Abstract
Minimal research has focused on understanding mechanisms underlying porcine reproductive and respiratory syndrome virus (PRRSV) induced reproductive failure. We have completed a large-scale project investigating phenotypic and genotypic predictors of reproductive PRRS severity in which numerous clinical, pathological, immunologic and viral responses were characterized in dams and fetuses. The goal was to determine which phenotypic responses were associated with fetal viral load and death after experimental infection of pregnant gilts with type 2 PRRSV, thereby elucidating mechanisms of reproductive PRRS in third trimester pregnant gilts. The presence of fetal infection and increasing RNA concentration at the maternal-fetal interface were strong predictors of the probability of fetal death, while PRRSV RNA concentration in dam sera and systemic tissues were not associated with the odds of fetal death. Fetal infection and death clustered, indicating that the status of adjacent fetuses is crucial for lateral transmission and fetal outcome. Several systemic immune responses of gilts were associated with fetal outcome and viral load: interferon-α contributed to the probability of fetal death, but absolute numbers of T helper cells in early infection, absolute numbers of myeloid cells over time and interleukin 12 levels appeared protective. These results suggest specific immune responses may either contribute to, or protect against, transplacental virus transmission. The WUR10000125 SNP on chromosome 4, associated with PRRS resilience in nursery pigs, was not associated with reproductive outcome. Whereas past research suggested that fetal death results from events occurring at the maternal-fetal interface, we conclude that viral replication within fetuses and spread of PRRSV to adjacent fetuses are pivotal events in the pathogenesis of reproductive PRRS.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-015-0251-7) contains supplementary material, which is available to authorized users.
Highlights
In spite of porcine reproductive and respiratory syndrome virus (PRRSV) reproductive disease contributing millions in losses annually [1], a proportionately small amount of research has focused on the reproductive form of the disease
Phenotypic outcomes of PRRSV infection measured in gilts and fetuses Detailed results on clinical signs, viral loads and litter outcomes including fetal preservation can be found in Ladinig et al [19]
The fetal mortality rate per litter ranged from 0% to 94.4%, with 50% of fetuses categorized as VIA, 9% as meconium stained (MEC), 8% as DEC, and 33% as AUT [19]
Summary
In spite of PRRSV reproductive disease contributing millions in losses annually [1], a proportionately small amount of research has focused on the reproductive form of the disease. Numerous phenotypic responses were characterized, including clinical signs, virus levels in serum and tissues, changes in leukocyte subsets in gilt blood, cytokine protein levels over time in gilt serum and supernatants of stimulated peripheral blood mononuclear cells (PBMC), gross and microscopic pathology, fetal preservation and mortality [17,18,19]. For this experiment, dams were selected from high and low birth weight (BW) litters in order to determine if BW of the dam influences PRRS severity. Genotyping for a major quantitative trait locus (QTL) on Sus scrofa chromosome (SSC) 4 conferring PRRSV resistance/susceptibility and explaining approximately 11 and 15% of the individual variation in weight gain and viral load, respectively, in experimentally infected nursery pigs [20,21,22] was performed on DNA from gilts, sires and non-autolyzed fetuses
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