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

作者：Yu Zhijian; Wang Zhanhui; Chen Jinjun; Li Hui; Lin Zhanzhou; Zhang Fan; Zhou Yuanping; Hou Jinlin^*

来源：Archives of Virology, 2008, 153(9): 1677-1684.

DOI：10.1007/s00705-008-0168-9

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.

• 出版日期2008-9
• 单位南方医科大学