|ROWLAND, R R|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/29/2006
Publication Date: 6/25/2006
Citation: Lunney, J.K., Petry, D., Johason, R., Zuckermann, F., Zimmerman, J., Rowland, R.R. 2006. Understanding swine immunity to porcine reproductive and respiratory syndrome virus (prrsv) infection - informing future vaccine design [abstract]. International Veterinary Vaccines and Diagnostics Conference (IVVDC), Oslo, Norway. p.107.
Technical Abstract: Porcine Reproductive and Respiratory Syndrome (PRRS) is the most economically significant disease facing the swine industry today, costing U.S. pork producers at least $560 million annually. This abstract describes some of the approaches we’ve tested to evaluate immunity to PRRSV. We plan to use this research to predict protective anti-PRRSV immune responses, and later to improve PRRSV vaccine design. Current modified live vaccines (MLV) are only partially effective against virus infection because they elicit a weak immune response that is not fully protective. Therefore we tested the cytokine, interferon-alpha (IFNA), as an MLV adjuvant. Despite stimulating higher levels of IFN-gamma (IFNG) gene expression in peripheral blood mononuclear cells this adjuvanated MLV provided no better protection against virus infection (Royaee et al, 2004). Further exploration will be required to decipher the immunobiology of PRRSV and to increase the immunogenicity of conventional MLV vaccines using IFNA and other adjuvants to insure protection even from heterologous PRRSV isolates. In another experiment host genomics was used to compare different lines of pigs and to identify factors correlated with PRRSV resistance/susceptibility. Previous work (Petry et al., 2005) had shown that there were statistically significant changes in viremia, weight change, and rectal temperature at 0, 4, 7, and 14 days post-PRRSV infection (dpi) between pig lines. Data presented here will address our evaluation of immune gene expression in RNA from frozen lung and bronchial lymph node (BLN) tissue of the 7 highest and lowest responders per line, and from each of their control littermates, as well as serum cytokine protein levels. Analyses of this data indicated that levels of interleukin-8 (IL8) may be predictive of resistance. Additionally, low (not high) levels of serum IFNG after infection may be associated with a PRRSV resistant phenotype. These data are critical for genetic association studies to fine map candidate genes and determine causative alleles of PRRSV resistance/susceptibility. Further genetic studies are required to affirm these associations. Most recently we have begun assessing immune gene and protein expression in lung, BLN, tonsil and blood samples collected from pigs after PRRSV infection. With this data we plan to highlight differences between samples collected from pigs persistently infected with PRRSV at 150 dpi versus pigs that cleared their infection in the first 28 dpi. We expect that this data will reveal differential gene expression associated with PRRSV clearance. Overall, by combining these diverse immune approaches, we expect to develop new hypotheses about protective anti-PRRSV responses and to identify novel regulatory pathways that would stimulate PRRSV immunity. Supported in part by USDA ARS CRIS funds as well as USDA PRRS CAP initiative grant funds.