Carthew P, Sparrow S
Res Vet Sci. 1980 Nov;29(3):289-92. doi: 10.1016/S0034-5288(18)32629-8.
The pathogenesis of Sendai virus infection was studied in athymic and AGUS rats. The infection was more severe in the athymic rats and caused considerable clinical disease. Virus was shown to replicate in the bronchial epithelium and persisted in athymic rats for the duration of the experiment (32 days). The characteristic changes of necrosis of the bronchial epithelium and subsequent hyperplasia also persisted in this group and was accompanied by quite extensive interstitial pneumonitis. The virus failed to evoke an antibody response in the athymic rats.
在无胸腺大鼠和无脾大鼠中研究了仙台病毒感染的发病机制。无胸腺大鼠的感染更为严重,并引发了相当严重的临床疾病。病毒在支气管上皮细胞中复制,并在无胸腺大鼠中在整个实验期间(32天)持续存在。支气管上皮细胞坏死及随后的增生等特征性变化在该组中也持续存在,并伴有相当广泛的间质性肺炎。病毒未能在无胸腺大鼠中引发抗体反应。