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Title:   Author  item
                                            Loving, Crystalitem
                                            Brockmeier, Susanitem
                                            Palmer, Mitchellitem
                                            Spear, Allynitem
                                            Faaberg, Kayitem
                                            Nicholson, Tracy
  Submitted to: Research Workers in Animal Diseases Conference Proceedings
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 10/1/2012
                                    Publication  Date: 12/2/2012
                                    Citation: Loving, C.L., Brockmeier, S.L., Palmer, M.V., Spear, A.R., Faaberg, K.S., Nicholson, T.L. 2012. Changes in circulating and thymic lymphocyte populations following infection with strains of North American or highly pathogenic PRRSV. Conference of Research Workers in Animal Diseases Annual Meeting. Paper No. 185.Interpretive Summary:
                                Technical Abstract: Recently, a highly pathogenic (HP) PRRSV strain has emerged in Asia, which causes severe clinical disease and mortality. Since its emergence, work has focused on characterizing the virus and host response following infection to determine the mechanism of enhanced virulence. PRRSV infection has been shown to cause a decrease in circulating T cell populations, lymphadenopathy and thymic atrophy; however, the relationship between these features in relation to HP-PRRSV has not been evaluated. Groups of pigs were challenged with one of two different North American isolates (VR-2332 or SDSU73) or one of two different HP-PRRSV isolates (SRV07 or JXwn06) for this study. Circulating T cell populations were enumerated on 1-4, 6, 8 and 10 days post-infection (dpi) using a newly developed flow cytometric based assay with whole blood. T-cell populations in the thymus and lymph node were evaluated on dpi 4 and 10. Regardless of the challenge strain, there was a significant decrease in the number of circulating CD3+ T-cells, including CD4 and CD8 subsets, following infection. The sharpest decline occurred between dpi 1 to 2 in VR-2332, SDSU73 and JXwn06 groups and between dpi 2 to 4 for SRV07 group. There was not a significant difference in the lowest number of circulating T cells between the SDSU73, SRV07 or JXwn06 groups. VR2332, SDSU73 and JXwn06 groups were viremic by dpi 1 while pigs challenged with SRV07 displayed a gradual increase in serum virus titers. The JXwn06 group had the greatest amount of virus in the sera beyond dpi 2; however, the number of circulating T-cells was similar between SDSU73 and JXwn06 groups. Thus, serum virus titers alone do not explain the decrease in circulating T-cells. There was a significant increase in the number of dead T-cells (CD4, CD8 and CD4/CD8) in the thymus of all PRRSV infected pigs, though SDSU73 and JXwn06 pigs were the most affected. There was not a significant increase in serum cortisol levels in any of the pigs. Taken together, there is a rapid decrease in the number of circulating T-cells following PRRSV infection, but, this effect does not appear to correlate to virulence, serum virus titers nor serum cortisol levels.


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