IAPV-induced arrested development in infected honey bee pupae

In the environment, honey bees are often exposed to pathogens throughout their entire life cycle. One of these pathogens is Israeli Acute Paralysis Virus (IAPV), which is especially virulent in white-eyed honey bee pupae, often resulting in developmental defects or mortality. Despite its impact, the mechanisms by which IAPV manipulates host physiology to enhance its replication remain poorly understood. Prior lab experiments showed that bees surviving oral IAPV infection as larvae developed normally until the white-eyed pupal stage, where development was arrested without overt signs of mortality – a phenotype also observed after direct pupal injection with IAPV. In this study, we investigate the host manipulation mechanism of IAPV to maximize its fitness by quantifying the cuticular hydrocarbon (CHC) profile of experimentally infected honey bee pupae and the transcripts of target genes that may induce an arrested development phenotype. Based on preliminary data, we predict that IAPV-infected bee pupae will exhibit a similar chemical profile to healthy bees to maximize IAPV replication without being discovered by worker bees and an upregulation of genes that stall development in the immature stage. These findings elucidate how IAPV exploits host physiology to propagate within honey bee colonies, offering insights into pathogen-host dynamics.