Temperature alters gene expression in mosquitoes during arbovirus infection

<jats:title>ABSTRACT</jats:title><jats:p>Arthropod-borne viruses (arboviruses) such as dengue, Zika and chikungunya constitute a significant proportion of the global disease burden. The principal vector of these pathogens is the mosquito <jats:italic>Aedes</jats:italic> (<jats:italic>Ae</jats:italic>.) <jats:italic>aegypti</jats:italic>, and its ability to transmit virus to a human host is influenced by environmental factors such as temperature. However, exactly how ambient temperature influences virus replication within mosquitoes remains poorly elucidated, particularly at the molecular level. Here, we use chikungunya virus (CHIKV) as a model to understand how the host mosquito transcriptome responds to arbovirus infection under different ambient temperatures. We exposed CHIKV-infected mosquitoes to 18 °C, 28 °C and 32 °C, and found higher temperature correlated with higher virus replication levels, particularly at early time points post-infection. Lower ambient temperatures resulted in reduced virus replication levels. Using RNAseq, we found that temperature significantly altered gene expression levels in mosquitoes, particularly components of the immune response. The highest number of significantly differentially expressed genes in response to CHIKV was observed at 28 °C, with a markedly more muted effect observed at either lower (18 °C) or higher (32 °C) temperatures. At the higher temperature, the expression of many classical immune genes, including <jats:italic>Dicer-2</jats:italic> in the RNAi pathway, was not substantially altered in response to CHIKV. Upregulation of Toll, IMD and JAK-STAT pathways was only observed at 28 °C. Time post infection also led to substantially different gene expression profiles, and this effect varied depending upon the which temperature mosquitoes were exposed to. Taken together, our data indicate temperature significantly modulates mosquito gene expression in response to infection, potentially leading to impairment of immune defences at higher ambient temperatures.</jats:p>