Bryson D G, Platten M F, McConnell S, McNulty M S
Veterinary Research Laboratories, Stormont, Belfast, Northern Ireland, United Kingdom.
Vet Pathol. 1991 Jul;28(4):293-9. doi: 10.1177/030098589102800405.
Ultrastructural changes were observed in bronchioles in acute and repair stages of respiratory syncytial virus pneumonia induced in eight young calves (calf Nos. 1-8) using a bovine strain of respiratory syncytial virus. Five of the calves were Friesians and three were Hereford x Friesians and all were male. Tissues from three mock-infected control calves (two Friesian, one Hereford x Friesian) were also examined. Calves were from 3 to 6 days old at the time of first inoculation, with the exception of calf No. 8, which was 2 weeks old. In the acute stage of the induced pneumonia, evidence of respiratory syncytial virus replication and release was demonstrable in both ciliated and non-ciliated bronchiolar epithelial cells, with the virus-releasing process most obvious at 4 and 5 days after infection. Respiratory syncytial virus infection of bronchiolar epithelium was associated with various changes, including hypertrophy, hyperplasia, and formation of syncytia. Necrosis of epithelial cell structures usually appeared to be preceded by their desquamation from bronchiolar walls. Respiratory syncytial virus infection resulted in considerable damage to the bronchiolar ciliary apparatus. Such damage was seen as early as 1 day post-infection and was still obvious at 10 days post-infection. Neutrophils were closely associated with respiratory syncytial virus infected epithelial cells and evidence of neutrophil fusion with infected epithelial cells was seen. These observations suggest that neutrophils may be involved in killing respiratory syncytial virus infected cells and that neutrophils might play an important role in early antiviral defense against respiratory syncytial virus at a time when antibody levels are low and other cellular defenses are not fully in play. Bronchiolar repair was evident from 6 days after infection and was well advanced at 10 and 13 days after infection.
利用牛呼吸道合胞病毒株，在8头幼龄犊牛（犊牛编号1 - 8）中诱发呼吸道合胞病毒肺炎，并观察其急性和修复期细支气管的超微结构变化。其中5头犊牛为弗里斯兰牛，3头为赫里福德×弗里斯兰杂交牛，均为雄性。还检查了3头 mock - 感染对照犊牛（2头弗里斯兰牛，1头赫里福德×弗里斯兰杂交牛）的组织。首次接种时犊牛年龄为3至6天，犊牛8号除外，其为2周龄。在诱发肺炎的急性期，在纤毛和非纤毛细支气管上皮细胞中均可证明呼吸道合胞病毒的复制和释放，病毒释放过程在感染后4至5天最为明显。细支气管上皮细胞的呼吸道合胞病毒感染与各种变化有关，包括肥大、增生和多核巨细胞形成。上皮细胞结构的坏死通常似乎先于其从细支气管壁脱落。呼吸道合胞病毒感染对细支气管纤毛装置造成了相当大的损害。这种损害在感染后1天就可见到，在感染后10天仍然明显。中性粒细胞与呼吸道合胞病毒感染的上皮细胞密切相关，可见中性粒细胞与感染上皮细胞融合的证据。这些观察结果表明，中性粒细胞可能参与杀死呼吸道合胞病毒感染的细胞，并且在抗体水平低且其他细胞防御尚未充分发挥作用时，中性粒细胞可能在早期抗病毒防御呼吸道合胞病毒中发挥重要作用。从感染后6天开始可见细支气管修复，在感染后10天和13天进展良好。
