Abstract
Summary Lifelong infection is regularly produced in mice inoculated intracerebrally with SMCA at birth. However, the progeny of such infected mice do not develop cataracts and virus cannot be recovered from them. Furthermore, neither induction of cataracts nor transplacental passage of SMCA virus was demonstrated in the progeny of susceptible pregnant dams inoculated intravenously with high-titered preparations of SMCA at intervals throughout the gestation period. SMCA-infected mother mice conferred solid protection against SMCA-induced cataracts on their progeny. Mice acquiring such maternal resistance and inoculated with SMCA were not able subsequently to protect their own progeny. Five consecutive generations of mice were inoculated intracerebrally with SMCA as newborn mice. The first, third and fifth generations were fully susceptible to cataracts, while the second and fourth generations were completely protected. Liver-spleen virus titers in protected generations were sharply reduced and eyes were nearly completely free of SMCA infection. Protected second generation SMCA-inoculated mice were not immunologically tolerant. When re-inoculated with SMCA at 45 days of age, they subsequently conferred protection against SMCA-induced cataracts on their progeny. Despite the fact that neutralizing antibody is not readily demonstrated in SMCA-infected mice, transfer of maternal antibody provides the most reasonable explanation for the protection against SMCA-induced cataract conferred on suckling mice by SMCA-infected dams.
Published Version
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