The Autographa californica Multiple Nucleopolyhedrovirus ac51 Gene Is Required for Efficient Nuclear Egress of Nucleocapsids and Is Essential for In Vivo Virulence.

Abstract

Alphabaculoviruses are lepidopteran-specific nucleopolyhedroviruses that replicate within the nucleus; however, the anterograde transport of the nucleocapsids of these viruses, which is an obligatory step for progeny virion production, is not well understood. In the present study, a unique Alphabaculovirus gene with unknown function, namely, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) ac51 gene, was found to be required for efficient nuclear egress of AcMNPV nucleocapsids. Our results indicate that ac51 is a late gene, and Ac51 protein was detectable from 24 to 72 h postinfection using an antibody raised against Ac51. Ac51 is distributed in both the cytoplasm and nuclei of infected cells. Upon ac51 deletion, budded virion (BV) production by 96 h posttransfection was reduced by approximately 1,000-fold compared with that of wild-type AcMNPV. Neither viral DNA synthesis nor viral gene expression was affected. Ac51 was demonstrated to be a nucleocapsid protein of BVs, and ac51 deletion did not interrupt nucleocapsid assembly and occlusion-derived virion (ODV) formation. However, BV production in the supernatants of transfected cells during a viral life cycle was substantially decreased when ac51 was deleted. Further analysis showed that, compared with wild-type AcMNPV, ac51 deletion decreased nucleocapsid egress, while the numbers of nucleocapsids in the nuclei were comparable. Deletion of ac51 also eliminated the virulence of AcMNPV in vivo Taken together, our results support the conclusion that ac51 plays an important role in the nuclear egress of nucleocapsids during BV formation and is essential for the in vivo virulence of AcMNPV.