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The constant pressure posed by parasites has caused species throughout the animal kingdom to evolve suites of mechanisms to resist infection. Individual barriers and physiological defenses are considered the main barriers against parasites in invertebrate species. However, behavioral traits and other non-immunological defenses can also effectively reduce parasite transmission and infection intensity. In social insects, behaviors that reduce colony-level parasite loads are termed \"social immunity.\" One example of a behavioral defense is resin collection. Honey bees forage for plant-produced resins and incorporate them into their nest architecture. This use of resins can reduce chronic elevation of an individual bee's immune response. Since high activation of individual immunity can impose colony-level fitness costs, collection of resins may benefit both the individual and colony fitness. However the use of resins as a more direct defense against pathogens is unclear. Here we present evidence that honey bee colonies may self-medicate with plant resins in response to a fungal infection. Self-medication is generally defined as an individual responding to infection by ingesting or harvesting non-nutritive compounds or plant materials. Our results show that colonies increase resin foraging rates after a challenge with a fungal parasite (Ascophaera apis: chalkbrood or CB). Additionally, colonies experimentally enriched with resin had decreased infection intensities of this fungal parasite. If considered self-medication, this is a particularly unique example because it operates at the colony level. Most instances of self-medication involve pharmacophagy, whereby individuals change their diet in response to direct infection with a parasite. In this case with honey bees, resins are not ingested but used within the hive by adult bees exposed to fungal spores. Thus the colony, as the unit of selection, may be responding to infection through self-medication by increasing the number of individuals that forage for resin.

Food quantity and macronutrients contribute to honey bee health and colony survival by mediating immune responses. We determined if this held true for bees injected with chronic bee paralysis virus (CBPV) and deformed wing virus (DWV), two common honey bee ssRNA viruses. Pollen-substitute diet and syrup consumption rates and macronutrient preferences of two Varroa-resistant stocks (Pol-Line and Russian bees) were compared to Varroa-susceptible Italian bees. Bee stocks varied in consumption, where Italian bees consumed more than Pol-Line and Russian bees. However, the protein: lipid (P:L) ratios of diet consumed by the Italian and Russian bees was greater than that of the Pol-Line bees. Treatment had different effects on consumption based on the virus injected. CBPV was positively correlated with syrup consumption, while DWV was not correlated with consumption. P:L ratios of consumed diet were significantly impacted by the interaction of bee stock and treatment, with the trends differing between CBPV and DWV. Variation in macronutrient preferences based on viral species may indicate differences in energetic costs associated with immune responses to infections impacting different systems. Further, virus species interacted with bee genotype, indicating different mechanisms of viral resistance or tolerance among honey bee genotypes.

Nutrition is an important component of social insect colony health especially in the face of stressors such as parasitism and viral infections. Honey bees are known to preferentially select nectar and pollen based on macronutrient and phytochemical contents and in response to pathogen loads. However, given that honey bees live in colonies, collective foraging decisions may be impacted directly by forager infection status but also by colony health. This field experiment was conducted to determine if honey bee viral infections are correlated with pollen and nectar foraging and if these associations are impacted more by colony or forager infection. By comparing regressions with and without forager and colony variables and through structural equation models, we were able to determine the relative contributions of colony and forager virus loads on forager decisions. We found that foragers had higher numbers and levels of BQCV and CBPV but lower levels of DWV viruses than their respective colonies. Overall, individuals appeared to forage based a combination of their own and colony health but with greater weight given to colony metrics. Colony parasitism by Varroa mites, positively correlated with both forager and colony DWV-B levels, was negatively associated with nectar weight. Further, colony DWV-B levels were negatively associated with individually foraged pollen protein: lipid ratios but positively correlated with nectar weight and sugar content. This study shows that both colony and forager health can simultaneously mediate individual foraging decisions and that the importance of viral infections and parasite levels varies with foraging metrics. Overall, this work highlights the continued need to explore the interactions of disease, nutrition, and genetics in social interactions and structures.

