AI Article Synopsis

  • * RNA sequencing revealed 159 genes that were expressed differently in infected mosquitoes compared to uninfected ones, and the role of Bruton's tyrosine kinase was further examined for its potential function in viral response.
  • * Although knocking down Bruton's tyrosine kinase did not alter viral replication, it did increase cell death in mosquitoes, hinting at a shared mechanism between mosquito and mammal immune responses to CHIKV.

Article Abstract

Chikungunya virus (CHIKV) is transmitted by mosquitoes and causes prolonged arthralgia in patients. After crossing the mosquito midgut barrier, the virus disseminates to tissues including the head and salivary glands. To better understand the interaction between and CHIKV, we performed RNASeq analysis on pools of mosquito heads and parts of the thorax 8 days post infection, which identified 159 differentially expressed transcripts in infected mosquitos compared to uninfected controls. After validation using RT-qPCR (reverse transcriptase-quantitative polymerase chain reaction), inhibitor of Bruton's tyrosine kinase (), which has previously been shown to be anti-inflammatory in mammals after viral infection, was further evaluated for its functional significance. Knockdown of using double-stranded RNA in a mosquito cell line showed no significant difference in viral RNA or infectivity titer. However, gene knocked-down cells showed increased apoptosis 24 hours post-infection compared with control cells, suggesting involvement of in the mosquito response to viral infection. Since in mammals promotes an inflammatory response and has been shown to be involved in osteoclastogenesis, a hallmark of CHIKV pathogenesis, our results suggest a possible conserved mechanism at play between mosquitoes and mammals. Taken together, these results will add to our understanding of interactions with CHIKV.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6789441PMC
http://dx.doi.org/10.3390/pathogens8030132DOI Listing

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