Impact of hepatitis B virus replication on Rho GTPases

Abstract

Hepatitis B Virus (HBV) is the cause of liver diseases such as hepatocellular carcinoma. It is important to understand its interaction with cellular proteins to determine prognosis. From literature review, it was shown that HBV specifically activated Rac1 GTPase through a proline-rich region in its protein HBx. Even though Cdc42 is an upstream activator of Rac1, HBx did not activate Cdc42. To demonstrate the impact of HBV replication in HepG2 cells on RhoA, a cell migration transwell assay was done. However, due to inconsistencies, the results from this experiment did not yield a definite conclusion about the impact of HBV replication on RhoA. This was despite successful transfection of HepG2 cells, and successful expression of RhoA and HBV vectors. Three possible scenarios were discussed: 1) that HBV does not activate RhoA; 2) HBV activates RhoA through its proline-rich region; and 3) HBV activates RhoA, but not through its proline-rich region. The possible reasons for the inconsistencies were discussed and several recommendations were suggested to improve future experiments.