Abstract: RNA viruses were sensed by pathogen-associated pattern recognition receptors (PRRs),such as Toll-like receptor 3,retinoic acid-inducible gene I,and melanoma differentiation-associated gene 5.PRRs activation leads to production of Type 1 interferon (IFN-α/β),which serves as the first line to defend against viruses.HAV has developed various strategies to evade the innate immune system and promote viral replication inside the host cells.The long-term co-evolution of HAV with hosts has promoted the development of effective immune evasion strategies that actively counteract host antiviral responses.Proteases encoded by HAV can cleave mitochondrial antiviral signaling protein,TIR domain-containing adaptor inducing IFN-β and nuclear factor-κB (NF-κB) essential modulator,which are key adaptor proteins in RIG-I-like receptor,Toll-like receptor 3 and NF-κB signaling,respectively.In this mini-review,we summarize the recent progress on the interaction between HAV and host,especially focusing on how HAV abrogates the antiviral effect of innate immune system.

Key words: HAV, MAVS, TRIF, Type 1 interferon