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A nonpathogenic variant of viral hemorrhagic septicemia virus has been selected which immunizes fish against a subsequent challenge with the wild-type virus strain. In this paper, we demonstrate that both the variant and the wild-type virus strains multiplied in spleen and kidney of infected fish, but the virus yield was lower for the variant and soon dropped below the sensitivity of our titration technique, which indicates that an early mechanism prevents the establishment of septicemia. This early mechanism could also be responsible for early protection since fish were already immunized 48 h postinfection with the variant. In a second step antibodies relayed that first defence mechanism to ensure long-lasting immunity. Antisera collected after immunization by the variant or the wild-type virus strain cross-reacted poorly in neutralization tests, which is in agreement with results obtained with plant lectins and proves that the variant is modified in its antigenic properties.

infection and immunity

Viral hemorrhagic septicemia of rainbow trout: relation between the G polypeptide and antibody production in protection of the fish after infection with the F25 attenuated variant