Resnick-Roguel N, Eldor A, Burstein H, Hy-Am E, Vlodavsky I, Panet A, Blajchman M A, Kotler M
Department of Molecular Genetics, Hebrew University, Hadassah Medical School, Jerusalem, Israel.
J Virol. 1990 Aug;64(8):4029-32. doi: 10.1128/JVI.64.8.4029-4032.1990.
Vascular endothelial cells are a target for blood-borne pathogens which may affect their integrity and thromboresistant properties. Here, we report that cultured bovine and human endothelial cells lose their thromboresistance following interaction with the avian hemangioma-inducing retrovirus. We show that the envelope (env) gene product, glycoprotein 85, is responsible for this effect, which appears soon after infection without viral replication or cell transformation. Induction of thrombogenicity is associated with a reduction in prostacyclin release and increased expression of tissue factor. These observations may explain the occurrence of thrombosis frequently observed in association with the hemangiosarcomas induced by avian hemangioma-inducing retrovirus. These unique endothelial cell-virus interactions may also be a model for the pathogenesis of various vascular diseases.
血管内皮细胞是血源性病原体的靶标,这些病原体可能会影响其完整性和抗血栓特性。在此,我们报告培养的牛和人内皮细胞在与禽血管瘤诱导逆转录病毒相互作用后会失去其抗血栓性。我们表明,包膜(env)基因产物糖蛋白85负责这种效应,这种效应在感染后很快出现,无需病毒复制或细胞转化。血栓形成性的诱导与前列环素释放减少和组织因子表达增加有关。这些观察结果可能解释了与禽血管瘤诱导逆转录病毒诱导的血管肉瘤相关的血栓形成的频繁发生。这些独特的内皮细胞-病毒相互作用也可能是各种血管疾病发病机制的模型。