We have previously shown, as for other viral infections (23, 24), that there is an age-dependent resistance to SBV infection in suckling mice (11) that could be attributed to the development of anatomic barriers, the reticuloendothelial system, and the IFN and immune responses, and thus, the increased pathogenicity of SBVp32 could be due to many factors. This evidence concerns the gene IFNA1 and viral infectious disease.