Department of Animal Breeding and Biotechnology, University of Hohenheim, Garbenstraße 17, D-70593 Stuttgart, Germany1
Federal Research Centre for Virus Diseases of Animals, D-72076 Tübingen, Germany2
Author for correspondence: Gerald Reiner. Present address: Professur für Schweinekrankheiten, Justus-Liebig-Universität Giessen, Frankfurter Strasse 112, D-35392 Giessen, Germany. Fax +49 641 201854. e-mail gerald.reiner{at}vetmed.uni-giessen.de
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Abstract |
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Introduction |
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Indications of genetic differences in serum-neutralization titres of pigs after vaccination with pseudorabies vaccine and individual differences in cell-mediated and humoral immunity and in susceptibility to PrV in pigs were observed by Rothschild et al. (1984) , Meeker et al. (1987a
, b
) and Hessing et al. (1994
, 1995
). However, no quantitative trait loci (QTL) have been identified to date for resistance against PrV. The objectives of this study were to map QTLs in a genome-wide scan for resistance/susceptibility to PrV in informative F2 pig families and to indicate candidate genes that are probably involved in resistance to PrV in swine.
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Methods |
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Eighty-five microsatellite markers were selected from the map produced by Rohrer et al. (1996) (http://sol.marc.usda.gov/) based on their position, ease of scoring and informativity. Markers were spaced evenly on the 18 porcine autosomes and on the pseudoautosomal region of the X chromosome (SSCX) (Fig. 2). The maximum interval based on the USDA map was 40 cM. Linkage was analysed with the software package CRIMAP (Green et al., 1990
) according to the guidelines of Keats et al. (1991)
. Sex-averaged maps were constructed.
QTL analysis was done according to an interval mapping strategy (Haley et al., 1994 ) with a monolocus regression analysis. The statistical model included effects of sex, age at challenge and family. Chromosome-specific empirical threshold values of the F statistic were estimated via permutation test (Churchill & Doerge, 1994
). The 5% genome-wide, 10% genome-wide and 5% chromosome-wide thresholds were estimated as 8·8, 7·9 and 5·6.
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Results |
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Discussion |
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Due to the limited number of F2 animals, QTL positions within chromosomes could not be mapped very precisely. Thus, the identification of candidate genes can only be assumed very roughly. Major QTLs on SSC9 and SSC6 are linked with the loci PRR1 [polio-related receptor 1, HveC (herpes virus entry protein C); Geraghty et al., 1998 ] and PRR2 (HveB; Eberle et al., 1995
). Both receptor proteins are involved in adsorption and penetration of PrV to the cell in rodent models. Initiation of infection by alphaherpesviruses requires a cascade of interactions between different virus and cellular membrane components (Karger & Mettenleiter, 1996
). Interaction of the receptors with virus glycoprotein gE seems to influence markedly the neurological spread of the infection (Kimman et al., 1992
; Kritas et al., 1994
; Husak et al., 2000
). To date, the effects of PRR1 and PRR2 on porcine PrV infection are unknown, and the linked QTLs presented in our study indicate the need for more specific investigation of these genes. Furthermore, the absence of QTLs in the region of the MHC must be mentioned, since Favoreel et al. (1999)
assumed an important role of this gene complex in resistance/susceptibility to PrV. However, a number of further components of the immune system can influence resistance/susceptibility to alphaherpesviruses (Sin et al., 1999
). Specific immunology against herpesviruses seems to be sustained by the IL-12/IFN-
pathway (Grob et al., 1999
; Zuckermann, 2000
). The IL-12 gene is located within an interleukin cluster on SSC2, close to the marker Swr349, a region associated with a QTL on temperature course. Further QTLs are linked to the IFN-
locus (SSC5) and the locus for an interferon receptor (SSC13). Thus, more specific research should include the candidate genes (PRR1, PRR2, IFN-
, IL-12, interferon receptor) and analyse their role in porcine PrV. Since our study elucidates genetic differences in resistance/susceptibility to PrV between Meishan and Large White pigs, these genetically diverse breeds are informative in elucidation of the role of host defence against PrV in swine.
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Acknowledgments |
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References |
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Received 9 August 2001;
accepted 18 September 2001.
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