4.4 Article

Transcriptional response of Wolbachia-transinfected Aedes aegypti mosquito cells to dengue virus at early stages of infection

Journal

JOURNAL OF GENERAL VIROLOGY
Volume 103, Issue 1, Pages -

Publisher

MICROBIOLOGY SOC
DOI: 10.1099/jgv.0.001694

Keywords

Aedes aegypti; dengue virus; differential gene expression; transcriptome; Wolbachia

Funding

  1. Australian Research Council [DP210101791]

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This study examines the transcriptional response of Wolbachia-transinfected Aedes aegypti cells to dengue virus (DENV) infection. Differential expression of immune genes, as well as genes related to post-transcriptional modifications, antioxidant enzymes, and heat-shock response, are identified. Additionally, several long non-coding RNAs show differential regulation. These findings provide insights into the initial virus recognition and transcriptional response of Wolbachia-transinfected Aedes aegypti to DENV infection.
Mosquito-borne flaviviruses are responsible for viral infections and represent a considerable public health burden. Aedes aegypti is the principal vector of dengue virus (DENV), therefore understanding the intrinsic virus-host interactions is vital, particularly in the presence of the endosymbiont Wolbachia, which blocks virus replication in mosquitoes. Here, we examined the transcriptional response of Wolbachia-transinfected Ae. aegypti Aag2 cells to DENV infection. We identified differentially expressed immune genes that play a key role in the activation of anti-viral defence such as the Toll and immune deficiency pathways. Further, genes encoding cytosine and N-6-adenosine methyltransferases and SUMOylation, involved in post-transcriptional modifications, an antioxidant enzyme, and heat-shock response were up-regulated at the early stages of DENV infection and are reported here for the first time. Additionally, several long non-coding RNAs were among the differentially regulated genes. Our results provide insight into Wolbachia-transinfected Ae. aegypti's initial virus recognition and transcriptional response to DENV infection.

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