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Title: Swine immunity and resistance to persistent Porcine Reproductive and Respiratory Syndrome virus (PRRSV) infection.

Author
item Lunney, Joan
item Kuhar, Daniel
item Prucnal, Elizabeth
item MOLINA, RAMON - IOWA STATE U, AMES IA
item CHRISTOPHER-HENNINGS, JANE - SOUTH DAKOTA STATE U
item NELSON, ERIC - SOUTH DAKOTA STATE U
item ZIMMERMAN, JEFFREY - IOWA STATE U, AMES IA
item ROWLAND, R R - KANSAS STATE U, MANHATTAN

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 10/7/2007
Publication Date: 11/30/2007
Citation: Lunney, J.K., Kuhar, D.J., Prucnal, E., Molina, R., Christopher-Hennings, J., Nelson, E., Zimmerman, J., Rowland, R.R. 2007. Swine immunity and resistance to persistent Porcine Reproductive and Respiratory Syndrome virus (PRRSV) infection. Proceedings 2007 PRRS Symposium. p.49.

Interpretive Summary:

Technical Abstract: Infection with Porcine Reproductive and Respiratory Syndrome virus (PRRSV) elicits a weak immune response that is not fully protective and that results in persistent infection in a subset of pigs. Despite substantial research efforts the exact components of a protective anti-PRRSV immune response are still not known, particularly as it effects on persistence. We hypothesized that the intensity and timing of the early cytokine responses to PRRSV infection might be a predictor of final PRRSV burden and persistence. We tested serum samples collected as part of the “Big Pig” project, an extensive analysis of virus replication and immunity in a population of 109 pigs (and 60 control pigs) sampled for up to 203 days post-PRRSV infection (dpi). We compared pigs that apparently cleared the viral infection from serum and tissues by the first 28 dpi, the Non-Persistent (NP) pigs, to Persistent (P) pigs that even at 150 dpi have evidence of long term persistent PRRSV infection. Sera, collected over the course of the PRRSV infection, were tested for relevant cytokine induction in response to infection from the groups of P, NP and C pigs. Statistical analyses indicated that innate cytokines were increased earliest. Serum interleukin-1beta (IL-1b) levels were elevated in all pigs prior to infection and these levels continued to decrease for the C pigs. The infected pigs exhibited continuing high IL-1b to 14 dpi. When IL-8 was examined at 7 dpi and 14 dpi NP pigs had higher concentrations of IL-8 than P pigs. This increased IL-8 was followed in time by an increased level of interferon-gamma (IFNg) at 28 dpi in NP pigs. P pigs only showed peak serum IFNg at 42 dpi. There appeared to be no changes in serum IL-10 associated with infection. In summary, serum cytokine protein levels indicate that NP pigs appeared to have earlier and higher serum innate cytokine, IL-8, followed by T helper 1, IFNg, levels than the P pigs. This immune cytokine trend correlated with NP pigs having lower serum and tissue viral loads; this might indicate that the NP immune response was more effective than that for P pigs and possibly enabled the NP pigs to prevent PRRSV infections to become persistent. These data will help predict protective anti-PRRSV responses and to identify novel regulatory pathways that would stimulate PRRSV immunity. Supported by USDA ARS and NRI PRRS CAP1 funds.