Honey bee approaching a flower. Image credit: Boris Smokrovic on Unsplash (CC0)
Honey bees are important pollinators of plants, including those that produce fruit, nut, and vegetable crops. They live in colonies of about 30,000 individuals, most of which are managed by beekeepers. Since 2008, honeybee colony deaths have been high; in the USA, these losses averaged 40% annually from 2008 to 2025. Beekeepers can divide one colony into two to help offset those losses, which helped maintain the overall US honey bee colony population at around 3 million colonies.
Many factors are associated with poor honey bee colony health and/or death, including lack of available forage (i.e., flowers from which bees collect nectar and pollen), chemical exposure, mites, and pathogens – including viruses. Honey bees are commonly infected with several viruses, and adults may harbor high levels of deformed wing virus and sacbrood virus, despite lacking morphological symptoms of these viruses (i.e., wing deformity and larval death, respectively).
Since flight requires a lot of energy, Kaku and Flenniken thought that virus-infected bees may have less energy, and that flight performance may be a suitable quantitative metric of bee health. To investigate the impact of asymptomatic virus infections on honey bees, these scientists measured the flight abilities of honey bees using a flight mill. The flight mill works similarly to a treadmill and enabled the researchers to measure how far and fast individuals flew after they were infected with viruses in the laboratory.
Deformed wing virus affected bees as they expected: they flew shorter distances at slower speeds compared to uninfected bees. Surprisingly, though, honey bees infected with sacbrood virus flew farther distances at faster speeds than uninfected bees. Their previous research showed that honey bees infected with sacbrood virus expressed more of the octopamine ß receptor 2, a cellular receptor that binds octopamine, a small molecule comparable to the “fight or flight” stimulating molecule in mammals called norepinephrine. Kaku and Flenniken confirmed the involvement of this pathway in the flight performance of virus-infected bees through pharmacological manipulation, flight performance assays, and analysis of associated gene expression.
Adding octopamine improved flight performance in bees infected with deformed wing virus but worsened flight performance in bees infected with sacbrood virus. Blocking octopamine receptors changed these effects. Gene expression analyses showed that the two viruses affected metabolism and octopamine production differently. These findings suggest that different viruses perturb octopamine signalling pathways in distinct manners, which in turn impact flight performance, potentially affecting foraging, colony health and virus spread.
Moreover, the results of Kaku and Flenniken demonstrate virus-specific impacts on honey bee flight, despite the lack of visible symptoms. Seemingly asymptomatic honey bees infected with deformed wing virus may not be able to fly as far from the colony to obtain food for the colony, whereas sacbrood virus-infected bees may be able to travel farther – though co-infections will neutralize those effects. Since octopamine alleviates the flight impairment of deformed wing virus-associated bees, it will be important to further investigate the pathways that govern the effects of viruses on honey bees. In the future, better understanding of virus-host interactions may lead to ways to reduce virus-associated honeybee colony deaths.
