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Journal of Virology, October 2008, p. 10295-10301, Vol. 82, No. 20
0022-538X/08/$08.00+0 doi:10.1128/JVI.00931-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Departments of Microbiology, Immunology,1 Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 731042
Received 5 May 2008/ Accepted 29 July 2008
The role of tumor necrosis factor alpha (TNF-
) was evaluated for CXCL10-deficient (CXCL10–/–) mice which succumbed to genital herpes simplex virus type 2 (HSV-2) infection and possessed elevated levels of virus and TNF-
but not other cytokines in the central nervous system (CNS) and vaginal tissue within the first 7 days following virus exposure. Anti-TNF-
but not control antibody treatment offsets the elevated mortality rate of CXCL10–/– mice, despite increased CNS viral titers. In addition, TNF-
neutralization suppressed recruitment of leukocyte subpopulations into the CNS, which is associated with reduced CCL2 and CXCL9 expression. Collectively, the results implicate TNF-
as the principal mediator of mortality in response to genital HSV-2 infection.
Published ahead of print on 6 August 2008.
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