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J. Virol. doi:10.1128/JVI.01008-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Innate recognition network driving the HSV induced corneal immunopathology: Role of Toll Pathway in the early inflammatory events in Stromal Keratitis

Comparative and experimental Medicine, College of Veterinary Medicine, University of Tennessee, Knoxville, TN, 37996-0845; Biosafety Research Institute and Department of Pathology, College of Veterinary Medicine, South Korea; Department of Medicine, University of Massachusetts Medical Center

^* To whom correspondence should be addressed. Email: btr{at}utk.edu.

	Abstract

Ocular infection with herpes simplex virus (HSV) sets off an array of events that succeed in clearing virus from the cornea but leaves the tissue with a CD4+ T cell orchestrated chronic inflammatory lesion that impairs vision. We demonstrate that Toll-like receptor (TLR) signaling forms a part of the recognition system that induces the syndrome that eventually culminates in immunopathology. Accordingly, in a comparison of the outcome of the infection in wild-type (WT) mice and those lacking TLR function it was apparent that the absence of TLR2, and to a lesser extent TLR9, resulted in significantly diminished lesions. Similarly mice lacking the adapter molecule MyD88 were resistant to lesion development but such animals were also unable to control infection with most succumbing to lethal encephalitis. The susceptibility of TLR4-/- animals was also evaluated. These animals developed lesions more rapidly that were more severe than in WT animals. We discuss the possible mechanisms by which early recognition of HSV constituents impact on the subsequent development of immunopathological lesions.

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