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Journal of Virology, December 2001, p. 12039-12046, Vol. 75, No. 24
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.24.12039-12046.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

SJL/J Mice Are Highly Susceptible to Infection by Mouse Adenovirus Type 1

Katherine R. Spindler,1,* Lei Fang,1 Martin L. Moore,1 Gwen N. Hirsch,1 Corrie C. Brown,2 and Adriana Kajon1,dagger

Department of Genetics, Franklin College of Arts and Sciences,1 and Department of Veterinary Pathology, College of Veterinary Medicine,2 University of Georgia, Athens, Georgia 30602

Received 29 June 2001/Accepted 10 September 2001

Mouse adenovirus type 1 (MAV-1) targets endothelial and monocyte/macrophage cells throughout the mouse. Depending on the strain of mouse and dose or strain of virus, infected mice may survive, become persistently infected, or die. We surveyed inbred mouse strains and found that for the majority tested the 50% lethal doses (LD50s) were >104.4 PFU. However, SJL/J mice were highly susceptible to MAV-1, with a mean LD50 of 10-0.32 PFU. Infected C3H/HeJ (resistant) and SJL/J (susceptible) mice showed only modest differences in histopathology. Susceptible mice had significantly higher viral loads in the brain and spleen at 8 days postinfection than resistant mice. Infection of primary macrophages or mouse embryo fibroblasts from SJL/J and C3H/HeJ mice gave equivalent yields of virus, suggesting that a receptor difference between strains is not responsible for the susceptibility difference. When C3H/HeJ mice were subjected to sublethal doses of gamma irradiation, they became susceptible to MAV-1, with an LD50 like that of SJL/J mice. Antiviral immunoglobulin G (IgG) levels were measured in susceptible and resistant mice infected by an early region 1A null mutant virus that is less virulent that wild-type virus. The antiviral IgG levels were high and similar in the two strains of mice. Taken together, these results suggest that immune response differences may in part account for differences in susceptibility to MAV-1 infection.

* Corresponding author. Mailing address: Department of Genetics, University of Georgia, Life Sciences Bldg., Athens, GA 30602-7223. Phone: (706) 542-8395. Fax: (706) 542-3910. E-mail: spindler{at}arches.uga.edu.

dagger Present address: Lovelace Respiratory Research Institute, Albuquerque, NM 87185.

Journal of Virology, December 2001, p. 12039-12046, Vol. 75, No. 24
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.24.12039-12046.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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