Skip to main content
ARS Home » Research » Publications at this Location » Publication #203604
Title: Differential immunity in pigs with high and low responses to porcine reproductive and respiratory syndrome virus (PRRSV) infection

Author
item PETRY, D - UNIV. OF NE
item Lunney, Joan
item Boyd, Patricia
item Kuhar, Daniel
item BLANKENSHIP, E - UNIV. OF NE
item JOHNSON, R - UNIV. OF NE

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/15/2007
Publication Date: 4/27/2007
Citation: Petry, D.B., Lunney, J.K., Boyd, P., Kuhar, D.J., Blankenship, E., Johnson, R.K. 2007. Differential immunity in pigs with high and low responses to porcine reproductive and respiratory syndrome virus (PRRSV) infection. Journal of Animal Science. 85:2075-2092. http://jas.fass.org/cgi/content/full/85/9/2075.

Interpretive Summary: Genetic resistance to infectious diseases has been shown in pigs but limited studies have shown genetic resistance to viral infections. In this study 400 pigs were tested; 100 Hampshire by Duroc crossbred pigs (HD) and 100 NE Index line pigs (I) were each infected and compared to non-infected controls. Porcine reproductive and respiratory syndrome virus (PRRSV) is the most economically important viral infections of pigs worldwide. Thus finding genes that determine genetic resistance is an important research goals. All 200 infected pigs, and their 200 littermate controls, were evaluated for resistance/susceptibility by comparing serum and tissue viremia (V), weight change (WT'), and clinical signs [rectal temperatures at 0, 4, 7, and 14 days post-infection (dpi)]. For the immune studies reported in this manuscript lung, bronchial lymph node (BLN), and blood tissue were collected at necropsy (14 dpi). Genetic analyses (principal component analyses) were used to rank pigs for resistance/susceptibility. Those pigs exhibiting different responses to PRRSV were separated into two groups, 1) the low (L) responders had low PRRSV burden, high WT', low V, and few lung lesions; and 2) the high (H) responders had high PRRS burden, low WT', high V, and many lesions. For these studies RNA was extracted from lung and BLN tissue of the seven highest H pigs and seven lowest L pigs per line, and from each of their littermate controls. Comparisons were performed on expression of 11 specific innate and T helper 1 immune markers. These were evaluated in a specific genetic design. Significant up-regulation in lung and/or lymph of infected pigs, relative to non-infected control pigs, occurred for all but one gene. Expression differences were greater in HD than I pigs. It was clear that there was significant down-regulation for certain immune genes in L pigs, relative to littermate controls, in lung and BLN, particularly in Line I. Serum levels of the immune cytokines affirmed the gene expression differences. Overall, high pre-infection serum levels of interleukin-8 (IL8) were significantly associated with the PRRSV-resistant, L pigs. Following infection, low expression of interferon-gamma (IFNG) in cDNA and in serum was also correlated with PRRSV resistance. Thus future tests will determine whether IL8 and IFNG levels can be used as biomarkers for genetic resistance to PRRSV infection. These genetic associations are important for future fine mapping. They are among the first candidate genes for PRRSV resistance and need to be tested to determine whether causative alleles can be revealed.

Technical Abstract: One hundred Hampshire by Duroc crossbred pigs (HD) and 100 NE Index line pigs (I) were infected with porcine reproductive and respiratory syndrome virus (PRRSV) and evaluated for resistance/susceptibility. Controls (100/line) were uninfected littermates to infected pigs. Viremia (V), weight change (WT'), and rectal temperature at 0, 4, 7, and 14 days post-infection (dpi) were recorded. Lung, bronchial lymph node (BLN), and blood tissue were collected at necropsy (14 dpi). The first principal component from principal component analyses of all variables was used to rank pigs for phenotypic response to PRRSV. Low (L) responders (low PRRS burden) had high WT', low V, and few lung lesions; high (H) responders (high PRRS burden) had low WT', high V, and many lesions. RNA was extracted from lung and BLN tissue of the seven highest and seven lowest responders per line, and from each of their littermates. Expression of 11 specific innate and T helper 1 immune markers was evaluated with cDNA in a 2*2*2 factorial design. Significant up-regulation in lung and/or lymph of infected pigs relative to controls occurred for all but one gene. Expression differences were greater in HD than I pigs. Significant down-regulation for certain immune genes in L pigs, relative to littermate controls, was detected in lung and BLN, particularly in Line I. Serum levels of the immune cytokines affirmed the gene expression differences. High pre-infection serum levels of interleukin-8 were significantly associated with PRRSV-resistant, L pigs. Following infection, low expression of interferon-gamma in cDNA and in serum was also correlated with PRRSV resistance. Important genetic associations for fine mapping candidate genes for PRRSV resistance and determining causative alleles were revealed.