Abstract
Replication of arboviruses in their arthropod vectors is controlled by innate immune responses. The RNA sequence-specific break down mechanism, RNA interference (RNAi), has been shown to be an important innate antiviral response in mosquitoes. In addition, immune signaling pathways have been reported to mediate arbovirus infections in mosquitoes; namely the JAK/STAT, immune deficiency (IMD) and Toll pathways. Very little is known about these pathways in response to chikungunya virus (CHIKV) infection, a mosquito-borne alphavirus (Togaviridae) transmitted by aedine species to humans resulting in a febrile and arthralgic disease. In this study, the contribution of several innate immune responses to control CHIKV replication was investigated. In vitro experiments identified the RNAi pathway as a key antiviral pathway. CHIKV was shown to repress the activity of the Toll signaling pathway in vitro but neither JAK/STAT, IMD nor Toll pathways were found to mediate antiviral activities. In vivo data further confirmed our in vitro identification of the vital role of RNAi in antiviral defence. Taken together these results indicate a complex interaction between CHIKV replication and mosquito innate immune responses and demonstrate similarities as well as differences in the control of alphaviruses and other arboviruses by mosquito immune pathways.
Highlights
Arthropod-borne viruses replicate in both their vertebrate host and arthropod vector
The first replicon, named CHIKVRep(3F)RLuc-SG-FFLuc, encodes a non-structural polyprotein with RLuc inserted into the C-terminal region of nsP3 and mRNA of FFLuc expressed from the viral subgenomic promoter instead of the mRNA of structural proteins
Chikungunya virus (CHIKV) infection of mosquitoes and their derived cell lines results in the production of small RNAs indicating that small RNA pathways are activate against CHIKV and that the presence of an RNA interference (RNAi) inhibitor resulted in increased virus replication and virus production [12]
Summary
Arthropod-borne viruses (arboviruses) replicate in both their vertebrate host and arthropod vector. This poses a unique problem for arboviruses as they are exposed to both the vertebrate and invertebrate immune systems. Interactions between the replicating virus and the mosquito immune defence system produce an outcome that can influence subsequent viral transmission, as shown for the flavivirus dengue (DENV) [3]. This emphasizes the importance of further understanding innate immunity in arbovirus vectors
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