BMC Microbiology (Jun 2019)

Transcriptome analysis of responses to bluetongue virus infection in Aedes albopictus cells

  • Junzheng Du,
  • Shandian Gao,
  • Zhancheng Tian,
  • Yanni Guo,
  • Di Kang,
  • Shanshan Xing,
  • Guorui Zhang,
  • Guangyuan Liu,
  • Jianxun Luo,
  • Huiyun Chang,
  • Hong Yin

DOI
https://doi.org/10.1186/s12866-019-1498-3
Journal volume & issue
Vol. 19, no. 1
pp. 1 – 11

Abstract

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Abstract Background Bluetongue virus (BTV) causes a disease among wild and domesticated ruminants which is not contagious, but which is transmitted by biting midges of the Culicoides species. BTV can induce an intense cytopathic effect (CPE) in mammalian cells after infection, although Culicoides- or mosquito-derived cell cultures cause non-lytic infection with BTV without CPE. However, little is known about the transcriptome changes in Aedes albopictus cells infected with BTV. Methods Transcriptome sequencing was used to identify the expression pattern of mRNA transcripts in A. albopictus cells infected with BTV, given the absence of the Culicoides genome sequence. Bioinformatics analyses were performed to examine the biological functions of the differentially expressed genes. Subsequently, quantitative reverse transcription–polymerase chain reaction was utilized to validate the sequencing data. Results In total, 51,850,205 raw reads were generated from the BTV infection group and 51,852,293 from the control group. A total of 5769 unigenes were common to both groups; only 779 unigenes existed exclusively in the infection group and 607 in the control group. In total, 380 differentially expressed genes were identified, 362 of which were up-regulated and 18 of which were down-regulated. Bioinformatics analyses revealed that the differentially expressed genes mainly participated in endocytosis, FoxO, MAPK, dorso-ventral axis formation, insulin resistance, Hippo, and JAK-STAT signaling pathways. Conclusion This study represents the first attempt to investigate transcriptome-wide dysregulation in A. albopictus cells infected with BTV. The understanding of BTV pathogenesis and virus–vector interaction will be improved by global transcriptome profiling.

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