Adult honeybees often carry viruses without any obvious signs, yet new research shows those infections are not harmless. A recent study reports that one common virus slows flight while another speeds it up, reshaping what a normal day in the air looks like for a forager.
The findings are important because flight is the most energetically costly activity for a bee and is essential for transporting food back to the colony.
The work comes from a research team led by Michelle L. Flenniken at Montana State University, in collaboration with lead author Naomi G. Kaku.
Researchers used flight performance as a clean readout of health, not because it is flashy, but because it is fundamental.
The study followed adult Apis mellifera three days after controlled infection to capture effects before other stressors muddy the waters.
Flight mills recorded distance, duration, and speed for 240 bees from multiple colonies. Tested individuals flew up to about 3.46 miles before exhaustion, offering a robust window into how infection changes real work capacity.
The team focused on two iflaviruses that many beekeepers already know by name, deformed wing virus and sacbrood virus. Both belong to a family of positive strand RNA viruses that are widespread in bees and other insects.
Each bee was either mock treated or inoculated, then flown on a miniaturized tether system that allowed accurate speed and distance tracking.
The setup minimized confounders and produced directly comparable flight metrics across groups.
The pattern was clear. Bees with high deformed wing virus loads flew 49 percent shorter distances than uninfected bees, while those with high sacbrood virus loads flew 53 percent farther.
Average and peak speeds shifted too. Peak speeds dropped with heavy deformed wing virus, and rose with heavier sacbrood virus, even though total flight time did not change in a meaningful way.
When both viruses were present at moderate levels, their opposing effects nearly canceled out, leaving flight distance close to baseline.
The canceling effect hides trouble because sacbrood virus is lethal to larvae and does not become a net positive at the colony scale.
The authors kept the analysis tight with linear mixed models that explained a large share of variation by accounting for virus load, bee weight, and equipment effects. That modeling choice matters when the goal is to separate signal from noise in behavior data.
One line of evidence points to octopamine, a core invertebrate neuromodulator often described as the insect fight or flight signal.
It ramps metabolic activity and neuromuscular transmission through the octopamine beta 2 receptor, and that receptor’s biology has been mapped for decades.
Sacbrood virus was associated with higher expression of the octopamine beta 2 receptor, and adding octopamine to bees infected with deformed wing virus countered the flight deficit.
Viruses do not act alone. The ectoparasitic mite Varroa destructor amplifies and transmits deformed wing virus and alters its population dynamics, which can raise virulence in managed colonies.
Across the United States, beekeeper surveys continue to report heavy losses that stress pollination services and business survival, with annual losses often near 40 percent over recent years.
A related virus influences behavior through a different mechanism. Kakugo virus, a close relative of deformed wing virus, has been associated with aggressive guard behavior in worker bees, as shown in peer-reviewed studies examining infected brains.
The new flight results extend this theme, showing that covert infections can reshape core tasks without visible symptoms. That makes detection and interpretation harder in the field.
Flight sets the radius for collecting nectar and pollen, and it governs how many trips a forager can complete on a good day. If many foragers fly shorter ranges or at lower peak speeds, colonies risk falling behind on calories even when flowers are available.
That risk scales up to farms that rely on pollination, so subtle changes at the level of an individual bee can nudge crop outcomes. It is a classic case where biology and economics share the same line in the ledger.
The study does not argue that sacbrood virus is beneficial because its larval toll remains severe. It does show that looking only for dead brood or deformed wings misses important adult performance costs that trace back to infection chemistry.
Better virus monitoring, steady mite control, and realistic expectations about “asymptomatic” adults will help align management with what the data say today. The mechanistic octopamine link gives physiology a seat at the table for future interventions.
“This study has organismal, colony, and ecosystem level implications,” wrote Kaku. The next wave of research will test how different diets, temperatures, and co-stressors interact with virus loads to shape flight and foraging.
Future studies will also investigate how frequently co-infections obscure risk in real-world apiaries, where multiple pathogens coexist.
The study is published in the journal Science Advances.
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