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Transcriptional profiles in bursal B-lymphoid DT40 cells infected with very virulent infectious bursal disease virus

文献类型： 外文期刊

作者： Quan, Rong 1 ; Zhu, Shanshan 1 ; Wei, Li 1 ; Wang, Jing 1 ; Yan, Xu 1 ; Li, Zixuan 2 ; Liu, Jue;

作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Live, 9 Shuguang Garden Middle Rd, Beijing 100097, Peoples R China

2.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Live, 9 Shuguang Garden Middle Rd, Beijing 100097, Peoples R

关键词： vvIBDV;Microarray;DT40 cells;Pathway analysis;Toll-like receptors;Inflammatory response;Bursa

期刊名称：VIROLOGY JOURNAL （ 影响因子：4.099； 五年影响因子：3.719 ）

ISSN： 1743-422X

年卷期： 2017 年 14 卷

页码：

收录情况： SCI

摘要： Background: Infectious bursal disease virus (IBDV) causes a highly contagious, immunosuppressive disease in chickens. The virus mainly infects immature B lymphocytes in the bursa of Fabricius (BF). Chicken B cell line DT40, an avian leukosis virus-induced B cell line, supports very virulent IBDV (vvIBDV) infection in vitro and thereby serves as a good model for investigating the infection and pathogenesis of this virus. However, a transcriptome-wide understanding of the interaction between vvIBDV and B cells has not yet been achieved. This study aimed to employ time-course DNA microarrays to investigate gene expression patterns in DT40 cells after infection with vvIBDV strain LX. Results: DT40 cells infected with vvIBDV exhibited alterations in the expression of many important host genes involved in signal transduction pathways, including MAPK signaling, PI3K/mTOR signaling, cell death and survival, BCR signaling, and antigen presentation. The changes in cellular mRNA levels identified by microarray analysis were confirmed for 8 selected genes using real-time reverse transcription-PCR. The upregulation of inflammatory cytokines and Toll-like receptors (TLRs) in the bursa of vvIBDV-infected chickens might involve excessive activation of the innate immune and inflammatory responses and contribute to tissue damage. Conclusions: The present study is the first to provide a comprehensive differential transcriptional profile of cultured DT40 cells in response to vvIBDV infection and further extends our understanding of the molecular mechanisms underlying vvIBDV infection and pathogenesis.

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