Limits...
Probing genetic control of swine responses to PRRSV infection: current progress of the PRRS host genetics consortium.

Lunney JK, Steibel JP, Reecy JM, Fritz E, Rothschild MF, Kerrigan M, Trible B, Rowland RR - BMC Proc (2011)

Bottom Line: Blood samples were collected at 0, 4, 7, 10, 14, 21, 28, 35 and 42 dpi for serum and whole blood RNA gene expression analyses; weekly weights were recorded for growth traits.All data have been entered into the PHGC relational database.The availability of PHGC samples provides a unique opportunity to continue to develop deeper phenotypes on every PRRSV infected pig.

View Article: PubMed Central - HTML - PubMed

Affiliation: Animal Parasitic Diseases Laboratory, BARC, ARS, USDA, Beltsville, MD 20705, USA. Joan.Lunney@ars.usda.gov.

ABSTRACT

Background: Understanding the role of host genetics in resistance to porcine reproductive and respiratory syndrome virus (PRRSV) infection, and the effects of PRRS on pig health and related growth, are goals of the PRRS Host Genetics Consortium (PHGC).

Methods: The project uses a nursery pig model to assess pig resistance/susceptibility to primary PRRSV infection. To date, 6 groups of 200 crossbred pigs from high health farms were donated by commercial sources. After acclimation, the pigs were infected with PRRSV in a biosecure facility and followed for 42 days post infection (dpi). Blood samples were collected at 0, 4, 7, 10, 14, 21, 28, 35 and 42 dpi for serum and whole blood RNA gene expression analyses; weekly weights were recorded for growth traits. All data have been entered into the PHGC relational database. Genomic DNAs from all PHGC1-6 pigs were prepared and genotyped with the Porcine SNP60 SNPchip.

Results: Results have affirmed that all challenged pigs become PRRSV infected with peak viremia being observed between 4-21 dpi. Multivariate statistical analyses of viral load and weight data have identified PHGC pigs in different virus/weight categories. Sera are now being compared for factors involved in recovery from infection, including speed of response and levels of immune cytokines. Genome-wide association studies (GWAS) are underway to identify genes and chromosomal locations that identify PRRS resistant/susceptible pigs and pigs able to maintain growth while infected with PRRSV.

Conclusions: Overall, the PHGC project will enable researchers to discover and verify important genotypes and phenotypes that predict resistance/susceptibility to PRRSV infection. The availability of PHGC samples provides a unique opportunity to continue to develop deeper phenotypes on every PRRSV infected pig.

No MeSH data available.


Related in: MedlinePlus

Different anti-viral reponses associated with PRRS resistance/susceptibility. PHGC pigs exhibited different anti-PRRSV infection responses as reflected in the serum viral levels after challenge. Circles, solid squares/long dashed lines – resistant pigs (1341, 1379, 1524, 1533); Triangles/solid lines= susceptible pigs (1451, 1391); Squares/short dashed line = pigs with virus reactivation (1341, 1474).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3108226&req=5

Figure 1: Different anti-viral reponses associated with PRRS resistance/susceptibility. PHGC pigs exhibited different anti-PRRSV infection responses as reflected in the serum viral levels after challenge. Circles, solid squares/long dashed lines – resistant pigs (1341, 1379, 1524, 1533); Triangles/solid lines= susceptible pigs (1451, 1391); Squares/short dashed line = pigs with virus reactivation (1341, 1474).

Mentions: Results have affirmed that all challenged pigs become PRRSV infected with peak viremia from 4-21 dpi (Rowland et al., manuscript in preparation). The PHGC results revealed the appearance of stratified subpopulations of PRRS resistant/ susceptible pigs, which exhibited wide variations in virus load and growth performance; examples of such anti-viral responses are shown in Figure 1. The greatest impact of PRRSV infection was on weight, with only about 30% of infected pigs in the same weight class as the reference control pigs (pigs from the same litters kept uninfected and weighed for the same 42 days). Plotting virus load versus average daily weight gain (ADWG) showed little correlation between growth and virus load. Multivariate statistical analyses of viral load and weight data have categorized PHGC pigs into 4 extreme categories including the most desirable, PRRS resistant low virus/high weight gain (Lv/Hg) pigs, the worst, PRRS susceptible high virus/ low weight gain (Hv/Lg) pigs, the PRRS tolerant, high virus/high weight gain (Hv/Hg) pigs, and the less thrifty, low virus/low weight gain (Lv/Lg) pigs. This statistical categorization of pigs from each PHGC trial provides a critical basis for selecting pigs and samples for detailed analyses of processes that control transcriptional and proteomic responses to PRRSV infection, as outlined in Table 1.


