Evidence map›Paper›PMID 40425709›Full record

ArticleScientific reports2025

Effects of venetoclax, a BCL2 inhibitor, in systemic chronic active Epstein-Barr virus disease.

Ayaka Ohashi, Miwako Nishio, Mayumi Yoshimori, Kaoru Koike, Morito Kurata, Hayato Tamai, Ken-Ichi Imadome, Ayako Arai

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Ayaka Ohashi *Department of Immunology and Parasitology, St. Marianna University School of Medicine, Kanagawa, Japan.
Miwako Nishio *Department of Hematology and Biophysical Systems Analysis, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Mayumi YoshimoriDepartment of Hematology and Biophysical Systems Analysis, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Kaoru KoikeDepartment of Hematology and Biophysical Systems Analysis, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Morito KurataDivision of Integrated Facilities, Pathology, Institute of Science Tokyo, Tokyo, Japan.
Hayato TamaiDepartment of Hematology and Oncology, St. Marianna University School of Medicine, Kanagawa, Japan.
Ken-Ichi ImadomeDepartment of Infectious diseases and Infection Control, Akiru Municipal Medical Center, Tokyo, Japan.
Ayako AraiDepartment of Hematology and Biophysical Systems Analysis, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan. ara.hema@marianna-u.ac.jp.

Funding

Japan Agency for Medical Research and Development 18ek0109334h0001Japan Agency for Medical Research and Development 21ek0109334h0004Japan Agency for Medical Research and Development 24ek0109609h0003Japan Society for the Promotion of Science 20K16410Ministry of Health, Labour and Welfare 24FC1001
6 · The paper itself

Abstract

Systemic chronic active Epstein-Barr virus disease (sCAEBV) is a chemotherapy-resistant, EBV-positive T- or NK-cell lymphoproliferative disorder characterized by persistent systemic inflammation driven by the activation of EBV-infected cells. In this study, we explored BCL2, an anti-apoptotic factor implicated in various hematopoietic malignancies, as a potential therapeutic target for sCAEBV, focusing on the effects of its inhibitor, venetoclax. We confirmed BCL2 expression in EBV-positive T- and NK-cell lines and peripheral blood mononuclear cells (PBMCs) from sCAEBV patients using western blotting. Immunofluorescence staining further revealed BCL2 expression in EBV-infected cells within patient-derived PBMCs. Venetoclax treatment reduced the viability of EBV-positive cell lines and patient-derived PBMCs in a dose-dependent manner and induced apoptosis in these cells. Moreover, venetoclax suppressed the mRNA expression of the inflammatory cytokine IFN-γ in patient-derived PBMCs. To evaluate the in vivo effects of venetoclax, we utilized sCAEBV xenograft model generated by transplanting patient-derived PBMCs into NOD/Shi-scid/IL-2Rγnull mice. No engraftment of EBV-infected cells was observed in mice treated with venetoclax, whereas one out of three mice in the untreated group exhibited engraftment of EBV-positive cells and tumor formation. Venetoclax treatment showed an insignificant trend to reducing IFN-γ levels in peripheral blood in established xenograft models. To our knowledge, this is the first report to suggest that venetoclax exerts not only anti-tumor effects but also potential anti-inflammatory effects in sCAEBV. BCL2 represents a promising therapeutic target to address the two pathological characteristics of sCAEBV: malignancy and inflammation.

Indexed as

Bridged Bicyclo Compounds, HeterocyclicEpstein-Barr Virus InfectionsProto-Oncogene Proteins c-bcl-2SulfonamidesAnimalsAntineoplastic AgentsApoptosisChronic DiseaseFemaleHerpesvirus 4, HumanHumansInterferon-gammaLeukocytes, MononuclearMaleMiceMice, Inbred NODAntineoplastic AgentsBCL2 protein, humanBridged Bicyclo Compounds, HeterocyclicInterferon-gammaProto-Oncogene Proteins c-bcl-2SulfonamidesvenetoclaxBCL2EBVsCAEBVSystemic chronic active Epstein-Barr virus diseaseVenetoclax

Identifiers

PMID40425709
PMCPMC12117165

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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.