4.7 Article

Transcriptomic profiles of striped snakehead cells (SSN-1) infected with snakehead vesiculovirus (SHVV) identifying IFI35 as a positive factor for SHVV replication

Journal

FISH & SHELLFISH IMMUNOLOGY
Volume 86, Issue -, Pages 46-52

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fsi.2018.11.031

Keywords

Transcriptomic sequence; SSN-1; SHVV; Differentially expressed genes; IFI35

Funding

  1. National Natural Science Fund [31572657, U31372563, 31872606]
  2. Special fund for marine economic development [GDME-2018C006]
  3. Modern Fishery Development from the Administration of Ocean and Fisheries of Guangdong Province [GDMF-2018004]
  4. Innovation and Strong Universities special fund from the Department of Education of Guangdong Province [KA170500G]
  5. Jiangsu Agriculture Science and Technology Innovation Found [CX(18)2012]
  6. Natural Science Foundation of the Jiangsu Higher Education Institutions of China [18KJB240003]
  7. Natural Science Foundation of Jiangsu Province [BK20180915]
  8. Projects of Shui Chan San Xin of Jiangsu Province [Y2016-33, D2017-3, D2015-15]
  9. Chinese Postdoctoral Science Foundation [189103]

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Snakehead vesiculovirus (SHVV) has caused great economic loss in snakehead fish culture in China. However, there is no effective strategy to prevent the epidemic of the virus. Understanding the host factors in response to virus infection is the basis for the prevention of viral disease. In this study, the transcriptomic profiles of SHVV-infected and mock-infected SSN-1 cells (derived from striped snakehead, Channa striatus) at 3 and 24 h (h) post of infection (poi) were obtained using high-throughput sequencing technique. A total of 93,372 unigenes were obtained. The differently expressed genes (DEGs) of SSN-1 cells upon SHVV infection were thereby identified, including 3668 and 3536 DEGs at 3 and 24 h poi, respectively. These DEGs were involved in many pathways of viral pathogenesis, including retinoic acid-inducible gene I (RIG-I) like receptors pathway, Toll-like receptor signaling pathway, NF-kappa B signaling pathway, PI3K-Akt signaling pathway and MAPK signaling pathway. Therefore, several immune-related DEGs were randomly selected and confirmed by quantitative real-time PCR (qRT-PCR). In addition, the effects of the interferon inducible protein 35 (IFI35) on SHVV replication were further investigated. Over-expression or inhibition of IFI35 significantly promoted or reduced SHVV replication at the level of viral gene expression, which indicated that IFI35 might be a positive factor for SHVV replication in SSN-1 cells. Our findings presented some valuable information, which will benefit for future study on SHVV-host interactions.

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