Abstract
Some strains of bluetongue virus cause congenital brain damage in bovine and ovine fetuses, as well as in neonatal mice. Two strains of bluetongue virus serotype 11 (UC-2 and UC-8) which differ in neuroinvasiveness were used to determine the biological basis for this difference. UC-2 and UC-8 were inoculated subcutaneously into newborn mice and virus was titrated from blood, plasma and brain tissues over 14 days. For the invasive UC-8 strain, 50-175 plaque forming units of virus per ml was found associated with the blood cells and no virus was detected in the plasma. The virus was detected in the brain at day one post inoculation, and again at day 7, increasing to day 11. The results indicate that UC-8 was able to reach the brain soon after inoculation and to replicate and/or remain in the blood circulation better than UC-2. Immunohistochemical examination of frozen brain sections revealed a sudden, multifocal appearance of UC-8 at day 9, with more viral antigen seen at days 11 and 13, which was barely detected by day 15. Viral antigen was not associated with blood vessels in the brain, indicating that the viral invasion was not from infected vascular endothelium. No virus was detected in the mice infected with strain UC-2.
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