Modification of host genes in the infected cells with parvovirus

大鼠细小病毒（RPV）在大鼠胸腺淋巴瘤C58（NT）R细胞系中增殖，并诱导细胞凋亡。感染后存活的耐药细胞表现出与亲本细胞克隆不同的表型，如抗凋亡和肿瘤抑制。为了阐明这一现象的分子机制，我们试图鉴定抗性细胞与亲本细胞之间差异表达的基因。根据代表性差异分析（RDA）结果，确定了6个已知基因和2个未知基因。PCR和北方印迹分析显示，亲代C58（NT）细胞中组织蛋白酶E、胸腺细胞ARPP和seladin-1表达下调，而抗性细胞克隆中睫状神经营养因子受体α（CNTFR_α）、小应激蛋白1相关蛋白和Molony鼠白血病病毒包膜基因表达增强。这些结果提示，CNTFR_α表达增强有助于诱导耐药细胞克隆对凋亡的抵抗。

Rat parvovirus (RPV) propagates in rat thymic lymphoma C58(NT)R cell line, and induces apoptosis. Resistant cells survived after infection reveal different phenotypes such as resistance to apoptosis and tummor suppression compared to parent cell clone. To elucidate the moleculer mechanism of this phenomenon, we tried to identify the genes which express differently between the resistant cells and the parental cell. From the results of representational difference analysis (RDA), 6 known genes and 2 unknown genes were determined. Cathepsin E, thymocyte ARPP and seladin-1 were down-expressed in the parental C58 (NT) cells, and ciliary neurotrophic factor receptor alpha (CNTFR_α), protein associating with small stress protein 1, and envelop gene of Molony murine leukemia virus were enhanced expression in the resistant cell clone, by PCR and Northern blot analysis. These results suggest that enhanced expresson of CNTFR_α contribute to induce resistance to apoptosis in the resistant cell clone.