Schnittler H J, Mahner F, Drenckhahn D, Klenk H D, Feldmann H
Institut für Virologie, Philipps-Universität Marburg, Germany.
J Clin Invest. 1993 Apr;91(4):1301-9. doi: 10.1172/JCI116329.
Marburg and Ebola virus, members of the family Filoviridae, cause a severe hemorrhagic disease in humans and primates. The disease is characterized as a pantropic virus infection often resulting in a fulminating shock associated with hemorrhage, and death. All known histological and pathophysiological parameters of the disease are not sufficient to explain the devastating symptoms. Previous studies suggested a nonspecific destruction of the endothelium as a possible mechanism. Concerning the important regulatory functions of the endothelium (blood pressure, anti-thrombogenicity, homeostasis), we examined Marburg virus replication in primary cultures of human endothelial cells and organ cultures of human umbilical cord veins. We show here that Marburg virus replicates in endothelial cells almost as well as in monkey kidney cells commonly used for virus propagation. Our data support the concept that the destruction of endothelial cells resulting from Marburg virus replication is a possible mechanism responsible for the hemorrhagic disease and the shock syndrome typical of this infection.
马尔堡病毒和埃博拉病毒属于丝状病毒科，可在人类和灵长类动物中引发严重的出血性疾病。该疾病的特征是泛嗜性病毒感染，常导致与出血相关的暴发性休克和死亡。所有已知的该疾病组织学和病理生理学参数都不足以解释其毁灭性症状。先前的研究表明，内皮细胞的非特异性破坏可能是一种机制。鉴于内皮细胞的重要调节功能（血压、抗血栓形成、内环境稳定），我们研究了马尔堡病毒在人内皮细胞原代培养物和人脐静脉器官培养物中的复制情况。我们在此表明，马尔堡病毒在内皮细胞中的复制情况几乎与常用于病毒繁殖的猴肾细胞一样好。我们的数据支持这样一种观点，即马尔堡病毒复制导致的内皮细胞破坏是造成这种感染典型的出血性疾病和休克综合征的一种可能机制。
