Honey bees are economically important pollinators of a wide variety of crops that have attracted the attention of both researchers and the public alike due to unusual declines in the numbers of managed bee colonies. Viral infections are thought to be a significant factor contributing to these declines, but viruses have proven a challenging pathogen to study in a bee model and interactions between viruses and the bee antiviral immune response remain poorly understood. In the work described here, we demonstrate the use of flock house virus (FHV) as a model system for the study of viral infections in bees and reveal an important role for ATP-sensitive inwardly rectifying potassium (KATP) channels in the regulation of the bee antiviral immune response. KATP channels couple cellular metabolism to the membrane potential of the cell and have been demonstrated to play an evolutionarily conserved role in mediating the innate immune response of both insects and mammals during a viral infection. Most of what is known about these ion channels is the result of work performed in mammalian systems, with insect studies being limited to only a few model species and physiological systems that have not included bees. Using FHV as a model for infection, we have shown that treatment with the KATP channel agonist pinacidil increases survival of bees while decreasing viral replication following infection with FHV, whereas treatment with the KATP channel antagonist tolbutamide decreases survival and increases viral replication. Our results suggest that KATP channels provide a significant link between cellular metabolism and the antiviral immune response in bees. This work represents a promising area for future research designed to enhance our understanding of honey bee disease tolerance and the factors that negatively impact pollinator health.

ATP-sensitive inwardly rectifying potassium channel regulation of viral infections in honey bees

254th National Meeting (2017)

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