Porcine reproductive and respiratory syndrome virus (PRRSV) has caused devastating losses to swine herds on a worldwide basis. It has been estimated that PRRSV costs the United States pork industry approximately $560 million per year. Reliable methods to prevent, control and/or eliminate PRRSV have not been achieved. It has been shown that various biological responses are different between breeds and lines of pigs when infected with PRRSV. If mechanisms of genetic control of susceptibility to PRRSV can be identified, then selection of pigs that have increased resistance to PRRSV may be possible. The primary objective of this project was to determine differences in growth rate and expression of specific immune function genes and levels of cytokines between pigs that are more resistant and more susceptible to PRRSV infection. Interleukin-8 (IL8) is a protein cytokine produced by the IL8 immune function gene. Previous data suggested that pre-inoculation levels of the IL8 kinase may predict a pig’s response to PRRSV infection. At 34 ± 5 days of age (8.2 ± 1.8 kg body weight), 220 weaned pigs free of PRRSV were transported from their farm of origin to the wean-to-finish barn at the Haskell Agricultural Laboratory (Concord, NE). The pigs were randomly allotted to one of 16 pens (2.4 m x 4.3 m) that held 12 to 14 pigs per pen. After a 19-day adjustment period, all pigs were weighed and blood samples were collected. The pigs were inoculated with PRRSV FL12 (104.8 TCID50/2 mL) by injection in the neck muscle 2 mL of virus preparation (one-half of dose on each side of neck). Blood was drawn at 4, 7, and 14 days post-inoculation to monitor response to virus. Body weight was recorded at 4, 7, 14, and 35 days post-inoculation and every two weeks after day 35. The correlations among weights at 0, 4, 7, 14 and 35 days after inoculation with PRRSV, viremia at 4, 7 and 14 days after inoculation, and pre-inoculation levels of IL8 were relatively low. Weight gain from 0 to 4, 4 to 7, 7 to 14, and 14 to 35 days after inoculation, viremia at 4, 7, and 14 days after inoculation, and pre-inoculation levels of IL8 were negatively correlated. Correlations of IL8 with all variables were low; thus, these data are not consistent with previous results. The data of this study are consistent with previous data in that weight gains and viremia are not highly correlated, but the two variables together are a good index of response to PRRSV. The distribution of pigs with various levels of viremia at 4, 7, and 14 days post-inoculation indicate that some pigs have low replication rates, while others have very high replication rates. This variation suggests underlying variation in the pig’s immune response to virus. The hypothesis is that some of the variation is due to the pig’s genetic makeup and that selection for genes that inhibit viral replication may reduce the incidence and severity of disease.
Contact Information:
Dr. Donald G. Levis
University of Nebraska – Lincoln
Northeast Research & Extension Center
601 East Benjamin Avenue, Suite 104
Norfolk, NE 68701-0812
Phone: (402) 370 4016""
E-mail: [email protected]