Role of DCP1-DCP2 complex regulated by viral and host microRNAs in DNA virus infection

The DCP1-DCP2 complex can regulate the antiviral immunity of animals by the decapping of retrovirus RNAs and the suppression of RNAi during RNA virus infection. However, the influence of DCP1-DCP2 complex on DNA virus infection and the regulation of DCP1-DCP2 complex by microRNAs (miRNAs) remain unclear. In this study, the role of miRNA-regulated DCP1-DCP2 complex in DNA virus infection was characterized. Our results showed that the DCP1-DCP2 complex played a positive role in the infection of white spot syndrome virus (WSSV), a DNA virus of shrimp. In the DCP1-DCP2 complex, the N-terminal regulatory domain of DCP2 was interacted with the EVH1 domain of DCP1. Furthermore, shrimp miRNA miR-87 inhibited WSSV infection by targeting the host DCP2 gene and viral miRNA WSSV-miR-N46 took a negative effect on WSSV replication by targeting the host DCP1 gene. Therefore, our study provided novel insights into the underlying mechanism of DCP1-DCP2 complex and its regulation by miRNAs in virus-host interactions. IMPORTANCE: During RNA virus infection, the DCP1-DCP2 complex can play important roles in the animal antiviral immunity by decapping retrovirus RNAs and suppressing RNAi. In the present study, the findings indicated that the silencing of DCP1 and DCP2 inhibited the infection of WSSV, a DNA virus of shrimp, suggesting that the DCP1-DCP2 complex facilitated DNA virus infection. Due to the suppressive role of the DCP1-DCP2 complex in shrimp RNAi against WSSV infection, the DCP1-DCP2 complex could promote WSSV infection in shrimp. The results showed that WSSV-miR-N46 and shrimp miR-87 could respectively suppress the expressions of DCP1 and DCP2 to affect virus infection. Therefore, our study contributed novel aspects of the DCP1-DCP2 complex and its regulation by miRNAs in virus-host interactions.