Hepatitis B virus dampens autophagy maturation via negative regulation of Rab7 expression
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- Zhou Tianhui
- Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
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- Jin Min
- ey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine
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- Ding Yongsen
- Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
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- Zhang Yi
- Biomedical Research Center, Zhongshan Hospital, Fudan University Shanghai Key Laboratory of Organ Transplantation
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- Sun Ye
- Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
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- Huang Shiqian
- Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine
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- Xie Qing
- Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
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- Xu Congfeng
- Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine ey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine
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- Cai Wei
- Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
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抄録
<p>Hepatitis B virus (HBV) infection brings a huge challenge for medical health practitioners. It has been reported that invaded HBV escapes autophagic degradation through inhibiting lysosome maturation following enhanced autophagy formation, which putatively contributes to HBV replication and infection. However, the underlying mechanism by which HBV escapes from autophagic degradation remains elusive. In this study, we monitored the autophagic process using HepG2 cells and mice without or with transient HBV DNA plasmid transfection (pHepG2) or stable HBV infection (HepG2.2.15 cells) in vitro and in vivo. The results of Western blot, transmission electron microscopy and confocal microscopy, confirmed that HBV induced autophagy, while the fusion of autophagosomes with lysosomes was arrested. Furthermore, Rab7, a small GTPase that functions as a molecular switch responsible for the autophagosome-lysosome fusion, was inhibited, suggesting a potential mechanism for HBV-induced inhibition of autophagic degradation. In conclusion, our study proposes a potential mechanism for how HBV escapes autophagic degradation, which might be a novel therapeutic target for controlling HBV infection.</p>
収録刊行物
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- BioScience Trends
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BioScience Trends 10 (4), 244-250, 2016
特定非営利活動法人 バイオ＆ソーシャル・サイエンス推進国際研究交流会