Submitted to: American Journal of Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/9/1998
Publication Date: N/A
Citation: N/A Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is a swine disease responsible for major losses to the industry. It is caused by the PRRS virus which can cause abortions, stillborn and weak pigs in sows, and a severe respiratory disease in young pigs. Recently, two modified-live virus vaccines have been developed and marketed for use in non-pregnant gilts and sows to reduce the reproductive failure caused by the PRRS virus. Anecdotal evidence, some field studies, and some limited experimental studies completed by the manufacturers of the vaccines support the use of the vaccines, however, there are some field studies that have suggested that modified-live vaccines are not efficacious and may even cause disease. The study reported here was an attempt to investigate the PRRS virus immune response in gilts. Results from this study suggest that swine can produce a protective immune response following exposure or vaccination with a live virus. The protective immune response results in reduced reproductive losses; however, this protection is not perfect and it may have a limited duration. Nevertheless, this study indicates that there may be a place for the use of PRRS virus vaccines in the reduction of reproductive losses.
Technical Abstract: Objectives of this study were to induce and evaluate homologous and heterologous porcine reproductive and respiratory syndrome virus (PRRSV) protective immunity in pregnant gilts. Forty gilts were divided into 5 equal groups. Two of the groups were immunized at or before breeding with a North American PRRSV isolate. All gilts were bred and protective homologous and heterologous immunity were evaluated by live virus challenge during late gestation, a stage of gestation that is the most susceptible to PRRSV-induced reproductive failure. Challenge virus was either the same PRRSV isolate (homologous) or an antigenically distinct European PRRSV (heterologous). Gilt and fetal tissues were tested for the presence of challenge virus. Lack of challenge virus in gilt tissues indicated protective immunity. Lack of challenge virus in fetal tissues indicated protection from reproductive losses. Complete homologous protection was demonstrated by a lack of challenge virus in gilt and fetal tissues. Heterologous protection was incomplete as indicated by a limited failure of gilt protective immunity (the presence of challenge virus in gilts) combined with significant protection from reproductive losses (the lack of challenge virus in fetal tissues). In conclusion, homologous protective immunity can be induced in gilts by exposure to live PRRSV. Heterologous protective immunity can be induced in gilts by exposure to live PRRSV; however, this immunity may have a shorter duration than homologous immunity. This study suggests the use of live virus vaccines may provide some protection against PRRSV-induced reproductive losses in the field. However, the protection may have a limited duration and it may be dependent on the antigenic relatedness of vaccine and field virus.