GTPase activity is not essential for the interferon-inducible MxA protein to inhibit the replication of hepatitis B virus

被引：0
作者：
Zhijian Yu
Zhanhui Wang
Jinjun Chen
Hui Li
Zhanzhou Lin
Fan Zhang
Yuanping Zhou
Jinlin Hou
机构：
[1] Nanfang Hospital,Department of Infectious Diseases
[2] Nanfang Medical University,undefined
来源：
Archives of Virology | 2008年 / 153卷
关键词：
HepG2 Cell; GTPase Activity; Recombinant Vector; GTPase Effector Domain; Nuclear Translocation Signal;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Multiple studies have established that GTPase activity is critical for MxA to act against RNA viruses. Recently, it was shown that MxA can also restrict the replication of hepatitis B virus (HBV), a DNA virus, but the requirements for GTPase activity in inhibition of HBV by MxA remain unknown. Here, we report that GTPase-defective mutants (K83A, T103A, and L612K) can downregulate extracellullar HBsAg and HBeAg and reduce the expression of extra- and intracellular HBV DNA in HepG2 cells to levels similar to that achieved by wild-type MxA. Furthermore, TMxA and T103, two nuclear forms of wild-type MxA and a GTPase-defective mutant (T103A) could only slightly decrease the expression of extra- and intracellular HBV DNA in HepG2 cells. In conclusion, GTPase activity is not essential for MxA protein to inhibit HBV replication, and MxA may have only a minimal effect on the replicative cycle of HBV in the nucleus.
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页码：1677 / 1684
页数：7
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