Pathogenesis of lesions in lymphoid tissue of mice infected with lymphocytic choriomeningitis (LCM) virus

Abstract

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.