ArticleCellular and molecular life sciences : CMLS2026
The BmCPV-derived viral small peptide vsp1S4(-) suppresses viral replication by triggering apoptosis via the ROS-JNK signalling pathway.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Viral antisense RNAs are generally considered noncoding. Here, we show that segment 4 of Bombyx mori cypovirus (BmCPV) encodes a 78-aa antisense-microprotein, vsp1S4(-), that triggers a host-restrictive reactive oxygen species (ROS)-c-Jun N-terminal kinase (JNK)-apoptosis axis. vsp1S4(-) localizes to mitochondria, induces superoxide release, and activates JNK signalling. Consequently, cells undergo caspase-3-dependent apoptosis and S-phase arrest, while the levels of the viral structural protein (VP7) and progeny virions are strongly suppressed. Pharmacologic interruption of either ROS with N-acetylcysteine (NAC) or JNK signalling with SP600125, a dominant-negative JNK effectively rescues VP7 expression and restores viral replication, confirming that vsp1S4(-)-elicited signalling shows antiviral activity. Thus, BmCPV autonomously limits its own propagation through an antisense-encoded peptide that weaponizes host mitochondrial ROS and JNK, representing a paradigm of programmed self-attenuation operating via antisense translation.
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