The capacity of hepatoviruses to disrupt MAVS-mediated innate immune responses has shaped evolution of both hepatoviruses and their hosts, and facilitates cross-species transmission of hepatitis A.
A recent publication in Science identifies the cytosolic adapter molecule MAVS as being responsible for species restriction of infection with hepatitis A virus as well as linking cytosolic immune sensing in infected hepatocytes with innate effector functions and protective adaptive immunity.