In contrast to Lewis (LEW) and Wistar rats, black hooded (BH) rats inoculated with Borna disease (BD) virus developed neither encephalitis nor clinical disease despite persistent replication of the virus in the central nervous system. In comparison to LEW rats, production of virus-specific antibodies was significantly delayed in BD-resistant BH rats, even though identical titres were finally reached. The different susceptibility in LEW and BH rats was studied further by investigating responses of F hybrid animals. Although these rats developed encephalitis, they did not become sick. The differences in host responses for BD virus were found to be genetically determined but were independent of class I or class II major histocompatibility complex gene products or to genes responsible for lymphocyte differentiation.


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