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Departments of Pediatrics and Microbiology, School of Medicine, State University of New York at Buffalo, Buffalo, New York
Abstract
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.
Footnotes
This work was supported in part by Research Grant AI-6227 and Training Grant AI-98 from the National Institute of Allergy and Infectious Diseases.
2 Recipient of Research Career Award AI-1136 from the National Institute of Allergy and Infectious Diseases.
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