The subversion of both RLR and TLR3 signaling likely contributes to the relatively lengthy, clinically silent incubation period that precedes acute liver injury in hepatitis A. This period is characterized by robust viral replication within the liver and shedding of virus in feces, which reaches a maximum at the onset of hepatic inflammation [10], [39]. The gene discussed is TLR3; the disease is hepatitis A virus infection.