Impact of climate- and urbanization-driven environmental change on Aedes aegypti susceptibility to Zika virus
As global temperatures rise and urbanization increases, the viable habitat for some mosquitoes will expand, allowing for increased spread of vector-borne diseases. Even in the most optimistic climate models, the risk of diseases transmitted by Aedes species mosquitoes is high, especially in Africa, where the disease burden is expected to shift from malaria to arboviruses. Our current understanding of how climate- and urbanization-driven expansion of mosquitoes, such as Ae. aegypti, into new environments will impact their capacity as a vector is limited. This expansion of mosquito habitats will be accompanied by changes in oviposition site access and microclimates the mosquitoes are exposed to. Increasing urbanization in Africa will shift the oviposition sites for Ae. aegypti natural containers in a sylvatic environment to human-made containers. The bacterial communities found in these different container types are a distinct characteristic determined by the environment and differ between human-made and natural containers. Larval-microbial interactions have been shown to influence adult traits, including susceptibility to Zika virus (ZIKV). Here, we tested the hypothesis that larval development with container-specific bacterial communities alters adult Ae. aegypti susceptibility to ZIKV. We found that plastic-derived microbiomes increase ZIKV susceptibility across multiple collection sites, with these effects largely driven by bacterial density. In addition to changes in larval habitats, the microclimate that mosquitoes are exposed to is expected to change in response to rising temperatures and urbanization. One microclimate variable is relative humidity; however, little is known about how it affects mosquito infection dynamics. Survival under desiccation stress is correlated with ZIKV infection rates in genetically diverse lines of Ae. aegypti originating from Senegal. Here, we investigated the genetic relationship between desiccation tolerance and ZIKV susceptibility by identifying transcripts differentially expressed in response to desiccation stress and probing their function in ZIKV infection in these Ae. aegypti lines. We found that the genetic response to desiccation stress differed between the genetically diverse lines from Senegal. We identified two candidate genes differentially expressed in response to desiccation stress and demonstrated that expression of both genes plays a role in ZIKV infection rates. Together, our results provide new insight into how urbanization-driven changes in larval habitat and desiccation tolerance shape Ae. aegypti – ZIKV interactions.
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The University of Texas Medical Branch at Galveston