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Journal of Virology, March 1999, p. 2058-2063, Vol. 73, No. 3
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

An Important Role for Major Histocompatibility Complex Class I-Restricted T Cells, and a Limited Role for Gamma Interferon, in Protection of Mice against Lethal Herpes Simplex Virus Infection

Ai-Xuan Holterman,1,dagger Kathleen Rogers,1 Kurt Edelmann,2 David M. Koelle,3,4 Lawrence Corey,3,4,5 and Christopher B. Wilson1,2,*

Departments of Pediatrics,1 Immunology,2 Medicine, Laboratory Medicine,3 and Microbiology,5 University of Washington, Seattle, Washington 98195, and the Fred Hutchinson Cancer Research Center, Seattle, Washington 981044

Received 25 August 1998/Accepted 2 December 1998

Herpes simplex virus (HSV) inhibits major histocompatibility complex (MHC) class I expression in infected cells and does so much more efficiently in human cells than in murine cells. Given this difference, if MHC class I-restricted T cells do not play an important role in protection of mice from HSV, an important role for these cells in humans would be unlikely. However, the contribution of MHC class I-restricted T cells to the control of HSV infection in mice remains unclear. Further, the mechanisms by which these cells may act to control infection, particularly in the nervous system, are not well understood, though a role for gamma interferon (IFN-gamma ) has been proposed. To address the roles of MHC class I and of IFN-gamma , C57BL/6 mice deficient in MHC class I expression (beta 2 microglobulin knockout [beta 2KO] mice), in IFN-gamma expression (IFN-gamma KO mice), or in both (IFN-gamma KO/beta 2KO mice) were infected with HSV by footpad inoculation. beta 2KO mice were markedly compromised in their ability to control infection, as indicated by increased lethality and higher concentrations of virus in the feet and spinal ganglia. In contrast, IFN-gamma appeared to play at most a limited role in viral clearance. The results suggest that MHC class I-restricted T cells play an important role in protection of mice against neuroinvasive HSV infection and do so largely by mechanisms other than the production of IFN-gamma .

* Corresponding author. Mailing address: Pediatrics, Box 356320, University of Washington School of Medicine, 1959 NE Pacific St., Seattle, WA 98195. Phone: (206) 543-3207. Fax: (206) 543-3184. E-mail: cbwilson{at}u.washington.edu.

dagger Present address: University of Illinois School of Medicine, Chicago, Ill.

Journal of Virology, March 1999, p. 2058-2063, Vol. 73, No. 3
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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