Azoulay-Dupuis E, Lambre C R, Soler P, Moreau J, Thibon M
J Comp Pathol. 1984 Apr;94(2):273-83. doi: 10.1016/0021-9975(84)90046-x.
Guinea-pigs were infected intranasally with influenza A Hong Kong 68 (H3N2) virus. Infective particles were re-isolated from lung homogenates up to 3 days after inoculation and indicated local replication. The subsequent lung inflammatory stages were studied by light microscopy, scanning and transmission electron microscopy (TEM). Lung alterations appeared after 24 h and intensified up to 7 days after virus inoculation, progressively decreasing until 3 weeks thereafter. The damage was reversible and complete restoration of structure was obtained within 5 weeks. The lesions commenced with the infiltration of bronchiolar and alveolar walls by polymorphonuclear cells, histiocytes and macrophages. A purulent exudate was seen to occupy the bronchiolar lumen. Cilia disappeared from tracheal and bronchiolar epithelia. Tracheal epithelium desquamated in some animals. TEM examination showed deterioration in type I pneumocytes, an increase in type II pneumocytes and concomitant damage to alveolar capillaries. Alveolar oedema and fibrinous deposits were seen. The pleura presented slight modifications. These results show that infection of guinea-pigs with influenza virus is a useful model for the study of lung pathology associated with a non-lethal respiratory viral infection.
将甲型香港68（H3N2）流感病毒经鼻内接种豚鼠。在接种后长达3天的时间里，可从肺匀浆中重新分离出感染性颗粒，表明病毒在局部复制。随后通过光学显微镜、扫描电子显微镜和透射电子显微镜（TEM）研究肺部炎症阶段。病毒接种后24小时出现肺部改变，并在接种后7天内加剧，此后逐渐减轻直至3周。损伤是可逆的，在5周内结构完全恢复。病变始于多形核细胞、组织细胞和巨噬细胞浸润细支气管和肺泡壁。可见脓性渗出物占据细支气管腔。气管和细支气管上皮的纤毛消失。一些动物的气管上皮发生脱落。透射电镜检查显示I型肺泡上皮细胞退变，II型肺泡上皮细胞增多，同时肺泡毛细血管受损。可见肺泡水肿和纤维蛋白沉积。胸膜有轻微改变。这些结果表明，豚鼠感染流感病毒是研究与非致死性呼吸道病毒感染相关的肺部病理学的有用模型。
