1887

Abstract

nucleopolyhedrovirus () and its homologues are highly conserved in genomes of all sequenced group I alphabaculoviruses and its function is still unknown. Transcriptional analysis revealed that is a very late gene initiated from a late transcriptional start motif TAAG. To examine its role in the virus, a knockout virus (vBm) was generated through homologous recombination in . Analysis of fluorescence microscopy, titration assays and electron microscopy examination showed that the deletion of did not affect viral replication and occlusion bodies formation , indicating that is not required for viral propagation. However, vBm did not result in cell lysis when wild-type virus infected cells began to lyse, and the vBm infected cells remained intact until 2 weeks post-infection. Quantification of polyhedra release from cells confirmed this observation. Accordingly, though deletion of did not reduce nucleopolyhedrovirus infectivity in bioassays, it did significantly disrupt the larval liquefaction, reducing the level of polyhedra release from infected host. Immunofluorescence analysis demonstrated that Bm58a was predominantly localized on the cellular membrane at the late stage of infection, which may contribute to its function of facilitating cell lysis and larval liquefaction. Our results suggest that although is not essential for viral propagation as an auxiliary gene, it is a key factor of virus-induced cell lysis and larval liquefaction and .

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2016-11-10
2024-04-19
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