Eldor A, Sela-Donenfeld D, Korner M, Pick M, Resnick-Roguel N, Panet A
Tel-Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Israel.
Haemostasis. 1996 Oct;26 Suppl 4:37-45. doi: 10.1159/000217284.
Endothelial injury caused by viruses usually involves viral replication or transformation. We report a novel mechanism of endothelial damage by a toxic viral protein. We have isolated a new retrovirus from hemangiosarcomas which appeared among layer hens. The isolated avian hemangiosarcoma virus (AHV) is capable of inducing hemangiomas in hens in-vivo and causes a cytopathic effect (CPE) and loss of thromboresistance in cultured bovine aortic endothelial cells (BAEC). These effects do not require viral replication and can be induced by purified AHV envelop glycoprotein (gp85). AHV causes CPE in BAEC through a typical programmed cell death (apoptosis). Quiescent G0/G1-BAEC are much more sensitive to AHV induced apoptosis than actively dividing cells. These experiments demonstrate the capacity of viral proteins to affect the integrity and functionality of vascular endothelial cells.
病毒引起的内皮损伤通常涉及病毒复制或转化。我们报告了一种由毒性病毒蛋白导致内皮损伤的新机制。我们从蛋鸡中出现的血管肉瘤中分离出一种新的逆转录病毒。分离出的禽血管肉瘤病毒（AHV）能够在母鸡体内诱导血管瘤，并在培养的牛主动脉内皮细胞（BAEC）中引起细胞病变效应（CPE）和血栓抵抗性丧失。这些效应不需要病毒复制，并且可以由纯化的AHV包膜糖蛋白（gp85）诱导。AHV通过典型的程序性细胞死亡（凋亡）在BAEC中引起CPE。静止的G0/G1期BAEC比活跃分裂的细胞对AHV诱导的凋亡更敏感。这些实验证明了病毒蛋白影响血管内皮细胞完整性和功能的能力。
