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CD8⁺ T cells control corneal disease following ocular infection with herpes simplex virus type 1

¹ Department of Ophthalmology & Visual Sciences, Washington University School of Medicine, 660 S. Euclid Avenue, Box 8096, St Louis, MO 63110, USA
² Department of Molecular Microbiology & Pathogenesis, Washington University School of Medicine, 660 S. Euclid Avenue, Box 8096, St Louis, MO 63110, USA
³ Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St Louis, MO 63104, USA

Correspondence
Patrick M. Stuart
stuart{at}vision.wustl.edu

The role that T cell subsets play in herpetic stromal keratitis (HSK) has been the subject of intense research efforts. While most studies implicate CD4⁺ T cells as the principal cell type mediating primary corneal disease, recent reports using knockout mice have suggested that both CD4⁺ and CD8⁺ T cell subsets may play integral roles in modulating the disease. Furthermore, recent studies suggest that CD8⁺ T cells are directly involved in maintaining virus latency in infected trigeminal ganglia. This work has addressed these discrepancies by infecting the corneas of mice lacking CD4⁺ and CD8⁺ T cells with herpes simplex virus type 1 (HSV-1) and monitoring both corneal disease and latent infection of trigeminal ganglia. Results indicated that mice lacking CD8⁺ T cells had more severe corneal disease than either BALB/c or B6 parental strains. In contrast, mice lacking CD4⁺ T cells had a milder disease than parental strains. When mice were evaluated for persistence of infectious virus, only transient differences were observed in periocular tissue and corneas. No significant differences were found in persistence of virus in trigeminal ganglia or virus reactivation from explanted ganglia. These data support the following conclusions. CD4⁺ T cells are not required for resistance to infection with HSV-1 and probably mediate HSK. Mice lacking CD8⁺ T cells do not display differences in viral loads or reactivation and thus CD8⁺ T cells are not absolutely required to maintain latency. Finally, CD8⁺ T cells probably play a protective role by regulating the immunopathological response that mediates HSK.

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