1887

Abstract

Apoptosis can protect lepidopteran insects against baculovirus infection by limiting viral replication. Baculoviruses counter this response by expressing anti-apoptotic proteins such as the caspase inhibitor P35, which is expressed by several baculoviruses including mutiple nucleopolyhedrovirus (AcMNPV). Mutants of AcMNPV that lack the gene induce apoptosis in cells, and replication of these mutants is severely curtailed in cell lines and larvae. However, cells from another lepidopteran species, , do not undergo apoptosis when infected with AcMNPV mutants lacking , and mutant and wild-type viruses replicate to equivalent levels in the cell line TN-368 and have equivalent infectivity in larvae by either oral or intrahaemocoelic injection. This has led to the conclusion that is not required for AcMNPV replication in . However, in this study it was found that stocks of mutant virus produced in TN-368 cells had defects in virion stability and infectivity. TN-368 cells infected with mutant AcMNPV exhibited caspase activity, despite a lack of apoptosis, and propagation of the mutant virus in the presence of a chemical caspase inhibitor restored the normal infection phenotype to the progeny virus. These results suggest that caspases can directly or indirectly damage baculovirus virions, and reveal a novel aspect of the role of apoptosis in antiviral defence.

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2009-03-01
2019-11-12
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