Probing genetic control of swine responses to PRRSV infection: current progress of the PRRS host genetics consortium.

Lunney JK, Steibel JP, Reecy JM, Fritz E, Rothschild MF, Kerrigan M, Trible B, Rowland RR - BMC Proc (2011)

Different anti-viral reponses associated with PRRS resistance/susceptibility. PHGC pigs exhibited different anti-PRRSV infection responses as reflected in the serum viral levels after challenge. Circles, solid squares/long dashed lines – resistant pigs (1341, 1379, 1524, 1533); Triangles/solid lines= susceptible pigs (1451, 1391); Squares/short dashed line = pigs with virus reactivation (1341, 1474).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3108226&req=5

Figure 1: Different anti-viral reponses associated with PRRS resistance/susceptibility. PHGC pigs exhibited different anti-PRRSV infection responses as reflected in the serum viral levels after challenge. Circles, solid squares/long dashed lines – resistant pigs (1341, 1379, 1524, 1533); Triangles/solid lines= susceptible pigs (1451, 1391); Squares/short dashed line = pigs with virus reactivation (1341, 1474).
Mentions: Results have affirmed that all challenged pigs become PRRSV infected with peak viremia from 4-21 dpi (Rowland et al., manuscript in preparation). The PHGC results revealed the appearance of stratified subpopulations of PRRS resistant/ susceptible pigs, which exhibited wide variations in virus load and growth performance; examples of such anti-viral responses are shown in Figure 1. The greatest impact of PRRSV infection was on weight, with only about 30% of infected pigs in the same weight class as the reference control pigs (pigs from the same litters kept uninfected and weighed for the same 42 days). Plotting virus load versus average daily weight gain (ADWG) showed little correlation between growth and virus load. Multivariate statistical analyses of viral load and weight data have categorized PHGC pigs into 4 extreme categories including the most desirable, PRRS resistant low virus/high weight gain (Lv/Hg) pigs, the worst, PRRS susceptible high virus/ low weight gain (Hv/Lg) pigs, the PRRS tolerant, high virus/high weight gain (Hv/Hg) pigs, and the less thrifty, low virus/low weight gain (Lv/Lg) pigs. This statistical categorization of pigs from each PHGC trial provides a critical basis for selecting pigs and samples for detailed analyses of processes that control transcriptional and proteomic responses to PRRSV infection, as outlined in Table 1.

Bottom Line: Blood samples were collected at 0, 4, 7, 10, 14, 21, 28, 35 and 42 dpi for serum and whole blood RNA gene expression analyses; weekly weights were recorded for growth traits.All data have been entered into the PHGC relational database.The availability of PHGC samples provides a unique opportunity to continue to develop deeper phenotypes on every PRRSV infected pig.

View Article: PubMed Central - HTML - PubMed

Affiliation: Animal Parasitic Diseases Laboratory, BARC, ARS, USDA, Beltsville, MD 20705, USA. Joan.Lunney@ars.usda.gov.

ABSTRACT

Background: Understanding the role of host genetics in resistance to porcine reproductive and respiratory syndrome virus (PRRSV) infection, and the effects of PRRS on pig health and related growth, are goals of the PRRS Host Genetics Consortium (PHGC).

Methods: The project uses a nursery pig model to assess pig resistance/susceptibility to primary PRRSV infection. To date, 6 groups of 200 crossbred pigs from high health farms were donated by commercial sources. After acclimation, the pigs were infected with PRRSV in a biosecure facility and followed for 42 days post infection (dpi). Blood samples were collected at 0, 4, 7, 10, 14, 21, 28, 35 and 42 dpi for serum and whole blood RNA gene expression analyses; weekly weights were recorded for growth traits. All data have been entered into the PHGC relational database. Genomic DNAs from all PHGC1-6 pigs were prepared and genotyped with the Porcine SNP60 SNPchip.

Results: Results have affirmed that all challenged pigs become PRRSV infected with peak viremia being observed between 4-21 dpi. Multivariate statistical analyses of viral load and weight data have identified PHGC pigs in different virus/weight categories. Sera are now being compared for factors involved in recovery from infection, including speed of response and levels of immune cytokines. Genome-wide association studies (GWAS) are underway to identify genes and chromosomal locations that identify PRRS resistant/susceptible pigs and pigs able to maintain growth while infected with PRRSV.

Conclusions: Overall, the PHGC project will enable researchers to discover and verify important genotypes and phenotypes that predict resistance/susceptibility to PRRSV infection. The availability of PHGC samples provides a unique opportunity to continue to develop deeper phenotypes on every PRRSV infected pig.

No MeSH data available.


Related in: MedlinePlus