Susceptibility to Fatal Pichinde Virus Infection in the Syrian Hamster
Pichinde virus, an arenavirus, causes a fatal infection in the inbred MHA strain of Syrian hamsters within 10 to 20 days of an intraperitoneal inoculation (1). High titres of virus are present, and death appears to be a direct consequence of the virus-induced necrosis in cells of the liver and spleen (2). Other strains of hamsters, including the inbred LSH strain and the random-bred LVG line, survive the infection. Resistance to the fatal virus infection is associated with an ability to limit Pichinde virus replication to low levels. The phenotypes of survival and the ability to limit viremia are each controlled by a single dominant gene (3, 4); it is not known whether the same gene controls both properties. Since the pathogenesis of Pichinde virus infection in Syrian hamsters resembles the pathogenesis of human arenavirus infections in several respects (5), an understanding of the events leading to the recovery of hamsters from Pichinde virus disease may contribute some insight into the factors controlling the human diseases. In this paper, early events of Pichinde virus infection and the immune response to the virus in the resistant and susceptible hamster strains are described.
KeywordsNatural Killer Cell Spleen Cell Syrian Hamster Natural Killer Activity Popliteal Lymph Node
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