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Published on: December 2, 2012
Inactivated Venezuelan equine encephalomyelitis virus vaccine complexed with specific antibody: enhanced primary
Complexes of formalinized Venezuelan equine encephalomyelitis (VEE) virus vaccine and specific IgG formed at antigen-antibody equivalence enhanced the immune responses of rhesus monkeys (Macaca mulatta). The predomonant class of antibody elicited by complexes was IgG. In contrast, lower titers of antibody and a more biphasic (IgG-IgM) response were observed after exposure of monkeys to the vaccine alone. In comparison to the response of monkeys primed with antigen, a more rapid secondary response was obtained in monkeys primed with the complexes of antigen and antibody formed at equivalence. A sustained level of protection of 88% was afforded mice 24 hr after immunization with antigen-antibody complexes; development of protection after administration of antigen required eight days to reach this level. Passive protection (80%-100%) was conferred by IgG controls for seven to eight days after immunization. This level of protection was not significantly affected by X-irradiation 24 hr prior to administration of IgG; however, protection in mice similarly irradiated prior to immunization with antigen-antibody complexes was significantly decreased. Early protection afforded by the complexes was not nonspecific (interferon) but was mediated by specific immunologic mechanisms and may be caused by an early formation of IgG.
Complexes of formalinized Venezuelan equine encephalomyelitis (VEE) virus vaccine and specific IgG formed at antigen-antibody equivalence enhanced the immune responses of rhesus monkeys (Macaca mulatta). The predomonant class of antibody elicited by complexes was IgG. In contrast, lower titers of antibody and a more biphasic (IgG-IgM) response were observed after exposure of monkeys to the vaccine alone. In comparison to the response of monkeys primed with antigen, a more rapid secondary response was obtained in monkeys primed with the complexes of antigen and antibody formed at equivalence. A sustained level of protection of 88% was afforded mice 24 hr after immunization with antigen-antibody complexes; development of protection after administration of antigen required eight days to reach this level. Passive protection (80%-100%) was conferred by IgG controls for seven to eight days after immunization. This level of protection was not significantly affected by X-irradiation 24 hr prior to administration of IgG; however, protection in mice similarly irradiated prior to immunization with antigen-antibody complexes was significantly decreased. Early protection afforded by the complexes was not nonspecific (interferon) but was mediated by specific immunologic mechanisms and may be caused by an early formation of IgG.
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