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

Quan, Rong, Zhu, Shanshan, Wei, Li, Wang, Jing, Yan, Xu, Li, Zixuan, Liu, Jue
Virology journal 2017 v.14 no.1 pp. 7
cell death, immunosuppression, signal transduction, genes, Infectious bursal disease virus, mitogen-activated protein kinase, bursa of Fabricius, cytokines, viruses, pathogenesis, gene expression regulation, virulence, B-lymphocytes, Toll-like receptors, avian leukosis, messenger RNA, models, DNA microarrays, transcription (genetics), chickens, antigen presentation, inflammation, reverse transcriptase polymerase chain reaction
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.