This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Norose, K.
Right arrow Articles by Heber-Katz, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Norose, K.
Right arrow Articles by Heber-Katz, E.

 Previous Article  |  Next Article 

Journal of Virology, April 2002, p. 3502-3510, Vol. 76, No. 7
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.7.3502-3510.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mapping of Genes Involved in Murine Herpes Simplex Virus Keratitis: Identification of Genes and Their Modifiers

Kazumi Norose,1 Akihiko Yano,1 Xiang-Ming Zhang,2 Elizabeth Blankenhorn,3 and Ellen Heber-Katz2*

Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan,1 The Wistar Institute,2 MCP Hahnemann University, Philadelphia, Pennsylvania3

Received 9 July 2001/ Accepted 5 December 2001

Herpes simplex keratitis (HSK) is an inflammatory response to viral infection and self antigens in the cornea and is a major cause of blindness. Using two strains of mice which are susceptible (129/SVEV) and resistant (C57BL/6) to herpes simplex virus (HSV) strain KOS, (129/SVEV x C57BL/6)F2 mice were generated and examined for their disease susceptibility in terms of clinical symptoms, ocular disease, and antibody production following corneal scarification with HSV (KOS). A genome-wide screen was carried out using microsatellite markers to determine the genetic loci involved in this response. Loci on chromosomes 4, 5, 12, 13, and 14 were shown to be involved in general susceptibility to clinical disease, whereas loci on chromosomes 10 and 17 were shown to be unique to ocular disease.


* Corresponding author. Mailing address: The Wistar Institute, 3601 Spruce St., Philadelphia, PA 19104. Phone: (215) 898-3710. Fax: (215) 898-3868. E-mail: heberkatz{at}wistar.upenn.edu.


Journal of Virology, April 2002, p. 3502-3510, Vol. 76, No. 7
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.7.3502-3510.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Halford, W. P., Balliet, J. W., Gebhardt, B. M. (2004). Re-Evaluating Natural Resistance to Herpes Simplex Virus Type 1. J. Virol. 78: 10086-10095 [Abstract] [Full Text]  
  • Luker, G. D., Prior, J. L., Song, J., Pica, C. M., Leib, D. A. (2003). Bioluminescence Imaging Reveals Systemic Dissemination of Herpes Simplex Virus Type 1 in the Absence of Interferon Receptors. J. Virol. 77: 11082-11093 [Abstract] [Full Text]