Moredun Research Institute, Pentlands Science Park, Midlothian EH26 0PZ, UK.
Virus Res. 2012 Oct;169(1):246-54. doi: 10.1016/j.virusres.2012.08.011. Epub 2012 Aug 25.
Malignant catarrhal fever is a lymphoproliferative disease of cattle and other ungulates caused by infection with gamma-herpesviruses of the genus Macavirus. These viruses do not establish a productive infection but instead replicate in a cell-associated fashion in T lymphocytes, leading to systemic immune dysregulation and a generally fatal outcome. Despite significant progress in understanding the pathology of this disease, its pathogenesis remains unclear. To identify genes and pathways affected in clinical MCF, sixteen bovine GeneCHIP microarrays were used to assay RNA from kidney and lymph node of four MCF-affected and four control Bos taurus steers. This is the first expression study of AlHV-1-MCF in the bovine host. Over 250 genes showed significant changes in gene expression in either lymph node or kidney, while expression of 35 genes was altered in both tissues. Pathway and annotation analysis of the microarray data showed that immune response and inflammatory genes were up-regulated in the kidney while proliferation-associated transcripts were additionally increased in the lymph node. The genes that showed the largest expression rises in both diseased tissues included cytotoxic enzymes and pro-inflammatory chemokines. These data are consistent with disease-induced stimulation of inflammatory responses involving interferon-γ, including cytotoxic T cell recruitment and activation in peripheral tissues containing virus-infected cells. However it remains unclear whether the tissue damage in MCF lesions is due entirely to the activity of infected cells or whether uninfected T cells, recruited and activated at lesion sites through the action of infected cells, contribute to the pathogenesis of MCF.
恶性卡他热是一种牛和其他有蹄类动物的淋巴组织增生性疾病,由马疱疹病毒属的γ疱疹病毒感染引起。这些病毒不能建立有效的感染,而是以细胞相关的方式在 T 淋巴细胞中复制,导致全身免疫失调和普遍致命的结果。尽管在了解这种疾病的病理学方面取得了重大进展,但它的发病机制仍不清楚。为了确定在临床 MCF 中受影响的基因和途径,使用 16 个牛基因芯片微阵列来检测来自 4 头 MCF 受影响和 4 头对照牛的肾脏和淋巴结中的 RNA。这是首次在牛宿主中对 AlHV-1-MCF 进行表达研究。超过 250 个基因在淋巴结或肾脏中的基因表达发生了显著变化,而 35 个基因的表达在两种组织中都发生了改变。微阵列数据的通路和注释分析表明,免疫反应和炎症基因在肾脏中上调,而与增殖相关的转录物在淋巴结中也增加。在两种病变组织中表达上升最大的基因包括细胞毒性酶和促炎趋化因子。这些数据与疾病诱导的涉及干扰素-γ的炎症反应刺激一致,包括细胞毒性 T 细胞在含有病毒感染细胞的外周组织中的募集和激活。然而,尚不清楚 MCF 病变中的组织损伤是否完全是由受感染细胞的活动引起的,还是通过受感染细胞的作用募集和激活的未感染 T 细胞对 MCF 的发病机制有贡献。