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<p>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.</p>

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

  • 期刊论文

  • 发表日期：

    2026年5月17日

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

摘要

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.