雪貂和人胎儿气管器官培养中呼吸道合胞病毒感染的发病机制

Pathogenesis of respiratory syncytial virus infection in ferret and fetal human tracheas in organ culture.

作者信息

Henderson F W, Hu S C, Collier A M

出版信息

Am Rev Respir Dis. 1978 Jul;118(1):29-37. doi: 10.1164/arrd.1978.118.1.29.

DOI:10.1164/arrd.1978.118.1.29

Abstract

The pathogenesis of human respiratory syncytial virus infection was studied in ferret and fetal human tracheas in organ culture. Although the patterns of virus growth were similar in these species, the sites and morphologic consequences of virus replication differed markedly. In human trachea, synthesis of respiratory syncytial virus occurred in a population of ciliated epithelial cells, whereas other cells in the epithelial layer were spared. Virus replication was associated with cell injury characterized by ballooning degeneration and syncytium formation. In ferret trachea, virus growth occurred in fibroblasts of the lamina propria and serosa. Ciliated epithelial cells did not contain viral antigen and remained histologically normal. These observations are relevant to understanding the pathogenesis of human disease and the evaluation of animal models of respiratory syncytial virus bronchiolitis.

摘要

在雪貂和人胎儿气管的器官培养中研究了人呼吸道合胞病毒感染的发病机制。尽管在这些物种中病毒生长模式相似，但病毒复制的部位和形态学后果却明显不同。在人气管中，呼吸道合胞病毒的合成发生在一群纤毛上皮细胞中，而上皮层中的其他细胞则未受影响。病毒复制与以气球样变性和多核巨细胞形成为特征的细胞损伤有关。在雪貂气管中，病毒生长发生在固有层和浆膜的成纤维细胞中。纤毛上皮细胞不含病毒抗原，组织学上保持正常。这些观察结果对于理解人类疾病的发病机制以及评估呼吸道合胞病毒细支气管炎的动物模型具有重要意义。