Evidence map›Paper›PMID 41108591›Full record

ArticleJournal of medical virology2025

Oral Microbiome and Inferred Functions Predict Kaposi's Sarcoma Progression.

Adam Officer, Wen Meng, David Spellman, Jeffrey Martin, Paige M Bracci, Mike McGrath, Yufei Huang, Shou-Jiang Gao

Abstract read
In one paragraph

Article in Journal of medical virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Adam OfficerCancer Virology Program, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania, USA.
Wen MengCancer Virology Program, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania, USA.ORCID 0000-0001-6771-0881
David SpellmanDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Jeffrey MartinDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA.
Paige M BracciDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA.
Mike McGrathDepartment of Medicine, The University of California at San Francisco, San Francisco, California, USA.
Yufei HuangCancer Virology Program, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania, USA.
Shou-Jiang GaoCancer Virology Program, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania, USA.ORCID 0000-0001-6194-1742

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 1988 to 2026
$158.0M
Cell Model for KSHV Infection and Genetic ManipulationR01CA096512 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Shou-Jiang Gao · 2003 to 2026
$7.4M
Regulation of KSHV replication by N6-methyladenosine (m6A) - Diversity SupplementR01CA124332 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GAO, SHOU-JIANG · 2007 to 2025
$5.0M
Impact of microbiota on AIDS-Kaposi’s sarcoma development and therapyR01CA284554 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Shou-Jiang Gao · 2023 to 2026
$3.1M
Citrulline-urea cycle in KSHV cellular transformationR01CA278812 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Shou-Jiang Gao · 2023 to 2026
$2.1M
Antiretroviral Therapy of AIDS-Related Kaposi's Sarcoma in AfricaR01CA119903 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MARTIN, JEFFREY N · 2005 to 2009
$1.9M
METTL16 and S-adenosylmethionine cycle in KSHV infectionR01CA291244 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Shou-Jiang Gao · 2025 to 2026
$1.3M
National Institutes of Health.NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA096512NCI NIH HHS R01 CA119903NCI NIH HHS R01 CA124332NCI NIH HHS R01 CA278812NCI NIH HHS R01 CA284554NCI NIH HHS R01 CA291244This study was supported by grants from the National Institutes of Health (CA096512, CA284554, CA278812, CA291244 and CA124332 to S.-J. Gao), UPMC Hillman Cancer Center Startup Fund to S.-J. Gao, S10OD028483 to the Center for Research Computing of the University of Pittsburgh, and in part by award P30CA047904. A. Officer is supported by T32CA186873.
6 · The paper itself

Abstract

Kaposi's sarcoma (KS) is a common cancer among people living with HIV and is caused by infection with Kaposi's sarcoma-associated herpesvirus (KSHV). While previous studies have linked the oral microbiome to KSHV infection and KS development, its role in KS progression remains poorly defined. We performed 16S rRNA gene sequencing targeting the V1-V2 and V3-V4 hypervariable regions to characterize the microbiome in 20 patients with AIDS-associated KS, including 10 with nonprogressive disease and 10 with progressive disease. Samples were obtained from three anatomical sites: oral cavity, peripheral blood, and tumor biopsies. The highest number of microbes were identified in the oral cavity at species, genus, and family levels. Beta diversity analysis revealed significant compositional differences in the oral microbiome between progressive and nonprogressive KS (p value = 0.044). Differential abundance analysis identified 16 species in the oral cavity associated with disease progression, compared to only three species in tumors and one in blood (p value < 0.05). Notably, Prevotella pallens and Megasphaera micronuciformis, both known producers of short-chain fatty acids, were significantly enriched in the oral microbiome of patients with progressive KS (log-fold changes = 2.8 and 2.4, respectively). Functional pathway inference revealed 39 differentially abundant microbial pathways in the oral cavity, including pathways related to denitrification, ubiquinone biosynthesis, and arginine metabolism (all p values < 0.05). Our findings provide the first evidence that specific oral microbiome alterations are associated with KS progression. The enrichment of short-chain fatty acid-producing bacteria and changes in microbial metabolic pathways may promote inflammation and KSHV lytic replication, offering potential mechanistic insights into KS pathogenesis and highlighting novel microbiome-based prognostic markers.

Indexed as

MicrobiotaMouthSarcoma, KaposiAdultAIDS-Related Opportunistic InfectionsBacteriaDisease ProgressionDNA, BacterialDNA, RibosomalFemaleHerpesvirus 8, HumanHumansMaleMiddle AgedRNA, Ribosomal, 16SSequence Analysis, DNADNA, BacterialDNA, RibosomalRNA, Ribosomal, 16SCancer progressioninflammationKaposi′s sarcomaKSHV lytic replicationmicrobiomeoral microbiomeshort‐chain fatty acids

Identifiers

PMID41108591
PMCPMC13045803

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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.