Department of Animal Science


Date of this Version



Published in J. Anim. Sci. 86:3279–3289 (2008). Copyright © 2008 American Society of Animal Science. Used by permission.


One hundred Hampshire × Duroc crossbred pigs and 100 Nebraska Index line pigs were infected with porcine reproductive and respiratory syndrome virus (PRRSV) and evaluated for resistance and susceptibility. Controls (100/line) were uninfected littermates to infected pigs. Viremia (V), BW change (WTΔ), and rectal temperature at 0, 4, 7, and 14 d postinfection were recorded. Lung, bronchial lymph node (BLN), and blood tissue were collected at necropsy (14 d postinfection). Infected pigs were classified as low or high responders to PRRSV based on the first principal component from principal component analyses of all variables. Low responders to PRRSV (low PRRSV burden) and their uninfected littermates were assigned to the low (L) class. High responders to PRRSV (high PRRSV burden) and their uninfected littermates were assigned to the high (H) class. Infected pigs in the L class had large WTΔ, low V, and few lung lesions; H-class pigs had small WTΔ, high V, and many lung lesions. Ribonucleic acid was extracted from lung and BLN tissue of the 7 highest and 7 lowest responders per line and from each of their control littermates. A control reference design was used, and cDNA from each reference sample tissue was prepared from pooled RNA extracted from 2 control pigs from each line whose infected littermates had a principal component value of 0. Design variables in data analyses were line (Index vs. Hampshire × Duroc), class (H vs. L), treatment (infected vs. uninfected controls), and slide/pig as error. Oligo differential expression was based on P < 0.01 occurring in both lung and BLN. Line and treatment effects were significant for 38 and 541 oligos, respectively, in both lung and BLN. Line × class interaction existed for expression of thymosin β-4, DEAD box RNA helicase 3, acetylcholinesterase, and Homo sapiens X (inactive)-specific transcript in both tissues. Treatment × class existed for expression of CCAAT/enhancer-binding δ protein, nuclear factor of κ light polypeptide gene enhancer in B cells inhibitor α, thioredoxin-interacting protein, major facilitator superfamily domain containing 1, and unknown sequences SS00012040 and SS00012343. Line × treatment and line × treatment × class interactions were not significant. Possible important genetic associations for fine-mapping candidate genes related to response to PRRSV and determining causative alleles were revealed.