PMID- 23403935
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130214
LR  - 20230502
IS  - 1664-8021 (Electronic)
IS  - 1664-8021 (Linking)
VI  - 3
DP  - 2012
TI  - Control of porcine reproductive and respiratory syndrome (PRRS) through genetic 
      improvements in disease resistance and tolerance.
PG  - 260
LID - 10.3389/fgene.2012.00260 [doi]
LID - 260
AB  - Infections caused by porcine reproductive and respiratory syndrome virus (PRRSV) 
      have a severe economic impact on pig production in North America, Europe, and 
      Asia. The emergence and eventual predominance of PRRS in the 1990s are the likely 
      result of changes in the pork industry initiated in the late 1970s, which allowed 
      the virus to occupy a unique niche within a modern commercial production system. 
      PRRSV infection is responsible for severe clinical disease, but can maintain a 
      life-long subclinical infection, as well as participate in several polymicrobial 
      syndromes. Current vaccines lessen clinical signs, but are of limited use for 
      disease control and elimination. The relatively poor protective immunity 
      following vaccination is a function of the virus's capacity to generate a large 
      degree of genetic diversity, combined with several strategies to evade innate and 
      adaptive immune responses. In 2007, the PRRS Host Genetics consortium (PHGC) was 
      established to explore the role of host genetics as an avenue for PRRS control. 
      The PHGC model for PRRS incorporates the experimental infection of large numbers 
      of growing pigs and has created the opportunity to study experimental PRRSV 
      infection at the population level. The results show that pigs can be placed into 
      distinct phenotypic groups, including pigs that show resistance (i.e., low virus 
      load) or pigs that exhibit "tolerance" to infection. Tolerance was illustrated by 
      pigs that gain weight normally in the face of a relatively high virus load. 
      Genome-wide association analysis has identified a region on chromosome 4 (SSC4) 
      correlated with resistance; i.e., lower cumulative virus load within the first 42 
      days of infection. The genomic region is near a family of genes involved in 
      innate immunity. The region is also associated with higher weight gain in 
      challenged pigs, suggesting that pigs with the resistance alleles don't seem to 
      simultaneously experience reduction in growth, i.e., that resistance and 
      tolerance are not antagonistically related. These results create the opportunity 
      to develop breeding programs that will produce pigs with increased resistance to 
      PRRS and simultaneously high growth rate. The identification of genomic markers 
      involved in actual tolerance will likely prove more difficult, primarily because 
      tolerance is difficult to quantify and because tolerance mechanism are still 
      poorly understood. Another avenue of study includes the identification of genomic 
      markers related to improved response following vaccination.
FAU - Rowland, Raymond R R
AU  - Rowland RR
AD  - Department of Diagnostic Medicine and Pathobiology, College of Veterinary 
      Medicine, Kansas State University Manhattan, KS, USA.
FAU - Lunney, Joan
AU  - Lunney J
FAU - Dekkers, Jack
AU  - Dekkers J
LA  - eng
PT  - Journal Article
DEP - 20121214
PL  - Switzerland
TA  - Front Genet
JT  - Frontiers in genetics
JID - 101560621
PMC - PMC3565991
OTO - NOTNLM
OT  - PRRS resistance
OT  - genome-wide association study
OT  - porcine reproductive and respiratory syndrome
EDAT- 2013/02/14 06:00
MHDA- 2013/02/14 06:01
PMCR- 2012/12/14
CRDT- 2013/02/14 06:00
PHST- 2012/04/18 00:00 [received]
PHST- 2012/11/05 00:00 [accepted]
PHST- 2013/02/14 06:00 [entrez]
PHST- 2013/02/14 06:00 [pubmed]
PHST- 2013/02/14 06:01 [medline]
PHST- 2012/12/14 00:00 [pmc-release]
AID - 10.3389/fgene.2012.00260 [doi]
PST - epublish
SO  - Front Genet. 2012 Dec 14;3:260. doi: 10.3389/fgene.2012.00260. eCollection 2012.