Abstract

Simple SummaryBaculoviruses arrest the cell cycle in the S or G2/M phase in insect cells, but the exact mechanism of this process still remains obscure. Bombyx mori nucleopolyhedrovirus (BmNPV), one of the best characterized baculoviruses, is an important pathogen in silkworms. In the present study, we determined that downregulation ofBmCDK1andBmCyclin Bexpression was required for BmNPV-mediated G2/M phase arrest, which plays an essential role in facilitating BmNPV replication. Further investigations showed that BmNPV IAP1 interacted with BmCDK1. The overexpression of the BmNPViap1gene led to the accumulation of cells in the G2/M phase, and BmNPViap1gene knockdown attenuated the effect of BmNPV-mediated G2/M phase arrest. These findings enhance the understanding of BmNPV pathogenesis, and indicate a novel mechanism through which baculoviruses impact the cell cycle progression.AbstractUnderstanding virus–host interaction is very important for delineating the mechanism involved in viral replication and host resistance. Baculovirus, an insect virus, can cause S or G2/M phase arrest in insect cells. However, the roles and mechanism of Baculovirus-mediated S or G2/M phase arrest are not fully understood. Our results, obtained using flow cytometry (FCM), tubulin-labeling, BrdU-labeling, and CellTiter 96®AQueous One Solution Cell Proliferation Assay (MTS), showed that Bombyx mori nucleopolyhedrovirus (BmNPV) induced G2/M phase arrest and inhibited cellular DNA replication as well as cell proliferation in BmN-SWU1 cells. We found that BmNPV induced G2/M arrest to support its replication and proliferation by reducing the expression ofBmCDK1andBmCyclin B. Co-immunoprecipitation assays confirmed that BmNPV IAP1 interacted with BmCDK1. BmNPViap1was involved in the process of BmNPV-induced G2/M arrest by reducing the content of BmCDK1. Taken together, our results improve the understanding of the virus–host interaction network, and provide a potential target gene that connects a