Petica M, Petrescu A, Prodescu S
The Stefan S. Nicolau Institute of Virology, Bucharest, Romania.
Rom J Virol. 1996 Jan-Dec;47(1-4):61-73.
Infections with respiratory syncytial virus Long strain, associated with influenza virus, A/Beijing 353/89 (H3N2) strain, parainfluenza virus type 3, 739-2D strain, and adenovirus type 3, were experimentally induced in white mice, causing histological, histochemical and histoenzymatic lesions at the respiratory system level, the severity of which exceeded the one observed in the controls infected with a single virus. The pathomorphological changes made up an inflammatory, predominantly infiltrative, lymphohistiocytic, then exudative and alterative picture. The severest and most frequent lesion was the diffuse interstitial, often peribronchiolovascular, bronchopneumonia, which might involve large parenchyma areas. Another highly frequent pulmonary lesion was the thickening of interalveolar septa, due to stasis hyperemia, oedema and the predominantly lymphocytic cytoinfiltrate. At the level of the extrapulmonary airways, the lesion present in all experimental models was the denudation of epithelium cilia. In the viral association in which influenza virus was included, an alteration, the hyalinosis of tunica media of the vessels, as well as of the Reisseisen's muscle, was also observed, in addition to the cytoinfiltrate; when the association was achieved with parainfluenza virus type 3, many macrophages and erythrocytes and a few fibroblasts appeared in the cytoinfiltrate, the alteration being the same as in the former model; when the association contained adenovirus, there appeared necrosis, abundant lymphocytes and lysis of the Reisseisen's muscle in the bronchopulmonary block. The associated infections were demonstrated by the presence of homologous serum antibodies and by positive IF reactions in the pulmonary tissue.
在白色小鼠中通过实验诱导感染呼吸道合胞病毒长株、与甲型流感病毒A/北京353/89(H3N2)株、副流感病毒3型739 - 2D株以及腺病毒3型相关的病毒,导致呼吸系统出现组织学、组织化学和组织酶学损伤,其严重程度超过了感染单一病毒的对照组。病理形态学变化构成了一种炎症性的、主要为浸润性的、淋巴组织细胞性的,然后是渗出性和变质性的病变情况。最严重且最常见的损伤是弥漫性间质性肺炎,通常为支气管血管周围性,可能累及大片实质区域。另一种常见的肺部损伤是肺泡间隔增厚,这是由于淤血、水肿以及主要为淋巴细胞的细胞浸润所致。在肺外气道层面,所有实验模型中均出现的损伤是上皮纤毛剥脱。在包含流感病毒的病毒联合感染中,除了细胞浸润外,还观察到血管中膜以及雷斯曼肌的透明样变性;当与副流感病毒3型联合感染时,细胞浸润中出现许多巨噬细胞、红细胞和少量成纤维细胞,病变与前一模型相同;当联合感染包含腺病毒时,在支气管肺组织中出现坏死、大量淋巴细胞以及雷斯曼肌溶解。通过同源血清抗体的存在以及肺组织中阳性免疫荧光反应证实了联合感染。