BmJun promotes viral proliferation and suppresses BmNPV-induced apoptosis in association with transcriptional upregulation of p35.

Abstract

Bombyx mori nucleopolyhedrovirus (BmNPV) is a major viral pathogen of silkworms, causing significant economic losses in the sericulture industry. BmNPV infection can induce host-cell apoptosis as an antiviral defense response, whereas the virus must suppress premature apoptosis to complete productive infection. However, the underlying mechanisms remain to be elucidated. Currently, no effective control strategies are available for managing BmNPV infection in silkworms. We previously observed a significant increase in BmJun protein levels after BmNPV infection. Members of the Jun protein family serve as important substrates in the JNK/MAPK signaling pathway and are vital for cellular responses to viral infections and apoptosis. Nevertheless, its function in B. mori has yet to be fully elucidated. Here, we showed that overexpression of BmJun significantly enhanced BmNPV proliferation. Subsequently, chromatin immunoprecipitation sequencing (ChIP-seq) revealed significant enrichment of BmJun at the promoter of the viral anti-apoptotic gene p35, and this association was further confirmed by ChIP-qPCR. Dual-luciferase reporter assays showed that BmJun activates p35 transcription through the -255 to -75 bp region of the p35 promoter. BmJun overexpression reduced host-cell apoptosis, consistent with its activation of the viral anti-apoptotic gene p35, thereby contributing to BmNPV proliferation. These findings suggest that BmJun may facilitate BmNPV proliferation by transcriptionally activating p35 and suppressing host-cell apoptosis. Together, these findings provide new insight into the molecular interactions between B. mori and BmNPV and advance our understanding of baculovirus pathogenesis.