Dequiedt F, Kettmann R, Burny A, Willems L
Department of Molecular Biology and Animal Physiology, Faculty of Agronomy, Gembloux, Belgium.
Virology. 1995 Jun 1;209(2):676-83. doi: 10.1006/viro.1995.1303.
To investigate the mechanisms of bovine leukemia virus (BLV)-induced leukemogenesis, we have examined the alterations of the p53 tumor-suppressor gene in sheep and in cattle. The sequences of the open reading frames as well as the intron/exon junctions of the ovine and bovine p53 genes were determined. Pathological samples were screened for the presence of p53 mutations using a single-strand conformational polymorphism assay. Five of ten BLV-induced bovine tumors harbored p53 mutations. In contrast, only one of seven samples corresponding to circulating leukocytes from cattle in persistent lymphocytosis showed an alteration of the p53 gene. Surprisingly, no p53 mutation was found among the 10 BLV-induced sheep tumors analyzed. Altogether, these data indicate that p53 mutations are linked to BLV-induced leukemogenesis in cattle at the transition to the lymphomic stage. These results also enlighten different molecular mechanisms involved in sheep and in cattle during BLV-induced pathogenesis.
为了研究牛白血病病毒（BLV）诱导白血病发生的机制，我们检测了绵羊和牛中p53肿瘤抑制基因的变化。确定了绵羊和牛p53基因开放阅读框以及内含子/外显子连接区的序列。使用单链构象多态性分析筛选病理样本中p53突变的存在情况。在10个BLV诱导的牛肿瘤中有5个存在p53突变。相比之下，在7个对应于持续性淋巴细胞增多症牛的循环白细胞的样本中，只有1个显示p53基因发生改变。令人惊讶的是，在分析的10个BLV诱导的绵羊肿瘤中未发现p53突变。总之，这些数据表明p53突变与牛在向淋巴瘤阶段转变时BLV诱导的白血病发生有关。这些结果也揭示了在BLV诱导的发病过程中绵羊和牛所涉及的不同分子机制。
