Bees—including solitary, social, wild, and managed species—are key pollinators of flowering plant species, including nearly three-quarters of global food crops. Their ecological importance, coupled with increased annual losses of managed honey bees and declines in populations of key wild species, has focused attention on the factors that adversely affect bee health, including viral pathogens. Genomic approaches have dramatically expanded understanding of the diversity of viruses that infect bees, the complexity of their transmission routes—including intergenus transmission—and the diversity of strategies bees have evolved to combat virus infections, with RNA-mediated responses playing a prominent role. Moreover, the impacts of viruses on their hosts are exacerbated by the other major stressors bee populations face, including parasites, poor nutrition, and exposure to chemicals. Unraveling the complex relationships between viruses and their bee hosts will lead to improved understanding of viral ecology and management strategies that support better bee health.

Honey bees are significant pollinators of agricultural crops and other important plant species. High annual losses of honey bee colonies in North America and in some parts of Europe have profound ecological and economic implications. Colony losses have been attributed to multiple factors including RNA viruses, thus understanding bee antiviral defense mechanisms may result in the development of strategies that mitigate colony losses. Honey bee antiviral defense mechanisms include RNA-interference, pathogen-associated molecular pattern (PAMP) triggered signal transduction cascades, and reactive oxygen species generation. However, the relative importance of these and other pathways is largely uncharacterized. Herein we review the current understanding of honey bee antiviral defense mechanisms and suggest important avenues for future investigation.

Bees are agriculturally and ecologically important plant pollinators. Recent high annual losses of honey bee colonies, and reduced populations of native and wild bees in some geographic locations, may impact the availability of affordable food crops and the diversity and abundance of native and wild plant species. Multiple factors including viral infections affect pollinator health. The majority of well-characterized bee viruses are picorna-like RNA viruses, which may be maintained as covert infections or cause symptomatic infections or death. Next generation sequencing technologies have been utilized to identify additional bee-infecting viruses including the Lake Sinai viruses and Rhabdoviruses. In addition, sequence data is instrumental for defining specific viral strains and characterizing associated pathogenicity, such as the recent characterization of Deformed wing virus master variants (DWV-A, DWV-B, and DWV-C) and their impact on bee health.

Honey bees are essential pollinators of numerous agricultural crops. Since 2006, honey bee populations have suffered considerable annual losses that are partially attributed to Colony Collapse Disorder (CCD). CCD is an unexplained phenomenon that correlates with elevated incidence of pathogens, including RNA viruses. Honey bees are eusocial insects that live in colonies of genetically related individuals that work in concert to gather and store nutrients. Their social organization provides numerous benefits, but also facilitates pathogen transmission between individuals. To investigate honey bee antiviral defense mechanisms, we developed an RNA virus infection model and discovered that administration of dsRNA, regardless of sequence, reduced virus infection. Our results suggest that dsRNA, a viral pathogen associated molecular pattern (PAMP), triggers an antiviral response that controls virus infection in honey bees.

In this short review, we present our current understanding of the role of viruses on honey bee health and address some overarching questions in honey bee virology.

Recent high annual losses of honey bee colonies are associated with many factors, including RNA virus infections. Honey bee antiviral responses include RNA interference and immune pathway activation, but their relative roles in antiviral defense are not well understood. To better characterize the mechanism(s) of honey bee antiviral defense, bees were infected with a model virus in the presence or absence of dsRNA, a virus associated molecular pattern. Regardless of sequence specificity, dsRNA reduced virus abundance. We utilized next generation sequencing to examine transcriptional responses triggered by virus and dsRNA at three time-points post-infection. Hundreds of genes exhibited differential expression in response to co-treatment of dsRNA and virus. Virus-infected bees had greater expression of genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expressed genes are not well characterized. To confirm the virus limiting role of two genes, including the well-characterized gene, dicer, and a probable uncharacterized cyclin dependent kinase in honey bees, we utilized RNAi to reduce their expression in vivo and determined that virus abundance increased, supporting their involvement in antiviral defense. Together, these results further our understanding of honey bee antiviral defense, particularly the role of a non-sequence specific dsRNA-mediated antiviral pathway.