Pathogenesis of Korean Type 1 (European Genotype) Porcine Reproductive and Respiratory Syndrome Virus in Experimentally Infected Pregnant Gilts

The aims of this study were to determine (1) the pathogenesis of experimental infection with a Korean type 1 porcine reproductive and respiratory syndrome virus (PRRSV) by defining the viral distribution and the sites of viral replication and (2) the relationship between viral replication and apoptosis in stillborn fetuses and live born piglets from infected pregnant gilts. At 3 weeks ante partum, four pregnant gilts were inoculated intranasally with Korean type 1 PRRSV. Stillborn fetuses from the infected gilts were of crown-to-rump length 25.8–27.1 cm consistent with fetal death between 106 and 110 days of gestation. Type 1 PRRSV was isolated from the fetal tissues and these isolates were shown to be identical to the challenge virus by sequence analysis. Type 1 PRRSV RNA was detected in the lung, lymph node, heart, tonsil, thymus, liver, adrenal gland and spleen of live born piglets and stillborn fetuses from the infected gilts. The mean number of apoptotic cells per unit area of lung (P = 0.003), heart (P = 0.011), thymus (P = 0.003), liver (P = 0.011) and spleen (P = 0.002) was significantly higher in stillborn fetuses than in live born piglets. Dual labelling showed that the majority of cells either contained type 1 PRRSV or were apoptotic, but not both. Apoptotic cells were more numerous than PRRSV+ cells. The results of the study demonstrated that type 1 PRRSV induces reproductive failure in pregnant gilts. Apoptosis induced by type 1 PRRSV may be associated with the incidence of stillborn fetuses in PRRSV-infected pregnant gilts.