Abstract
Fresh sera from normal rhesus monkeys, guinea pigs, and rabbits inactivated 90%-99% of the infectivity of Vero cell-passaged, attenuated strains of Junin virus (JV) within 60 minutes. Selective depletion studies showed that inactivation occurred by the classical complement pathway. Complement had little effect on virulent JV strains. Adsorption of the fresh sera with JV-infected Vero cells showed that inactivation was not mediated by low levels of antibodies in normal sera. The cells used for propagation of the virus affected inactivation: virus passaged in Vero cells (a continuous African green monkey kidney line) was more susceptible than virus passaged in FRhL-2 cells (a diploid strain derived from fetal rhesus monkey lung). Complement was important for in vitro neutralization of virulent JV strains by immune sera but was unnecessary for neutralization of attenuated strains. Thus, complement may be important in host resistance to Argentine hemorrhagic fever in two ways: first, complement activation may contribute to the attenuated phenotype of some strains; and second, complement may be necessary for efficient neutralization of virulent strains.
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