Evidence map›Paper›PMID 41905531›Full record

ArticleVirologica Sinica2026

EBV nuclear antigen 1 hijacks DDX5/BZLF1 axis to facilitate viral lytic replication.

Li Yang, Shuyu Xin, Shen Li, Pengfei Cao, Zeyu Sun, Mingjuan Jiang, Yujie Xin, Xiaoling Su, Jing Yang, Jianhong Lu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virologica Sinica, 2026. 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

10 authors.

Li YangDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Shuyu XinDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Shen LiDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Pengfei CaoKey Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Zeyu SunState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Mingjuan JiangDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Yujie XinDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Xiaoling SuState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Jing YangDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China.
Jianhong LuDepartment of Medical Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China; Key Laboratory of Cancer Carcinogenesis and Invasion of Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Central South University, Changsha 410078, China; Department of Microbiology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi 830017, China. Electronic address: jianhlu@csu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) lytic replication is a key driver of viral dissemination and tumorigenicity in epithelial malignancies, such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC). However, the underlying molecular mechanism and effective therapeutic strategy remain largely unknown. Here, we analyzed the EBV nuclear antigen 1 (EBNA1) interactome and identified DEAD-box helicase 5 (DDX5) as its novel partner. The N-terminal region (amino acids 1-88) of EBNA1 and the C-terminal domain of DDX5 were crucial for their binding. EBNA1 stabilized the DDX5 protein by impeding its proteasomal degradation via K48-linked polyubiquitin. EBNA1 facilitated EBV lytic replication in a DDX5-dependent manner. Furthermore, DDX5 bound to the promoter of BZLF1, which is the key switch of EBV reactivation, thus transactivating BZLF1 to drive viral lytic replication. Moreover, the small molecule inhibitor FL118 was able to disrupt this process by promoting DDX5 degradation, unveiling FL118 as a new potential antiviral drug. Our findings established a new functional axis of EBNA1/DDX5/BZLF1, adding to the knowledge about the role of EBNA1 in the regulation of EBV life cycle, particularly lytic replication. The study also provided a potential therapeutic strategy for EBV-associated epithelial tumors.

Indexed as

DEAD-box RNA HelicasesEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanTrans-ActivatorsVirus ReplicationEpstein-Barr Virus InfectionsHumansPromoter Regions, GeneticProtein BindingBZLF1 protein, Herpesvirus 4, HumanDdx5 protein, humanDEAD-box RNA HelicasesEBV-encoded nuclear antigen 1Epstein-Barr Virus Nuclear AntigensTrans-ActivatorsDead-box helicase 5 (DDX5)Epstein-Barr virus (EBV)Epstein-Barr virus nuclear antigen 1 (EBNA1)FL118Lytic replication

Identifiers

PMID41905531
PMCPMC13215960

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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.