Morin M J, Warner A, Fields B N
Department of Microbiology & Molecular Genetics, Harvard Medical School, Boston, Massachusetts, USA.
J Virol. 1996 Jan;70(1):541-8. doi: 10.1128/JVI.70.1.541-548.1996.
We undertook the present study to elucidate the pathogenesis of the pathologic response to reovirus infection in the lungs and further understand the interactions of reoviruses with pulmonary cells. We found that reoviruses were capable of causing acute pneumonia in 25- to 28-day-old Sprague-Dawley rats following intratracheal inoculation with the reoviruses type 1 Lang (T1L) and type 3 Dearing (T3D). The onset of the pneumonia was rapid, marked by type I alveolar epithelial cell degeneration, type II alveolar epithelial cell hyperplasia, and the infiltration of leukocytes into the alveolar spaces. More neutrophils were recruited into the lungs during T3D infection than during T1L infection, and the serotype difference in the neutrophil response was mapped to the S1 gene of reovirus. Viral replication in the lungs was required for the development of pneumonia due to T1L and T3D infections, and replication occurred in type I alveolar epithelial cells. T1L grew to higher titers in the lungs than did either T3D or type 3 clone 9, and the S1 gene was found to play a role in determining the level of viral replication. We propose that experimental reovirus infection in the lungs can serve as a model for the pathogenesis of viral pneumonia in which pulmonary inflammation results following direct infection of lung epithelial cells.
我们开展本研究以阐明肺部对呼肠孤病毒感染的病理反应的发病机制，并进一步了解呼肠孤病毒与肺细胞的相互作用。我们发现，用1型朗（T1L）和3型迪林（T3D）呼肠孤病毒经气管内接种后，呼肠孤病毒能够在25至28日龄的斯普拉格-道利大鼠中引起急性肺炎。肺炎发病迅速，其特征为I型肺泡上皮细胞变性、II型肺泡上皮细胞增生以及白细胞浸润到肺泡腔。在T3D感染期间比T1L感染期间有更多的中性粒细胞被募集到肺中，并且中性粒细胞反应中的血清型差异被定位到呼肠孤病毒的S1基因。由于T1L和T3D感染导致的肺炎发展需要病毒在肺中复制，并且复制发生在I型肺泡上皮细胞中。T1L在肺中的滴度比T3D或3型克隆株9更高，并且发现S1基因在决定病毒复制水平方面发挥作用。我们提出，肺部的实验性呼肠孤病毒感染可作为病毒性肺炎发病机制的模型，其中肺部炎症是在肺上皮细胞直接感染后发生的。
