Pathogenicity of three type 2 porcine reproductive and respiratory syndrome virus strains in experimentally inoculated pregnant gilts

•PRRSV strain KS06-483 appeared less virulent than NVSL 97-7895 and KS06-72109.•High and low virulent PRRSV strains were equally able to cross the placental barrier.•Important cytokines in reproductive PRRS were CCL2, IFNα and IFNγ.•Higher PRRS viral loads in fetuses increased odds of fetal death.•Higher frequency of lesions in fetal and maternal tissues in dead versus live infected fetuses.

Mechanisms of reproductive failure resulting from infection with porcine reproductive and respiratory syndrome virus (PRRSV) are still poorly understood. Presented herein are the results of a side-by-side evaluation of the pathogenicity of three type 2 PRRSV strains in a reproductive model, from a pilot study used to develop experimental conditions and laboratory methods for a larger experiment. Pregnant gilts were experimentally infected with PRRSV at gestation day 85 or served as uninfected negative controls. After 21 days, all gilts and fetuses were necropsied. Clinical signs, litter outcome, viral load, cytokine levels, and pathology were compared from samples collected among pigs exposed to the three PRRSV strains. Based on differences in histologic lesions, and fetal weights, and numeric differences in gilt serum cytokine levels, litter outcome and virus replication in fetal tissues KS06-483 appeared less virulent than NVSL 97-7895 and KS06-72109 isolates. Levels of chemokine ligand 2 (CCL2), interferon alpha (IFNα), and interferon gamma (IFNγ) were increased in PPRRSV-infected compared to non-infected gilts (0.01 > P < 0.06). Inoculation with NVSL 97-7895 induced higher levels of all three cytokines. All three PRRSV isolates were able to induce high mean viral load in individual litters, which was closely related to the proportion of PRRSV positive fetuses in the litter. Viral load in fetal samples was also positively associated with viral load at the maternal–fetal interface. All but one dead fetus were positive for PRRSV RNA, and higher concentrations of PRRSV RNA in fetal thymus increased the odds of fetal death. Our results suggest that virus replication in fetal tissues and the maternal–fetal interface, but not in other gilt tissues, are important for the outcome of reproductive PRRS. Additionally, our data indicate that umbilical lesions decreased corresponding to the use of pentobarbital sedation prior to euthanasia of pregnant gilts by captive bolt.