With long-term evolution, sophisticated mechanisms are formed by viruses to break host defense and utilize host proteins to facilitate their amplification. Here we found protein moloney leukemia virus 10(MOV10), which was identified as a putative RNA helicase and P-body component, interacts with 5’UTR of enterovirus 71(EV71) genome and facilitates viral IRES-dependent translation. Silencing of cellular MOV10 by siRNA could restrict EV71 replication, while dose-escalating over-expression of MOV10 had a first increase then decrease effect on viral replication. We also overexpressed C-term and N-term of MOV10 separately before EV71 infection, and found that N-term of MOV10 could restrict VP1 expression. We also found MOV10 co-localized with nuclear proteins TDP43, FUS and HuR after viral infection. Taken together, our data indicate a dual function of MOV10 in EV71 amplification for the first time, but the detailed mechanism still remains to be further investigated. |