环状DNA
表观遗传学
cccDNA
乙型肝炎病毒
DNA
共价键
遗传学
乙型肝炎
生物
病毒学
计算生物学
病毒
生物信息学
化学
基因组
基因
有机化学
作者
Ji‐Hua Ren,Sheng‐Tao Cheng,Fang Ren,Huiying Gu,Daiqing Wu,Xinyan Yao,Ming Tan,Ailong Huang,Juan Chen
标识
DOI:10.1016/j.gendis.2024.101215
摘要
Human hepatitis B virus (HBV) infection is the major cause of acute and chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma. Although the application of prophylactic vaccination programs has successfully prevented the trend of increasing HBV infection prevalence, the number of HBV-infected people remains very high. Approved therapeutic management efficiently suppresses viral replication; however, HBV infection is rarely completely resolved. The major reason for therapeutic failure is the persistence of covalently closed circular DNA (cccDNA), which forms viral minichromosomes by combining with histone and nonhistone proteins in the nucleus. Increasing evidence indicates that chromatin-modifying enzymes, viral proteins, and noncoding RNAs are essential for modulating the function of cccDNA. Therefore, a deeper understanding of the regulatory mechanism underlying cccDNA transcription will contribute to the development of a cure for chronic hepatitis B. This review summarizes the current knowledge of cccDNA biology, the regulatory mechanisms underlying cccDNA transcription, and novel anti-HBV approaches for eliminating cccDNA transcription.
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