Mechanisms of resistance and hypersensitivity in herpes simplex keratitis.
Laboratory studies show that systemic immunity protects the corneal epithelium against herpes simplex virus (HSV) infection, this protection probably being humoral in origin. It can be shown that hyperimmune gammaglobulin (HGG) has a similar protective action when instilled up to 2 hours after the induction of the ulcerative disease. Topical steroids enhance proliferation of HSV in epithelial disease, but at low dilutions there is some evidence that resistance is enhanced. Human studies of systemic immunity show that there is a response in cell-mediated immunity (CMI) after primary and recurrent ulcerative disease. Certain patients with severe stromal keratitis have evidence of CMI deficiency compared to controls or to patients with epithelial disease. To prevent virus spread into the stroma, early use of antiviral therapy is essential. Stromal disease does not only represent a hypersensitivity phenomenon, but is probably associated with virus proliferation in the keratocytes. Potent steroid medication will theoretically deplete immuno-protective responses, and promote further virus proliferation. Therefore the lowest possible concentrations achieving a clinical response should be employed.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis; D000936:Antigen-Antibody Complex; D003315:Cornea / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity; D007111:Immunity, Cellular; D007635:Keratitis, Dendritic / Q000188:drug therapy / Q000276:immunology*; D008213:Lymphocyte Activation; D011817:Rabbits; D014762:Viral Interference
D000305:Adrenal Cortex Hormones; D000914:Antibodies, Viral; D000936:Antigen-Antibody Complex