Involvement of virus infection in the pathogenesis of pulmonary fibrosis

在流感病毒感染小鼠肺中发现了超氧阴离子（O_2）和氧化亚硝酸盐等自由基的显著生成，这些分子种被认为是流感病毒的潜在致病原理。这一发现对理解病毒的发病机制具有许多重要意义：即，直接的病毒细胞毒性涉及细胞凋亡效应只是病毒感染引起的几种类型事件的一小部分。氧自由基的毒性和反应性可能是由于宿主对病毒复制器官的过度反应而产生的，这可能解释了不仅在小鼠流感病毒感染中观察到的组织损伤机制，而且在其他类型的病毒疾病中也观察到组织损伤，特别是那些急性程度较低但潜伏期较长的病毒，其中通常涉及免疫相互作用。更多地关注宿主源性因子的作用的研究可能会为理解病毒在肺中的发病机制以及其他病因不明的肺部疾病（如特发性间质性肺炎/肺纤维化）提供新的思路。

Free radicals such as superoxide anion(O_2) and nitrite oxide were found generated markedly in influenza virus infected mouse lung, and these molecular species were identified as the potent pathogenic principle. This finding has many important implications for understanding of the viral pathogenesis : namely, the direct viral cytotoxicity referred cytopahtic effect is only a fraction of several types of events induced by virus infection. The toxicity and reactivity of oxygen radicals, which are presumably generated in excess amount by the over reaction of host's immune response against the virus replicating organs, may explain the mechanism of tissue injuries observed not only in infuluenza virus infection in mice but also in other types of virus diseases, especially those viruses with less acute but with longer incubation period, in which immunological interactions are usually involved. Research focused more on the role of host-derived factors may shed new light on the understanding of viral pathogenesis in the lung as wel as other pulmonary disorders with uncertain etiology, such as idiopathic interstitial pneumonia/pulmonary fibrosis.