When wild honey bee colonies ( Apis mellifera ) nest in hollow tree cavities, they coat the rough cavity walls with a continuous layer of propolis, a substance comprised primarily of plant resins. Studies have shown that the resulting “propolis envelope” leads to both individual- and colony-level health benefits. Unfortunately, the smooth wooden boxes most commonly used in beekeeping do little to stimulate propolis collection. As a result, most managed bees live in hives that are propolis-poor. In this study, we assessed different surface texture treatments (rough wood boxes, boxes outfitted with propolis traps, and standard, smooth wood boxes) in terms of their ability to stimulate propolis collection, and we examined the effect of propolis on colony health, pathogen loads, immune gene expression, bacterial gene expression, survivorship, and honey production in both stationary and migratory beekeeping contexts. We found that rough wood boxes are the most effective box type for stimulating propolis deposition. Although the use of rough wood boxes did not improve colony survivorship overall, Melissococcus plutonius detections via gene expression were significantly lower in rough wood boxes, and viral loads for multiple viruses tended to decrease as propolis deposition increased. By the end of year one, honey bee populations in migratory rough box colonies were also significantly larger than those in migratory control colonies. The use of rough wood boxes did correspond with decreased honey production in year one migratory colonies but had no effect during year two. Finally, in both stationary and migratory operations, propolis deposition was correlated with a seasonal decrease and/or stabilization in the expression of multiple immune and bacterial genes, suggesting that propolis-rich environments contribute to hive homeostasis. These findings provide support for the practical implementation of rough box hives as a means to enhance propolis collection and colony health in multiple beekeeping contexts.

The ectoparasite Varroa destructor is the greatest threat to managed honey bee ( Apis mellifera ) colonies globally. Despite significant efforts, novel treatments to control the mite and its vectored pathogens have shown limited efficacy, as the host remains naïve. A prospective solution lies in the development of Varroa -resistant honey bee stocks, but a paucity of rigorous selection data restricts widespread adoption. Here, we characterise the parasite and viral dynamics of a Varroa -resistant honey bee stock, designated ‘Pol-line’, using a large-scale longitudinal study. Results demonstrate markedly reduced Varroa levels in this stock, diminished titres of three major viruses (DWV-A, DWV-B, and CBPV), and a two-fold increase in survival. Levels of a fourth virus that is not associated with Varroa —BQCV—do not differ between stocks, supporting a disruption of the transmission pathway. Further, we show that when decoupled from the influence of Varroa levels, viral titres do not constitute strong independent predictors of colony mortality risk. These findings highlight the need for a reassessment of Varroa etiology, and suggest that derived stocks represent a tractable solution to the Varroa pandemic.

Declines in managed honey bee populations are multifactorial but closely associated with reduced virus immunocompetence and thus, mechanisms to enhance immune function are likely to reduce viral infection rates and increase colony viability. However, gaps in knowledge regarding physiological mechanisms or ‘druggable’ target sites to enhance bee immunocompetence has prevented therapeutics development to reduce virus infection. Our data bridge this knowledge gap by identifying ATP-sensitive inward rectifier potassium (K ATP ) channels as a pharmacologically tractable target for reducing virus-mediated mortality and viral replication in bees, as well as increasing an aspect of colony-level immunity. Bees infected with Israeli acute paralysis virus and provided K ATP channel activators had similar mortality rates as uninfected bees. Furthermore, we show that generation of reactive oxygen species (ROS) and regulation of ROS concentrations through pharmacological activation of K ATP channels can stimulate antiviral responses, highlighting a functional framework for physiological regulation of the bee immune system. Next, we tested the influence of pharmacological activation of K ATP channels on infection of 6 viruses at the colony level in the field. Data strongly support that K ATP channels are a field-relevant target site as colonies treated with pinacidil, a K ATP channel activator, had reduced titers of seven bee-relevant viruses by up to 75-fold and reduced them to levels comparable to non-inoculated colonies. Together, these data indicate a functional linkage between K ATP channels, ROS, and antiviral defense mechanisms in bees and define a toxicologically relevant pathway that can be used for novel therapeutics development to enhance bee health and colony sustainability in the field.

The ongoing decline of honey bee health worldwide is a serious economic and ecological concern. One major contributor to the decline are pathogens, including several honey bee viruses. However, information is limited on the biology of bee viruses and molecular interactions with their hosts. An experimental protocol to test these systems was developed, using injections of Israeli Acute Paralysis Virus (IAPV) into honey bee pupae reared ex-situ under laboratory conditions. The infected pupae developed pronounced but variable patterns of disease. Symptoms varied from complete cessation of development with no visual evidence of disease to rapid darkening of a part or the entire body. Considerable differences in IAPV titer dynamics were observed, suggesting significant variation in resistance to IAPV among and possibly within honey bee colonies. Thus, selective breeding for virus resistance should be possible. Gene expression analyses of three separate experiments suggest IAPV disruption of transcriptional homeostasis of several fundamental cellular functions, including an up-regulation of the ribosomal biogenesis pathway. These results provide first insights into the mechanisms of IAPV pathogenicity. They mirror a transcriptional survey of honey bees afflicted with Colony Collapse Disorder and thus support the hypothesis that viruses play a critical role in declining honey bee health.

