Disruption of Autographa Californica Multiple Nucleopolyhedrovirus ac111 Results in Reduced per os Infectivity in a Host-Dependent Manner

The Autographa californica multiple nucleopolyhedrovirus (AcMNPV) gene is highly conserved in lepidopteran-specific baculoviruses, and its function in the AcMNPV life cycle is still unknown. To investigate the function of , an -knockout AcMNPV (vAc111KO) was constructed through homologous recombination in . Viral growth curve analysis and plaque assays showed that the deletion of had no effect on infectious budded virion production. Quantitative real-time polymerase chain reaction analysis confirmed that viral DNA replication was unaffected in the absence of . Electron microscopy revealed that the deletion did not affect nucleocapsid assembly, occlusion-derived virion formation, or the embedding of occlusion-derived virions into the occlusion bodies. However, in vivo bioassays showed that although the deletion of did not affect the infectivity of AcMNPV in larvae, it led to an approximately five-fold reduction in infectivity of AcMNPV in larvae, and vAc111KO took approximately 21 h longer to kill larvae than the wild-type viruses. Taken together, our results demonstrated that although is not essential for virus replication in vitro, it plays an important role in the infectivity of AcMNPV in a host-dependent manner.