Abstract
Multiple contributory factors have been postulated in the pathogenesis of hemorrhagic encephalopathy of the rat, an entity induced by rat virus infection of sucklings. These include: (1) the direct attack of virus upon vascular endothelium with resultant thrombotic and hemorrhagic effects; (2) the triggering of consumptive coagulopathy by the vascular injury; and (3) the production of a deficiency coagulopathy secondary to viral hepatitis. This report describes a new feature of rat virus infection, the involvement of the pool of developing megakaryocytes. This cellular lesion, although unsupported by evidence of depressed platelet levels, or disturbed platelet function, suggests that a direct viral attack upon platelet-forming elements may be an additional contributory factor in the pathogenesis of hemorrhagic encephalopathy. The complex of pathogenetic factors for hemorrhagic encephalopathy of the rat indicates that this entity offers an excellent experimental model for study of the general problem of the pathophysiology of disturbances of blood coagulation in virus infections.
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