Abstract
Herpes simplex virus 1 (HSV-1) infection of the cornea leads to a potentially blinding disease, termed herpetic stromal keratitis (HSK) that is characterized by lesions of an immunoinflammatory nature. In spite of the fact that HSK typically presents as a recurrent disease due to reactivation of virus which latently infects the trigeminal ganglia, most murine studies of HSK have employed a primary and not recurrent model of the disease. This report documents the several recurrent models of HSK that have been developed and how data generated from these models differs in some important aspects from data generated following primary infection of the cornea. Chief among these differences is the fact that recurrent HSK takes place in the context of an animal that has a preexisting anti-HSV immune response, while primary HSK occurs in an animal that is developing such a response. We will document both differences and similarities that derive from this fundamental difference in these models with an eye towards possible vaccines and therapies that demonstrate promise in treating HSK.
Highlights
Herpes simplex virus 1 (HSV-1) infection of the cornea leads to a potentially blinding disease, termed herpetic stromal keratitis (HSK) that is characterized by lesions of an immunoinflammatory nature
In a completely different set of studies to determine the role of IL-10 during HSK, it was reported that intraocular treatment of mice with IL-10 reduced corneal disease from 95% to 36% [43, 70]
Role of T Cells in Maintaining Viral Latency. In addition to their role in mediating corneal disease, T cells have been implicated in maintaining viral latency in the infected trigeminal ganglia (TG). This role for T cells comes primarily from work done in the laboratory of Robert Hendricks, who reported that CD8+ T cells surround latently infected TG neurons in mice infected with HSV-1 [89,90,91,92]
Summary
Herpetic stromal keratitis (HSK) is a potentially blinding corneal inflammation that accompanies herpes simplex virus type 1 (HSV-1) infection of the eye. Later Shimeld et al developed a model in which mice are infected with the McKrae strain of HSV-1 and given passive immunization in the form of pooled serum The eyes of these latently infected mice are exposed to UV-B irradiation at least 30 days following primary infection to induce reactivation [11,12,13,14]. It should be noted that while infections with these various strains of HSV-1 display differences in corneal pathology and neurovirulence, the immunological components of corneal disease are remarkably similar when compared on the basis of virus strain used or the strain of mouse being infected as the following discussion will illustrate
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