Semester of Graduation

Summer 2019


Master of Science (MS)



Document Type



Colonies of managed honey bees are annually being lost at an unsustainable rate, partly due to reduced immunocompetence that leads to acute viral outbreaks and mortality. To aid in restoring honey bee health despite the myriad of environmental stressors, this thesis focuses on identifying novel physiological pathways that can mitigate virus-mediated mortality through increased immune function. Previous work has demonstrated that a family of potassium ion channels, termed KATP channels, mediate the survival of honey bees during infection from a model virus, suggesting KATP channels may drive antiviral immunity. Interestingly, these channels have been linked to the regulation of reactive oxygen species (ROS), which are known to function as an immune system stimulator during virus infection. Thus, the overarching goal of this thesis study was to validate the linkage between KATP channels, ROS, and bee survivorship. Our findings in this thesis provide evidence that pinacidil, a KATP channel activator, is capable of dramatically reducing antioxidant levels in bees during chemically-induced ROS, suggesting KATP channels play a part in regulating levels of ROS. Further, mortality was significantly reduced in bees from colonies that had heavy mite infestations, which supports the notion that ROS is an intermediate molecule for immune health. While additional investigation is required to fully characterize the relationship between KATP channels, ROS, and antiviral immunity, this study has begun to fill significant gaps in knowledge pertaining to mechanisms honey bees use to regulate their antiviral immune response.



Committee Chair

Swale, Daniel



Included in

Entomology Commons