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Microarray analysis of differential gene expression profiles in blood cells of naturally BLV-infected and uninfected Holstein–Friesian cows

Brym, P., Kamiński, S.
Molecular biology reports 2017 v.44 no.1 pp. 109-127
B-lymphocytes, Bovine leukemia virus, Holstein, apoptosis, complement, cows, cytotoxicity, enzootic bovine leukosis, gene expression regulation, genes, herds, immune response, innate immunity, microarray technology, oligonucleotides, pathogenesis, quantitative polymerase chain reaction, rearing, reverse transcriptase polymerase chain reaction, seroprevalence
The aim of the present study was to examine gene expression changes in response to bovine leukemia virus (BLV) infection, in an effort to determine genes that take a part in molecular events leading to persistent lymphocytosis (PL), and to better define genes involved in host response to BLV infection. Using bovine 70-mer oligonucleotide spotted microarrays (BLOPlus) and qRT-PCR validation, we studied global gene expression profiles in blood cells in vivo of 12 naturally BLV-infected Polish Holstein cows, and 12 BLV non-infected controls of the same breed and reared in herds with high BLV seroprevalence. With an arbitrary cut-off value of 1.5-fold change in gene expression, we identified the down-regulation of 212 genes (M value ≤−0.585) and the up-regulation of 158 genes (M value of ≥0.585) at 1% false discovery rate in BLV-positive animals in comparison to the BLV-negative group. The gene set enrichment analysis demonstrated that the differentially expressed (DE) genes could be classified to diverse biological processes, including immune response of host blood cells. Interestingly, our data indicated the potential involvement of the innate immunity, including complement system activation, NK-cell cytotoxicity and TREM-1 signaling, during the BLV-induced pathogenesis. We showed the occurrence of numerous regulatory processes that are targeted by BLV-infection. We also suggest that a complex network of interrelated pathways is disturbed, causing the interruption of the control of B-cell proliferation and programmed cell death.