College of Life Sciences and Laboratory for Marine Biology and Biotechnology of Qingdao National Laboratory for Marine Science and Technology, Zhejiang University, Hangzhou, 310058, People's Republic of China.
College of Life Sciences and Laboratory for Marine Biology and Biotechnology of Qingdao National Laboratory for Marine Science and Technology, Zhejiang University, Hangzhou, 310058, People's Republic of China.
Fish Shellfish Immunol. 2019 Sep;92:21-30. doi: 10.1016/j.fsi.2019.05.058. Epub 2019 May 27.
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.
DCP1-DCP2 复合物可通过逆转录病毒 RNA 的脱帽和 RNA 病毒感染期间 RNAi 的抑制来调节动物的抗病毒免疫。然而，DCP1-DCP2 复合物对 DNA 病毒感染的影响以及 microRNAs（miRNAs）对 DCP1-DCP2 复合物的调节仍不清楚。在本研究中，表征了 miRNA 调节的 DCP1-DCP2 复合物在 DNA 病毒感染中的作用。我们的结果表明，DCP1-DCP2 复合物在虾的 DNA 病毒白斑综合征病毒（WSSV）的感染中发挥了积极作用。在 DCP1-DCP2 复合物中，DCP2 的 N 端调节结构域与 DCP1 的 EVH1 结构域相互作用。此外，虾 miRNA miR-87 通过靶向宿主 DCP2 基因抑制 WSSV 感染，而病毒 miRNA WSSV-miR-N46 通过靶向宿主 DCP1 基因对 WSSV 复制产生负效应。因此，本研究为 DCP1-DCP2 复合物及其在病毒-宿主相互作用中的 miRNA 调节的潜在机制提供了新的见解。
在 RNA 病毒感染期间，DCP1-DCP2 复合物通过脱帽逆转录病毒 RNA 和抑制 RNAi，在动物抗病毒免疫中发挥重要作用。在本研究中，研究结果表明，DCP1 和 DCP2 的沉默抑制了虾白斑综合征病毒（一种虾的 DNA 病毒）的感染，这表明 DCP1-DCP2 复合物促进了 DNA 病毒的感染。由于 DCP1-DCP2 复合物在虾 RNAi 对 WSSV 感染的抑制作用，DCP1-DCP2 复合物可能促进了 WSSV 在虾中的感染。结果表明，WSSV-miR-N46 和虾 miR-87 可以分别抑制 DCP1 和 DCP2 的表达，从而影响病毒感染。因此，我们的研究为 DCP1-DCP2 复合物及其在病毒-宿主相互作用中的 miRNA 调节提供了新的方面。
