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Journal of Virology, September 2005, p. 11517-11522, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11517-11522.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Identification of Quantitative Trait Loci for Susceptibility to Mouse Adenovirus Type 1{dagger}

Amanda R. Welton,1 Elissa J. Chesler,2 Carla Sturkie,3,{ddagger} Anne U. Jackson,4 Gwen N. Hirsch,3,§ and Katherine R. Spindler1*

Department of Microbiology and Immunology,1 Department of Biostatistics, University of Michigan, Ann Arbor, Michigan 48109,4 Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163,2 Department of Genetics, University of Georgia, Athens, Georgia 306063

Received 6 May 2005/ Accepted 10 June 2005

Adult SJL/J mice are highly susceptible to mouse adenovirus type 1 (MAV-1) infections, whereas other inbred strains, including BALB/cJ, are resistant (K. R. Spindler, L. Fang, M. L. Moore, C. C. Brown, G. N. Hirsch, and A. K. Kajon, J. Virol. 75:12039-12046, 2001). Using congenic mouse strains, we showed that the H-2s haplotype of SJL/J mice is not associated with susceptibility to MAV-1. Susceptibility of MAV-1-infected (BALB/cJ x SJL/J)F1 mice was intermediate between that of SJL/J mice and that of BALB/cJ mice, indicating that susceptibility is a genetically controlled quantitative trait. We mapped genetic loci involved in mouse susceptibility to MAV-1 by analysis of 192 backcross progeny in a genome scan with 65 simple sequence length polymorphic markers. A major quantitative trait locus (QTL) was detected on chromosome 15 (Chr 15) with a highly significant logarithm of odds score of 21. The locus on Chr 15 alone accounts for 40% of the total trait variance between susceptible and resistant strains. QTL modeling of the data indicated that there are a number of other QTLs with small effects that together with the major QTL on Chr 15 account for 54% of the trait variance. Identification of the major QTL is the first step in characterizing host genes involved in susceptibility to MAV-1.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Michigan Medical School, 1150 W. Medical Center Dr., 6723 Medical Science Bldg. II, Ann Arbor, MI 48109-0620. Phone: (734) 615-2727. Fax: (734) 764-3562. E-mail: krspin{at}umich.edu.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} Present address: Department of Horticulture, University of Georgia, Athens, Georgia.

§ Present address: Department of Animal and Dairy Science, University of Georgia, Athens, Georgia.


Journal of Virology, September 2005, p. 11517-11522, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11517-11522.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.







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