Grass carp reovirus VP56 and VP35 induce formation of viral inclusion bodies for replication
Chu Zhang,
Hui Wu,
Hao Feng,
Yong-An Zhang,
Jiagang Tu
Affiliations
Chu Zhang
State Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Engineering Research Center of Green Development for Conventional Aquatic Biological Industry in the Yangtze River Economic Belt, Ministry of Education, College of Fisheries, Huazhong Agricultural University, Wuhan, China
Hui Wu
State Key Laboratory of Developmental Biology of Freshwater Fish, College of Life Science, Hunan Normal University, Changsha, China
Hao Feng
State Key Laboratory of Developmental Biology of Freshwater Fish, College of Life Science, Hunan Normal University, Changsha, China
Yong-An Zhang
State Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Engineering Research Center of Green Development for Conventional Aquatic Biological Industry in the Yangtze River Economic Belt, Ministry of Education, College of Fisheries, Huazhong Agricultural University, Wuhan, China; Corresponding author
Jiagang Tu
State Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Engineering Research Center of Green Development for Conventional Aquatic Biological Industry in the Yangtze River Economic Belt, Ministry of Education, College of Fisheries, Huazhong Agricultural University, Wuhan, China; Corresponding author
Summary: Viral inclusion bodies (VIBs) are subcellular structures required for efficient viral replication. How type II grass carp reovirus (GCRV-II), the mainly prevalent strain, forms VIBs is unknown. In this study, we found that GCRV-II infection induced punctate VIBs in grass carp ovary (GCO) cells and that non-structural protein 38 (NS38) functioned as a participant in VIB formation. Furthermore, VP56 and VP35 induced VIBs and recruited other viral proteins via the N-terminal of VP56 and the middle domain of VP35. Additionally, we found that the newly synthesized viral RNAs co-localized with VP56 and VP35 in VIBs during infection. Taken together, VP56 and VP35 induce VIB formation and recruit other viral proteins and viral RNAs to the VIBs for viral replication, which helps identify new targets for developing anti-GCRV-II drugs to disrupt viral replication.
