HBx function in immune evasion
HBx directly interacts with, and inhibits host MAVS protein by inducing its ubiquitination and targeting it for degradation (Wei et al. 2010) Rating=2, (Kumar et al. 2011) Rating=2. It therefore plays a role in immune evasion. MAVS is localized to the outer mitochondrial membrane and coordinates many signaling events. It plays a pivotal role in the induction of antiviral and inflammatory pathways and is also involved in the coordination of apoptosis.
This activity of HBx is presumably true. Indeed hepatitis A (Yang et al. 2007) Rating=2, hepatitis B and hepatitis C (Li et al. 2005) Rating=2 proteins have been described as being able to counteract MAVS antiviral signaling. This suggests that hepatocytes antiviral defenses could likely involve MAVS.
Unlike most mammalian viruses, hepatitis A, B or C virus do not directly counteract interferon signaling JAK-STAT pathway, suggesting that hepatocytes must be poorly exposed to IFN upon infection and that no selective pressure would induce the virus to counteract this pathway.