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Review
. 2014 Aug;59(1-3):81-108.
doi: 10.1007/s12026-014-8549-5.

Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic

J E Butler  1 , K M Lager, William Golde, Kay S Faaberg, Marek Sinkora, Crystal Loving, Y I Zhang
Affiliations
Review

Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic

J E Butler et al. Immunol Res. 2014 Aug.

Abstract

Porcine reproductive and respiratory disease syndrome (PRRS) is a viral pandemic that especially affects neonates within the "critical window" of immunological development. PRRS was recognized in 1987 and within a few years became pandemic causing an estimated yearly $600,000 economic loss in the USA with comparative losses in most other countries. The causative agent is a single-stranded, positive-sense enveloped arterivirus (PRRSV) that infects macrophages and plasmacytoid dendritic cells. Despite the discovery of PRRSV in 1991 and the publication of >2,000 articles, the control of PRRS is problematic. Despite the large volume of literature on this disease, the cellular and molecular mechanisms describing how PRRSV dysregulates the host immune system are poorly understood. We know that PRRSV suppresses innate immunity and causes abnormal B cell proliferation and repertoire development, often lymphopenia and thymic atrophy. The PRRSV genome is highly diverse, rapidly evolving but amenable to the generation of many mutants and chimeric viruses for experimental studies. PRRSV only replicates in swine which adds to the experimental difficulty since no inbred well-defined animal models are available. In this article, we summarize current knowledge and apply it toward developing a series of provocative and testable hypotheses to explain how PRRSV immunomodulates the porcine immune system with the goal of adding new perspectives on this disease.

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Figures

Fig. 1
Fig. 1
The critical window of immunological development. Neonates are vulnerable during this period since their adaptive immune system is undeveloped, and they depend on innate and passive immunity. Within this period, healthy gut colonization takes place which drives the development of adaptive immunity and both oral tolerance and immune homeostasis develop. In some mammals, passive maternal antibodies are provided in utero as well as post-natally through suckling. The colors are a result of blending overlapping events. Modified from Butler and Sinkora [237]
Fig. 2
Fig. 2
Viremia in swine infected at different ages. Viremia is persistent when animals are infected as piglets. From Klinge et al. [121]
Fig. 3
Fig. 3
In piglets, the appearance of neutralizing antibodies is delayed, but other antibodies appear shortly after infection. From Lopez et al. [101]
Fig. 4
Fig. 4
(top) Plasma Ig levels in isolator piglets infected with PRRSV, PCV2, SIV, and sham controls. (bottom) Corresponding data from the BAL of these piglets. Dpi days post-infection, SIV swine influenza, PCV-2 porcine circovirus type 2. Note split y-axis
Fig. 5
Fig. 5
B lymphocytes and B cell subpopulation in isolator piglets infected with the same three viruses as in Fig. 4. Noteworthy is the apparent loss of the primed B cell subset (CD2−CD21−) in PRRSV-infected piglets
Fig. 6
Fig. 6
a Antibody repertoire diversification measured as a repertoire diversification index (RDI). PRRS = isolator piglets infected with PRRSV; GF = germfree controls; C/V = isolator piglets colonized with benign E. coli or infected with SIV; PIC = young, helminth-infected conventionally reared pigs (PIC). b Hydropathicity profiles calculated from sequence analysis of the HCDR3 region of Ig from PRRSV-infected piglets compared to PIC animals (top) and compared to newborns (bottom). The numbers in parentheses indicate the number of sequences examined. Hydrophobic HCDR3 regions I and II are a feature of an undiversified pre-immune repertoire whereas region III is characteristic of a diversified repertoire. From Butler et al. [153]
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References

    1. Rossow KD. Porcine reproductive and respiratory syndrome. Vet Path. 1998;35:1–20. doi: 10.1177/030098589803500101. - DOI - PubMed
    1. Albina E. Epidemiology of porcine reproductive and respiratory syndrome (PRRS): an overview. Vet Microbiol. 1997;55:309–316. doi: 10.1016/S0378-1135(96)01322-3. - DOI - PubMed
    1. Collins JE, Benfield DA, Christianson WT, Harris L, Hennings JC, Shaw DP, Goyal SM, McCullough S, Morrison RB, Joo HS, et al. Isolation of swine infertility and respiratory syndrome virus (isolate ATCC VR-2332) in North America and experimental reproduction of the disease in gnotobiotic pigs. J Vet Diagn Invest. 1992;4:117–126. doi: 10.1177/104063879200400201. - DOI - PubMed
    1. Wensvoort G, Terpstra C, Pol JM, ter Laak EA, Bloemraad M, de Kluyver EP, Kragten C, van Buiten L, den Besten A, Wagenaar F, et al. Mystery swine disease in The Netherlands: the isolation of Lelystad virus. Vet Q. 1991;13:121–130. doi: 10.1080/01652176.1991.9694296. - DOI - PubMed
    1. Dunowska M, Biggs PJ, Zheng T, Perrott MR. Identification of a novel nidovirus associated with a neurological disease of the Australian brushtail possum (Trichosurus vulpecula) Vet Microbiol. 2012;156:418–424. doi: 10.1016/j.vetmic.2011.11.013. - DOI - PMC - PubMed

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