Evidence map›Paper›PMID 42143639›Full record

ArticleVirus genes2026

Activation-induced cytidine deaminase (AID) suppresses the activity of HBV EnhII/CP by downregulating FANCE expression.

Weiping Zhou, Biao Yang, Ye Sun, Yuxin Bai, Xuanhe Fu, Bing Nie, Ying Li, Xing Tian, Zhongjia Jiang, Guangyan Liu

Abstract read
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Article in Virus genes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Weiping ZhouDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Biao YangDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Ye SunDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Yuxin BaiDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Xuanhe FuDepartment of Immunology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Bing NieDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Ying LiDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China.
Xing TianDepartment of Physiology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China. tianxing@symc.edu.cn.
Zhongjia JiangLiaoning Province Key Laboratory for Phenomics of Human Ethnic Specificity and Critical Illness, Shenyang, 110034, China. 908345440@qq.com.
Guangyan LiuDepartment of Pathogen Biology, School of Basic Medicine, Shenyang Medical College, Shenyang, 110034, China. liuguangyan@symc.edu.cn.

Funding

Liaoning Province Science and Technology plan joint plan (Natural Science Foundation-General Program) 2024-MSLH-457Natural Science Foundation of Liaoning Province of China 2025-MS-292The Natural Science Foundation Program (Doctoral Research Start-Up Project) of Liaoning Province of China 2024-BS-278
6 · The paper itself

Abstract

Activation-induced cytidine deaminase (AID) is a host restriction factor known to suppress hepatitis B virus (HBV) replication. However, the precise mechanisms underlying its antiviral activity remain incompletely understood. Combining RNA-Seq and functional assays, our study reveals a novel pathway by which AID inhibits HBV replication via downregulating the expression of Fanconi anemia complementation group E (FANCE). Our findings demonstrate that AID significantly reduces FANCE expression, and that FANCE promotes viral replication by specifically activating the HBV enhancer II/core promoter (EnhII/CP), a key transcriptional regulatory element. Combinatorial regulation experiments further confirm that FANCE is involved in AID-mediated HBV transcription. These results identify a novel downstream gene of AID, broaden the perspective on the host antiviral immune network against HBV, and provides a rationale for potential antiviral strategies targeting the FANCE regulatory axis.

Indexed as

Cytidine DeaminaseHepatitis BHepatitis B virusAICDA (Activation-Induced Cytidine Deaminase)Down-RegulationEnhancer Elements, GeneticHep G2 CellsHost-Pathogen InteractionsHumansPromoter Regions, GeneticVirus ReplicationAICDA (Activation-Induced Cytidine Deaminase)Cytidine DeaminaseActivation-induced cytidine deaminase (AID)Fanconi anemia complementation group E (FANCE)HBV

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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.