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Different effects of HBV and its viral proteins on TRAIL‐induced apoptosis and their distinct mechanisms
Author(s) -
Du Juan,
Liang Xiaohong,
Chen Youhai,
Liu Yugang,
Cui Min,
Han Lihui,
Liu Suxia,
Qu Zhonghua,
Zhang Zhiyong,
Sun Wensheng
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.856.8
Subject(s) - hbx , apoptosis , hepatitis b virus , tunel assay , biology , pathogenesis , virology , fulminant hepatitis , immunology , hepatitis , microbiology and biotechnology , cancer research , virus , genetics
TNF‐related apoptosis‐inducing ligand (TRAIL) has recently been implicated in the death of hepatocytes during HBV infection, but the mechanisms are not well understood. To determine the role of TRAIL in HBV infection, we examined the effects of HBV genome and its viral proteins on TRAIL‐induced apoptosis. TUNEL assay showed HBV genome or HBx protein significantly increased TRAIL‐induced apoptosis through upregulating Bax expression. Similarly, C‐terminally truncated middle hepatitis B surface protein (MHBs(t)) sensitized hepatocytes to TRAIL‐induced apoptosis through involving ERK2. By contrast, other HBV proteins played an opposite role in TRAIL‐induced apoptosis although the mechanisms remain to be elucidated. These results establish different HBV proteins have different effects on TRAIL‐induced hepatocyte apoptosis. If the pro‐apoptotic proteins, such as HBx, are dominant, HBV infected hepatocytes may die as a consequence and fulminant hepatitis may develop. While, if the anti‐apoptotic viral proteins prevail, the infected hepatocytes may not undergo apoptosis and chronic HBV infection may ensue. These findings clarify the roles of imbalanced apoptosis in the pathogenesis of hepatitis B infection. This work is supported by the Natural Science Fund of China (No.30772031, No.30700973).