One hundred Hampshire X 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 (WTĢ), 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 WTĢ, low V, and few lung lesions; H-class pigs
had small WTĢ, 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 X 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 ƒÀ-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 ƒÂ protein, nuclear factor of ƒÈ light polypeptide gene enhancer in B cells inhibitor ƒ¿, 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.