Infiltrating the hive mind: Immune and viral effects on behavior of the honey bee (Apis mellifera)
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Pathogens are important to the ecology of all organisms. This thesis describes host-pathogen interactions between Apis mellifera and Israeli acute paralysis virus (Dicistroviridae). Viral pathogens are critical factors in honey bee health, but effects of viral infection on honey bee behavior are difficult to study and can manifest differently across contexts. Collectively, this work seeks to better describe these host-pathogen interactions between honey bees and their viruses.
Firstly, we fed bees with viral sequence-based dsRNA, as a sham-virus to elicit RNA interference-based anti-viral immune response. We paired these bees with untreated bees and observed their interactions. Notably, we found that dsRNA-treated bees trophallaxed less than control bees, but found no differences in other social interactions. We hypothesize that anti-viral immune response likely induces sickness signals to conspecifics in the affected bee, reducing trophallaxis, but this signal might only be received through other social interaction (e.g. antennation, etc).
Secondly, we fed bees virus or sham-virus, paired them with unmodified partner bees, and observed their interactions. Both virus-infection and sham-infection elicited reduced trophallaxis; virus-infection led to reduced physical contact and antennation. Virus-infected bees were also more active than other bee types, suggesting infection could induce early onset foraging, previously described as altruistic self-removal, from a colony. We found support for adaptive sickness behavior, as virus-infected bees were more socially isolated, potentially preventing infection spread within the hive.
Finally, we explore how drifting in apiary settings is affected by honey bee-virus interactions. We paired bees with virus-infected, sham-infected and control bees from a different colony and observed their interactions. Virus-infected bees experienced more non-agonistic interactions and less aggression than either normal or sham-infected bees. We also found subtle shifts in cuticular hydrocarbon profiles among treatments. These results indicate drifting behavior has likely been co-opted by viral pathogens to enhance transmission between colonies, especially in apiary settings, and that virus-infection likely modifies chemical signals in the host to make them more acceptable.
Collectively, these chapters present the first description of potential adaptive honey bee behavioral manipulation by viruses, and highlight the need to reduce pathogen spread in apiaries by improving honey bee management practices.