The synergistic interactions between the ectoparasitic mite Varroa destructor and Deformed wing virus (DWV) lead to the reduction in lifespan of the European honey bee Apis mellifera and often have been implicated in colony losses worldwide. However, to date, the underlying processes and mechanisms that form the multipartite interaction between the bee, mite, and virus have not been fully explained. To gain a better understanding of honey bees’ defense response to Varroa mite infestation and DWV infection, the DWV titers and transcription profiles of genes originating from RNAi, immunity, wound response, and homeostatic signaling pathways were monitored over a period of eight days. With respect to DWV, we observed low viral titers at early timepoints that coincided with high levels of Toll pathway transcription factor Dorsal, and its downstream immune effector molecules Hymenoptaecin, Apidaecin, Abaecin, and Defensin 1. However, we observed a striking increase in viral titers beginning after two days that coincided with a decrease in Dorsal levels and its corresponding immune effector molecules, and the small ubiquitin-like modifier (SUMO) ligase repressor of Dorsal, PIAS3. We observed a similar expression pattern for genes expressing transcripts for the RNA interference (Dicer/Argonaute), wound/homeostatic (Janus Kinase), and tissue growth (Map kinase/Wnt) pathways. Our results demonstrate that on a whole, honey bees are able to mount an immediate, albeit, temporally limited, immune and homeostatic response to Varroa and DWV infections, after which downregulation of these pathways leaves the bee vulnerable to expansive viral replication. The critical insights into the defense response upon Varroa and DWV challenges generated in this study may serve as a solid base for future research on the development of effective and efficient disease management strategies in honey bees.

The ongoing decline of honey bee health worldwide is a serious economic and ecological concern. One major contributor to the decline are pathogens, including several honey bee viruses. However, information is limited on the biology of bee viruses and molecular interactions with their hosts. An experimental protocol to test these systems was developed, using injections of Israeli Acute Paralysis Virus (IAPV) into honey bee pupae reared ex-situ under laboratory conditions. The infected pupae developed pronounced but variable patterns of disease. Symptoms varied from complete cessation of development with no visual evidence of disease to rapid darkening of a part or the entire body. Considerable differences in IAPV titer dynamics were observed, suggesting significant variation in resistance to IAPV among and possibly within honey bee colonies. Thus, selective breeding for virus resistance should be possible. Gene expression analyses of three separate experiments suggest IAPV disruption of transcriptional homeostasis of several fundamental cellular functions, including an up-regulation of the ribosomal biogenesis pathway. These results provide first insights into the mechanisms of IAPV pathogenicity. They mirror a transcriptional survey of honey bees afflicted with Colony Collapse Disorder and thus support the hypothesis that viruses play a critical role in declining honey bee health.

Non-target impacts of insecticide treatments are a major public and environmental concern, particularly in contemporary beekeeping. Therefore, it is important to understand the physiological mechanisms contributing to insecticide sensitivity in honey bees. In the present studies, we sought to evaluate the role of esterases as the source of variation in insecticide sensitivity. To address this question, the following objectives were completed: 1) Evaluated esterase activity among honey bee stocks, 2) Assessed the correlation of esterase activity with changes in insecticide sensitivity with honey bee age, 3) Established if esterases can be used as a biomarker of insecticide exposure, and 4) Examined the effects of Varroa mite infestation and viral infection on esterase activity. Results indicated that honey bees have a dynamic esterase capacity that is influenced by genetic stock and age. However, there was no consistent connection of esterase activity with insecticide sensitivity across genetic stocks or with age, which suggests other factors are more critical for determining insecticide sensitivity. The trend of increased esterase activity with age in honey bees suggests this physiological transition is consistent with enhanced metabolic rate with age. The esterase inhibition with naled but not phenothrin or clothianidin indicates that reduced esterase activity levels may only be reliable for sublethal doses of organophosphate insecticides. The observation that viral infection, but not Varroa mite infestation, reduced esterase activity shows viruses have extensive physiological impacts. Taken together, these data suggest that honey bee esterase activity toward these model substrates may not correlate well with insecticide sensitivity. Future studies include identification of esterase substrates and inhibitors that are better surrogates of insecticide detoxification in honey bees as well as investigation on the usefulness of esterase activity as a biomarker of pesticide exposure, and viral infection.