Abstract
Summary
The present study of experimental herpes simplex virus keratoconjunctivitis of the rabbit was undertaken to compare virus production, interferon and antibody production in those eye tissues which show typical clinical signs. Although corneal epithelial lesions coincided with peak virus titers in the cornea, conjunctival lesions began 5 days after peak virus titers in the conjunctiva. Iritis developed in the absence of detectable HSV in that tissue. Thus, virus titers were not always correlated with onset of clinical signs. Simarily, appearance of local antibody did not correlate with elimination of HSV from the cornea or conjunctiva. Stromal disease coincided with the appearance of serum antibody and iritis ensued 2 days earlier than local antibody in this tissue. Since iris antibody exceeded serum antibody by a factor of 10 on Day 8, it is likely that it was produced by immunocompetent cells invading the iris. The inability of the HSV infection to induce detectable concentrations of interferon and the relative insensitivity of HSV to the action of interferon indicates that the interferon system may not play an important role during natural recovery from HSV infection of rabbit eyes. Topical treatment with In·Cn beginning 1 hr after HSV infection induced low levels of conjunctival interferon, a 10-fold decrease in conjunctival virus as well as a slight suppression of circulating antibody, but only a slight protective effect.
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