Skip to main content
ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Parasitic Diseases Laboratory » Research » Publications at this Location » Publication #310135

Research Project: FUNCTIONAL GENOMIC APPROACHES FOR CONTROLLING DISEASES OF SWINE

Location: Animal Parasitic Diseases Laboratory

Title: Pathogenicity of three type 2 Porcine Reproductive and Respiratory Syndrome virus strains in experimentally inoculated pregnant gilts

Author
item LADINIG, ANDREA - University Of Saskatchewan
item DETMER, SUSAN - University Of Saskatchewan
item CLARKE, KYLE - University Of Saskatchewan
item ASHLEY, CAROLYN - University Of Saskatchewan
item ROWLAND, RAYMOND - Kansas State University
item Lunney, Joan
item HARDING, JOHN - University Of Saskatchewan

Submitted to: Virus Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/18/2015
Publication Date: 3/18/2015
Publication URL: http://handle.nal.usda.gov/10113/61247
Citation: Ladinig, A., Detmer, S.E., Clarke, K., Ashley, C., Rowland, R.R., Lunney, J.K., Harding, J.C. 2015. Pathogenicity of three type 2 Porcine Reproductive and Respiratory Syndrome virus strains in experimentally inoculated pregnant gilts. Virus Research. 203:24-35.

Interpretive Summary: Porcine Reproductive and Respiratory Syndrome (PRRS) causes major losses to the pig industry, $642,000/year in the US alone. For breeding herds losses are due to abortions, early farrowings, fetal death, as well as the birth of weak, congenitally infected piglets resulting in elevated pre-weaning mortality. In spite of extensive research, immunologic control mechanisms against reproductive PRRS virus (PRRSv) infection remain poorly understood. This study involved a side-by-side evaluation of the pathogenicity of three type 2 PRRSv strains in a reproductive model. It served as a pilot study to develop experimental conditions and laboratory methods for a larger reproductive PRRS study. Pregnant gilts were experimentally infected with one of 3 different PRRSv isolates (KS06-483, NVSL 97-7895, and KS06-72109) in their third trimester (at gestation day 85) or kept as uninfected negative controls. After 21 days infection, 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, gilt serum cytokine levels, fetal weights, and numeric differences in litter outcome and virus replication in fetal tissues KS06-483 appeared less virulent than NVSL 97-7895 and KS06-72109 isolates. Based on these results virus isolate NVSL 97-7895 was chosen for the larger reproductive PRRS study.

Technical Abstract: Mechanisms of reproductive failure resulting from infection with porcine reproductive and respiratory syndrome virus (PRRSv) are still poorly understood. The present study, a side-by-side evaluation of the pathogenicity of three type 2 PRRSv strains in a reproductive model, was used as a pilot study to develop experimental conditions and laboratory methods for a larger experiment. Pregnant gilts were experimentally infected with PRRSv at gestation day 85 or kept 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, gilt serum cytokine levels, fetal weights, and numeric differences in litter outcome and virus replication in fetal tissues KS06-483 appeared less virulent than NVSL 97-7895 and KS06-72109 isolates. Chemokine ligand 2 (CCL2), interferon alpha (IFNa), and interferon gamma (IFN') were the most important cytokines in reproductive PPRRSv infection. 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; higher concentrations of PRRSv RNA in fetal thymus increased the odds of fetal death. Therefore, our data suggest that virus replication in fetal tissues and the maternal-fetal interface, but not in other gilt tissues, is important for the outcome of reproductive PRRS. Additionally, we showed that umbilical lesions decreased corresponding to the use of pentobarbital sedation prior to euthanasia of pregnant gilts by captive bolt.