Mims C A, Tosolini F A
Br J Exp Pathol. 1969 Dec;50(6):584-92.
Mice infected with lymphocytic choriomeningitis virus (LCM) may show prominent lesions in the spleen. The lesions originate in perifollicular collections of large pale cells, and consist of fibrinoid-type deposits which may replace lymphoid follicles. They stain negatively for amyloid. Similar lesions may occur in lymph nodes. In local lymph nodes after footpad infection, the lesions are very severe, leading to lymphatic blockade and obliterative necrosis of the node. The thymus shows changes attributable to the action of corticosteroids. These changes are seen in mice infected lethally with cowpox as well as in LCM virus infection. They are produced by injections of hydrocortisone and prevented by bilateral adrenalectomy. The pathogenesis of the fibrinoid-type lesions is discussed, and also the role of the immune response, of corticosteroids, and of direct viral activity in the pathogenesis of lymphoid lesions in LCM virus infection. Mice infected with LCM virus develop focal eosinophilic necrosis in the liver, and immunological mechanisms are thought to account for these lesions.
感染淋巴细胞性脉络丛脑膜炎病毒（LCM）的小鼠脾脏可能会出现明显病变。这些病变起源于滤泡周围大的淡色细胞聚集，由类纤维蛋白样沉积物组成，可能会取代淋巴滤泡。它们对淀粉样蛋白染色呈阴性。类似病变也可能出现在淋巴结中。在足垫感染后的局部淋巴结中，病变非常严重，导致淋巴管阻塞和淋巴结的闭塞性坏死。胸腺显示出归因于皮质类固醇作用的变化。在感染致死性牛痘的小鼠以及LCM病毒感染中都可见到这些变化。它们由注射氢化可的松产生，并可通过双侧肾上腺切除术预防。讨论了类纤维蛋白样病变的发病机制，以及免疫反应、皮质类固醇和直接病毒活性在LCM病毒感染中淋巴样病变发病机制中的作用。感染LCM病毒的小鼠肝脏会出现局灶性嗜酸性坏死，免疫机制被认为是这些病变的原因。
