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ARS Home » Research » Publications at this Location » Publication #187941
Title: CAN PIGS BE GENETICALLY SELECTED FOR PRRSV RESISTANCE? IS RESISTANCE DUE TO IMMUNE GENES?

Author
item JOHNSON, RODGER - U NEBRASKA LINCOLN NE
item PETRY, DEREK - MONSANTO, ST. LOUIS MO
item Lunney, Joan

Submitted to: National Hog Farmer
Publication Type: Popular Publication
Publication Acceptance Date: 12/3/2005
Publication Date: 12/15/2005
Citation: Johnson, R., Petry, D., Lunney, J.K. 2005. Can pigs be genetically selected for prrsv resistance? is resistance due to immune genes?. National Hog Farmer. p19-22

Interpretive Summary: The most important disease affecting US pork production is porcine reproductive and respiratory syndrome (PRRS). National Pork Board has estimated losses due to PRRS cost producers $600M each year. Identification of genetically resistant breeding stock would be a significant advance for PRRS control. Work from Dr. Rodger Johnson's group at the University of Nebraska at Lincoln has proven that genetic variation in resistance to PRRS virus (PRRSV) infection exists. Infected low responder Nebraska Index pigs had the lowest viremia at day 14 (Table 1), low clinical signs in their lungs, and greater weight gain, than high responder I pigs and low and high responder Hampshire-Duroc cross (HD) pigs. If underlying genetic variation determines whether pigs will effectively limit virus replication after infection with PRRSV, the next question is - Which genes are involved? Likely targets for infection control are immune genes. Table 2 lists some of these genes: innate (non-specific) immune factors; interferon-gamma (IFNG) related genes, termed T helper 1 (Th1) genes; or regulatory T cell genes, such as interleukin-10 (IL10). To evaluate the role of these immune genes, a collaboration funded by the USDA PRRS CAP grant was established between Nebraska scientists and Dr. Joan Lunney's lab at BARC-ARS-USDA. Overall, HD pigs had greater magnitude of difference in expression of immune genes in their lung and lymph node tissue at 14 days post infection than I pigs. Significant under-expression for certain immune genes of L pigs, relative to controls, was detected in lung and lymph node tissues, particularly in I pigs. Serum levels of the immune cytokines affirmed the lung gene expression ifferences. Following infection, low expression of interferon-gamma (IFNG) in cDNA and in serum was correlated with resistance. High pre-infection serum levels of the innate cytokine, interleukin-8 (IL8), were significantly associated with PRRSV resistant, L pigs. This may implicate that activation of the innate immune system helps to prevent viral expansion. These data outline targets for future studies of genetic association, to determine if specific immune gene alleles are associated with PRRSV resistance. Such studies will help determine the actual causative alleles, thus enabling producers to decrease breeding of PRRSV susceptible pigs, and select for PRRSV resistant stock.

Technical Abstract: The most important disease affecting US pork production is porcine reproductive and respiratory syndrome (PRRS). National Pork Board has estimated losses due to PRRS cost producers $600M each year. Identification of genetically resistant breeding stock would be a significant advance for PRRS control. Work from Dr. Rodger Johnson's group at the University of Nebraska at Lincoln has proven that genetic variation in resistance to PRRS virus (PRRSV) infection exists. Infected low responder Nebraska Index pigs had the lowest viremia at day 14 (Table 1), low clinical signs in their lungs, and greater weight gain, than high responder I pigs and low and high responder Hampshire-Duroc cross (HD) pigs. If underlying genetic variation determines whether pigs will effectively limit virus replication after infection with PRRSV, the next question is - Which genes are involved? Likely targets for infection control are immune genes. Table 2 lists some of these genes: innate (non-specific) immune factors; interferon-gamma (IFNG) related genes, termed T helper 1 (Th1) genes; or regulatory T cell genes, such as interleukin-10 (IL10). To evaluate the role of these immune genes, a collaboration funded by the USDA PRRS CAP grant was established between Nebraska scientists and Dr. Joan Lunney's lab at BARC-ARS-USDA. Overall, HD pigs had greater magnitude of difference in expression of immune genes in their lung and lymph node tissue at 14 days post infection than I pigs. Significant under-expression for certain immune genes of L pigs, relative to controls, was detected in lung and lymph node tissues, particularly in I pigs. Serum levels of the immune cytokines affirmed the lung gene expression ifferences. Following infection, low expression of interferon-gamma (IFNG) in cDNA and in serum was correlated with resistance. High pre-infection serum levels of the innate cytokine, interleukin-8 (IL8), were significantly associated with PRRSV resistant, L pigs. This may implicate that activation of the innate immune system helps to prevent viral expansion. These data outline targets for future studies of genetic association, to determine if specific immune gene alleles are associated with PRRSV resistance. Such studies will help determine the actual causative alleles, thus enabling producers to decrease breeding of PRRSV susceptible pigs, and select for PRRSV resistant stock.