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Multigenic control of resistance to Sendai virus infection in mice

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/42554

Title: Multigenic control of resistance to Sendai virus infection in mice
Authors: Simon, A. Y. Browse this author
Moritoh, K. Browse this author
Torigoe, D. Browse this author
Asano, A. Browse this author
Sasaki, N. Browse this author →KAKEN DB
Agui, T. Browse this author →KAKEN DB
Keywords: Sendai virus
Resistance
DBA/2
C57BL/6
Quantitative trait locus
Issue Date: Dec-2009
Publisher: Elsevier B.V.
Journal Title: Infection, Genetics and Evolution
Volume: 9
Issue: 6
Start Page: 1253
End Page: 1259
Publisher DOI: 10.1016/j.meegid.2009.08.011
PMID: 19733691
Abstract: Experimental infection of mice with Sendai virus (SeV) is frequently used as a model of viral pathogenesis of human respiratory disease. To understand the differences in host response to SeV among mice strains, we carried out genetic mapping studies in DBA/2 (D2) (susceptible) and C57BL/6 (B6) (resistant) mice. F1, F2, and N2 backcrossed mice were generated and examined for their disease resistance and susceptibility. For the determination of virulence, percentage body weight loss and survival time were used as phenotypes. We, then, carried out a genome wide scan on 108 backcrossed mice for linkage with percentage body weight loss as phenotype. A major quantitative trait locus (QTL) showing significant linkage was mapped to the distal portion of Chr4 (SeV1). In addition, two other QTLs showing suggestive statistical linkage were also detected on Chr 8 and 14. We, further, performed genome scan for interactions with least squares analysis of variance of all pairs of informative makers in backcrossed progenies. We identified a highly significant epistatic interaction between D3Mit182 and D14Mit10, then denoted as SeV2 and SeV3, respectively, and the latter was the same locus showing a suggestive level on Chr 14 in QTL analysis. Considered genotypes of these three loci, we could account for more than 90% of genetic effect on the differential response to SeV infection between B6 and D2 mice. These findings revealed a novel gene interactions controlling SeV resistance in mice and will enable the identification of resistance genes encoded within these loci.
Type: article (author version)
URI: http://hdl.handle.net/2115/42554
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 安居院 高志

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