Abstract
Among inadequately immunized laboratory animals dying of rabies, a small but consistent proportion succumb after an incubation period shorter than that of any of the unvaccinated controls and this phenomenon has been termed 'early death'. It has also been shown that, after immunosuppression either with cyclophosphamide or by thymectomy and irradiation, rabies-infected animals survive longer with decreased incidence of paralysis. It appears that 'early death' also occurs in humans who have been treated (unsuccessfully) with vaccine, with or without accompanying serum therapy, after exposure to rabies. Collectively, these studies suggest that there is a immunopathological component in rabies virus infection. We have therefore investigated a model of lethal rabies infection in immunosuppressed mice and have concluded that B lymphocytes or antibody specific for rabies play a part in the causation of early death. Accordingly the immune response to rabies has a dual role, sometimes favouring survival but sometimes enhancing the disease.
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