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

Author:

Sun Yuechao,Zhang Xiaobo

Abstract

AbstractThe DCP1-DCP2 complex can regulate the animal antiviral immunity by the decapping of retrovirus RNAs and the suppression of RNAi pathway. 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, we investigated the role of miRNA-regulated DCP1-DCP2 complex in DNA virus infection. Our results suggested that the DCP1-DCP2 complex played a positive role in the infection of white spot syndrome virus (WSSV), a DNA virus of shrimp. The N-terminal regulatory domain of DCP2 was interacted with the EVH1 domain of DCP1, forming the DCP1-DCP2 complex. Furthermore, a host shrimp miRNA (miR-87) inhibited WSSV infection by targeting the host DCP2 gene and a 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.The DCP1-DCP2 complex can regulate the animal antiviral immunity by the decapping of retrovirus RNAs and the suppression of RNAi pathway. In the present study, the findings indicated that the silencing of the DCP1-DCP2 complex 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 RNAi pathway against virus infection, the DCP1-DCP2 complex could promote WSSV infection in shrimp. In this context, our study contributed a novel aspect of the DCP1-DCP2 complex in virus-host interactions. Our study revealed that the host and viral miRNAs could regulate the DCP1-DCP2 complex to affect virus infection. Therefore, our study provided novel insights into the miRNA-mediated regulation of DCP1-DCP2 complex took great effects on RNAi immunity of invertebrates against virus infection.

Publisher

Cold Spring Harbor Laboratory

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