Meeting Abstract
Honey bees (Apis mellifera) play a vital role in pollinating both agricultural crops and wild plants. However, over the past several decades honey bee populations have been declining in a phenomenon known as Colony Collapse Disorder (CCD). The ectoparasitic mite, Varroa destructor, has been a large contributor to CCD, as it is known to transfer viruses that may ultimately lead to colony loss. As previously shown, varroa mites enhance the effects of these infections as well, causing abnormalities in bee physiology and behavior. Looking specifically at physiology, our project analyzed how a dicistrovirus, cricket paralysis virus (CrPV), affects the gene expression of vitellogenin. Vitellogenin is linked with regulatory behaviors; low amounts promote frantic foraging behaviors that may aid in CCD. Honey bees were divided into the following groups: No injection control, Vehicle injection control, CrPV, or V. destructor protein + CrPV (VP+CrPV). Bees were halved and used in both viral quantification using TCID50 assays and gene expression analysis using quantitative reverse transcription PCR (RT-qPCR). Vitellogenin mRNA was quantified alongside CrPV viral RNA with the use of β-actin as a reference gene. VP+CrPV exposed bees had an 89.2% higher level of viremia compared to CrPV-infected bees only, according to TCID50 results. Control bees exhibited no viremia. Relative vitellogenin expression was significantly lower in the VP+CrPV and CrPV infected bees compared to control bees. These results uncover a potentially substantial physiological relationship between viral disease and vitellogenin that may inform us about some of the underlying mechanisms of colony collapse disorder.
