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Journal of Virology, April 2000, p. 3517-3524, Vol. 74, No. 8
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Pathogenesis of Herpes Simplex Virus-Induced Ocular Immunoinflammatory Lesions in B-Cell-Deficient Mice

Shilpa P. Deshpande, Mei Zheng, Massoud Daheshia, and Barry T. Rouse*

Department of Microbiology, University of Tennessee, Knoxville, Tennessee 37996-0845

Received 22 November 1999/Accepted 19 January 2000

The role of B cells and humoral immunity in herpes simplex virus (HSV) ocular infections was studied in immunoglobulin µ chain gene-targeted B-cell-deficient mice (µK/O). At doses of virus well tolerated by immunocompetent mice, heightened susceptibility of µK/O mice to herpetic encephalitis as well as to herpetic stromal keratitis (HSK) was observed. An explanation was sought for the increased severity of HSK in the µK/O mice. First, the lack of antibody responses in µK/O mice resulted in longer viral persistence and dissemination to the corneal stroma, the site of inflammation. Prolonged virus expression in the corneal stroma was suggested to cause bystander activation of Th1-type CD4+ T cells, further contributing to the severity of HSK lesion expression in µK/O mice. Second, µK/O mice generated minimal Th2 cytokine responses compared to wild-type mice. Such responses might serve to downregulate the severity of Th1-mediated HSK lesions.

* Corresponding author. Mailing address: Department of Microbiology, M409, Walters Life Science Building, University of Tennessee, Knoxville, TN 37996-0845. Phone: (423) 974-4026. Fax: (423) 974-4007. E-mail: btr{at}utk.edu.

Journal of Virology, April 2000, p. 3517-3524, Vol. 74, No. 8
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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