Common Bee Viruses Alter Flight Performance Through Stress Pathways

Honey bees infected with common viruses show drastically altered flight performance and energy regulation driven by chemical signaling pathways, according to a study published in eLife.

Researchers Naomi G. Kaku and Michelle L. Flenniken at Montana State University investigated how invisible viral infections change insect behavior. High annual honey bee colony losses, which averaged 40 percent in the United States between 2008 and 2025, are closely linked to pathogens such as viruses. Many adult bees harbor high levels of viruses without displaying obvious external signs like wing deformities or larval death, making it vital to understand how these silent infections impact daily survival.

How Two Common Honey Bee Viruses Diverge in Flight Effects

To measure the subtle impacts of asymptomatic infections, the scientists tracked individual honey bee flight endurance, distance, and speed using specialized flight mills that act like insect treadmills. They focused on two prevalent pathogens with positive single-stranded RNA genomes: deformed wing virus, which replicates in Varroa destructor mites, and sacbrood virus, which is mechanically transmitted.

Deformed wing virus infected bees performed exactly as expected by flying significantly shorter distances and at slower speeds compared to uninfected controls. Mock-infected bees with low virus levels flew an estimated 45 meters, whereas bees harboring high deformed wing virus loads flew only about 9 meters. In contrast, honey bees infected with sacbrood virus displayed a surprising enhancement, flying farther distances and at faster speeds than healthy bees.

The Role of the Octopamine Stress Response Pathway

The research team explored whether these contrasting physical outcomes were tied to octopamine, a small neurohormone molecule in invertebrates that acts similarly to the mammalian fight-or-flight hormone norepinephrine. Octopamine orchestrates energy mobilization, temperature regulation, and movement by binding to specific cellular receptors such as the octopamine beta-2 receptor.

To test the mechanism, the authors exposed virus-infected honey bees to octopamine, epinastine, which is an octopamine receptor antagonist that blocks signaling, or a combination of both through injections and diet. Administering octopamine successfully rescued flight deficits in deformed wing virus infected bees, increasing their flight duration to levels comparable to healthy controls. However, treating sacbrood virus infected bees with octopamine unexpectedly diminished their flight performance.

Gene Expression Reveals Complex Metabolic Trade-Offs

Transcriptome analyses and quantitative polymerase chain reaction assays revealed that the two viruses perturb metabolic pathways and chemical synthesis differently. Sacbrood virus infections naturally induced higher expression of the octopamine receptor and key synthesis enzymes including tyrosine decarboxylase, which converts tyrosine to tyramine, and tyramine beta-hydroxylase, which converts tyramine into octopamine.

When sacbrood virus infected bees received extra octopamine supplementation, the expression of these synthesis genes dropped, pointing to a potential feedback loop that regulates internal neurohormone concentrations. Meanwhile, treating deformed wing virus infected bees with octopamine activated glucose metabolism genes and mitochondrial energy production pathways, helping explain their physical recovery on the flight mill.

Broader Implications for Colony Health and Miticide Use

These findings demonstrate that invisible virus infections reshape insect stamina through neurohormonal pathways, which may alter foraging efficiency and disease transmission inside the hive. The authors note that agricultural chemicals like amitraz, which are miticides used to control Varroa mites and act as octopamine receptor agonists, might interact with these stress pathways. Because managed colonies frequently experience coinfections, cumulative exposure to miticides and viral stress could create unintended physiological harms that warrant further study.

The research was published in eLife on November 9, 2026.