-1/2 histone deacetylases (HDACs) and downregulate expression of silent information regulator-1 (SIRT1). SCFAs also downregulate expression of enhancer of zeste homolog2 (EZH2) and suppressor of variegation 3-9 homolog1 (SUV39H1), which are two histone N-lysine methyltransferases (HLMTs). By suppressing the different components of host epigenetic regulatory machinery, SCFAs increase histone acetylation and decrease repressive histone trimethylations to transactivate the viral chromatin. These new findings provide mechanistic support that SCFAs from periodontal pathogens stimulate KSHV replication and infection in the oral cavity and are potential risk factors for development of oral Kaposi's sarcoma (KS). IMPORTANCE: About 20% of KS patients develop KS lesions first in the oral cavity, while other patients never develop oral KS. It is not known if the oral microenvironment plays a role in oral KS tumor development. In this work, we demonstrate that a group of metabolic by-products, namely, short-chain fatty acids, from bacteria that cause periodontal disease promote lytic replication of KSHV, the etiological agent associated with KS. These new findings provide mechanistic support that periodontal pathogens create a unique microenvironment in the oral cavity that contributes to KSHV replication and development of oral KS.

Indexed as

Virus ReplicationAdultAgedCoinfectionDown-RegulationEnhancer of Zeste Homolog 2 ProteinFatty Acids, VolatileFemaleFusobacterium nucleatumHerpesvirus 8, HumanHumansMaleMethyltransferasesMiddle AgedPeriodontal DiseasesPolycomb Repressive Complex 2Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanFatty Acids, VolatileMethyltransferasesPolycomb Repressive Complex 2Repressor ProteinsSUV39H1 protein, human

Identifiers

PMID24501407
PMCPMC3993761
OpenAlexW2092778130

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.