Zika (ZIKV) and dengue virus (DENV) are transmitted to humans by Aedes mosquitoes. However, the molecular interactions between the vector and ZIKV remain largely unexplored. In this work, we further investigated the tropism of ZIKV in two different Aedes aegypti strains and show that the virus infection kinetics, tissue migration, and susceptibility to infection differ between mosquito strains. We also compare the vector transcriptome changes upon ZIKV or DENV infection demonstrating that 40% of the mosquito’s midgut infection-responsive transcriptome is virus-specific at 7 days after virus ingestion. Regulated genes included key factors of the mosquito’s anti-viral immunity. Comparison of the ZIKV and DENV infection-responsive transcriptome data to those available for yellow fever virus and West Nile virus identified 26 genes likely to play key roles in virus infection of Aedes mosquitoes. Through reverse genetic analyses, we show that the Toll and the Jak/Stat innate immune pathways mediate increased resistance to ZIKV infection, and the conserved DENV host factors vATPase and inosine-5′-monophosphate dehydrogenase are also utilized for ZIKV infection.

The unprecedented rate of change in the Arctic climate is expected to have major impacts on the emergence of infectious diseases and host susceptibility to these diseases. It is predicted that malaria parasites will spread to both higher altitudes and latitudes with global warming. Here we show for the first time that avian Plasmodium transmission occurs in the North American Arctic. Over a latitudinal gradient in Alaska, from 61°N to 67°N, we collected blood samples of resident and migratory bird species. We found both residents and hatch year birds infected with Plasmodium as far north as 64°N, providing clear evidence that malaria transmission occurs in these climates. Based on our empirical data, we make the first projections of the habitat suitability for Plasmodium under a future-warming scenario in Alaska. These findings raise new concerns about the spread of malaria to naïve host populations.

Transmission of dengue virus (DENV) requires successful completion of the infection cycle in the Aedes aegypti vector, which is initiated in the midgut tissue after ingestion of an infectious blood meal. While certain Ae. aegypti midgut-associated bacteria influence virus infection, little is known about the midgut-associated fungi (mycobiota), and how its members might influence susceptibility to DENV infection. We show that a Talaromyces (Tsp_PR) fungus, isolated from field-caught Ae. aegypti, render the mosquito more permissive to DENV infection. This modulation is attributed to a profound down-regulation of digestive enzyme genes and trypsin activity, upon exposure to Tsp_PR-secreted factors. In conclusion, we show for the first time that a natural mosquito gut-associated fungus can alter Ae. aegypti physiology in a way that facilitates pathogen infection.

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