ArticleCommunications biology2023
Host-driven temperature dependence of Deformed wing virus infection in honey bee pupae.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Opposite seasonal and spatial dynamics of DWV-A and DWV-B suggest distinct transmission pathways in managed honey bees (Apis mellifera L.) colonies.Scientific reports · 2026Article
- Urban landscapes tend to increase the presence of pathogenic protozoa, microsporidia and viruses, but likely decrease the abundance of viruses in wild bees and wasps.Insect science · 2025Article
- Article
- A simulated natural heatwave perturbs bumblebee immunity and resistance to infection.The Journal of animal ecology · 2024Article
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The temperature dependence of infection reflects changes in performance of parasites and hosts. High temperatures often mitigate infection by favoring heat-tolerant hosts over heat-sensitive parasites. Honey bees exhibit endothermic thermoregulation-rare among insects-that can favor resistance to parasites. However, viruses are heavily host-dependent, suggesting that viral infection could be supported-not threatened-by optimum host function. To understand how temperature-driven changes in performance of viruses and hosts shape infection, we compared the temperature dependence of isolated viral enzyme activity, three honey bee traits, and infection of honey bee pupae. Viral enzyme activity varied <2-fold over a > 30 °C interval spanning temperatures typical of ectothermic insects and honey bees. In contrast, honey bee performance peaked at high (≥ 35 °C) temperatures and was highly temperature-sensitive. Although these results suggested that increasing temperature would favor hosts over viruses, the temperature dependence of pupal infection matched that of pupal development, falling only near pupae's upper thermal limits. Our results reflect the host-dependent nature of viruses, suggesting that infection is accelerated-not curtailed-by optimum host function, contradicting predictions based on relative performance of parasites and hosts, and suggesting tradeoffs between infection resistance and host survival that limit the viability of bee 'fever'.
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Registered trials
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