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Quasispecies groups in the core promoter region of hepatitis B virus

Hepatobiliary & Pancreatic Diseases International 2002年第3期1卷 392-396页

作者： Hong Deng Jing Dong Jun Cheng Kun-Jing Huangfu Shuang-Shuang Shi Yuan Hong Xi-Min Ren Li Li the Department of Communicable Diseases, the Second Hospital of Xi’an an Jiaotong University, Xi’an 710004, China and the Gene Therapy Research Center, Institute of Infections Diseases, the 302 Hospital of PLA, Beijing 100039, China Department of Communicable Diseases the Second Hospital of Xi'an Jiaotong University Xi'an 710004 China. dhpd@***

Objectives: To investigate the mutation of the basic core promoter (BCP) of hepatitis B virus (HBV) and clarify the significance of HBV quasispecies groups in patients with chronic HBV infection. Methods: A set of specific primers was synthesized according to the HBV DNA sequence of a Chinese strain. The BCP was amplified by PCR method from the serum of 40 patients with chronic HBV infection, and the PCR products of 2 patients were subcloned into pGEM Teasy vectors. Polyacrylamide gel elec- trophoresis (PAGE) was employed to display the de- letion mutations, and clones with differential length were selected to be sequenced. Sequence comparison was made to find the difference. Results: Two or three bands were displayed by PAGE in 60% patients. The results of sequence anal- ysis showed that there are some kinds of mutations in the BCP region. The substitution always occurs in TATA-like boxes, especially from T to C on 140 site. The deletion mutations were detected in TA1, TA2 and TA3. The 8bp, 20bp deletion mutations fre- quently happened. Conclusions: There is a hot deletion region in the BCP. The deletion and the substitution in the TATA- like box may influence the expression of preC/C pro- tein. The sequencing results indicate that there are HBV quasispecies groups in patients with chronic HBV infection.

关键词： hepatitis B virus basic core promoter mutation polyacrylamide gel electrophoresis quasispecies

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Hepatitis B virus core protein as a Rab-GAP suppressor driving liver disease progression

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Science Bulletin 2024年第16期69卷 2580-2595页

作者： Yu Su Fan Bu Yuanfei Zhu Le Yang Qiong Wu Yuan Zheng Jianjin Zhao Lin Yu Nan Jiang Yongxiang Wang Jian Wu Youhua Xie Xinxin Zhang Yueqiu Gao Ke Lan Qiang Deng Key Laboratory of Medical Molecular Virology(MOE/NHC/CAMS) School of Basic Medical SciencesShanghai Institute of Infectious Disease and BiosecurityFudan UniversityShanghai 200032China Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection Fudan UniversityShanghai 200032China Department of Infectious Diseases Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China Laboratory of Cellular Immunity Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghai 201203China State Key Laboratory of Virology College of Life SciencesWuhan UniversityWuhan 430072China

Chronic hepatitis B virus(HBV)infection can lead to advanced liver ***,we establish a transgenic murine model expressing a basic core promoter(BCP)-mutated HBV *** previous studies on the wild-type virus,the BCP-mutated HBV transgenic mice manifest chronic liver injury that culminates in cirrhosis and tumor development with ***,agonistic anti-Fas treatment induces fulminant hepatitis in these mice even at a negligible *** the BCP mutant exhibits a striking increase in HBV core protein(HBc)expression,we posit that HBc is actively involved in hepatocellular ***,HBc interferes with Fis1-stimulated mitochondrial recruitment of Tre-2/Bub2/Cdc16 domain family member 15(TBC1D15).HBc may also inhibit multiple Rab GTPase-activating proteins,including Rab7-specific TBC1D15 and TBC1D5,by binding to their conserved catalytic *** cells under mitochondrial stress,HBc thus perturbs mitochondrial dynamics and prevents the recycling of damaged ***,sustained HBc expression causes lysosomal consumption via Rab7 hyperactivation,which further hampers late-stage autophagy and substantially increases apoptotic cell ***,we show that adenovirally expressed HBc in a mouse model is directly cytopathic and causes profound liver injury,independent of antigen-specific immune *** findings reveal an unexpected cytopathic role of HBc,making it a pivotal target for HBV-associated liver disease *** BCP-mutated HBV transgenic mice also provide a valuable model for understanding chronic hepatitis B progression and for the assessment of therapeutic strategies.

关键词： Apoptosis basic core promoter Mitophagy Rab7 Transgenic mice

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