Microbes increase thermal sensitivity in the mosquito Aedes aegypti, with the potential to change disease distributions.

The mosquito Aedes aegypti is the primary vector of many disease-causing viruses, including dengue (DENV), Zika, chikungunya, and yellow fever. As consequences of climate change, we expect an increase in both global mean temperatures and extreme climatic events. When temperatures fluctuate, mosquito vectors will be increasingly exposed to temperatures beyond their upper thermal limits. Here, we examine how DENV infection alters Ae. aegypti thermotolerance by using a high-throughput physiological 'knockdown' assay modeled on studies in Drosophila. Such laboratory measures of thermal tolerance have previously been shown to accurately predict an insect's distribution in the field. We show that DENV infection increases thermal sensitivity, an effect that may ultimately limit the geographic range of the virus. We also show that the endosymbiotic bacterium Wolbachia pipientis, which is currently being released globally as a biological control agent, has a similar impact on thermal sensitivity in Ae. aegypti. Surprisingly, in the coinfected state, Wolbachia did not provide protection against DENV-associated effects on thermal tolerance, nor were the effects of the two infections additive. The latter suggests that the microbes may act by similar means, potentially through activation of shared immune pathways or energetic tradeoffs. Models predicting future ranges of both virus transmission and Wolbachia's efficacy following field release may wish to consider the effects these microbes have on host survival. Author summary: Changes in global climate, which include higher temperatures and more frequent extreme temperature events, are expected to cause dramatic shifts in the distributions of infectious diseases. The geographic range of the mosquito Aedes aegypti continues to expand, risking greater incidence of viral diseases including dengue (DENV), Zika, chikungunya, and yellow fever. One emerging solution to control these viruses is the release of the insect bacterium Wolbachia, whose infection in mosquitoes reduces virus transmission to humans. However, the effects of rising temperatures on the efficacy of this tool are unclear. Here, we studied whether DENV and Wolbachia can alter the thermal sensitivity of the mosquito Ae. aegypti by using a heat-based physiological assay. We demonstrate that, separately, DENV and Wolbachia infections increase mosquito thermal sensitivity, causing more rapid death when mosquitoes are exposed to extreme heat. The impacts of the microbes on mosquito thermal sensitivity were similar but not additive, suggesting they effect the mosquito in similar ways. Our work demonstrates that future global projections of DENV transmission risk and of Wolbachia's potential efficacy may need to consider the impact of these microbes on vector survival. [ABSTRACT FROM AUTHOR]