Adenovirus 12 and dermatitis herpetiformis.
J. Handley, June O’Neill, Joanne H. Connolly, D. Burrows
Abstract
J. Handley, June O’Neill, Joanne H. Connolly, D. Burrows
Abstract
Previous studies have shown that A-gliadin, a major gluten-derived peptide known to activate the gluten-sensitive enteropathy (GSE) of coeliac disease (CD), and the non-structural E1B peptide produced during early lytic gastrointestinal infection with human adenovirus type 12 (AD12) share an identical twelve amino acid sequence. It is suggested that immunological cross reactivity between these two peptides may play an important role in the pathogenesis of CD. As a milder but histologically identical GSE is found in the majority of patients with dermatitis herpetiformis (DH), a condition also thought to be caused by dietary gluten, we postulated that AD12 may also be involved in the pathogenesis of DH. To test this we assayed sera from 40 patients with DH and 18 healthy controls for AD12-neutralizing antibodies as evidence of past viral exposure. Detectable AD12 antibodies (titre of 13 or higher) were found in only 15% (6/40) of DH patients, compared with 27.8% (5/18) controls (not significant). These findings do not support a causative role for AD12 in the pathogenesis of DH.
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Previous studies have shown that A-gliadin, a major gluten-derived peptide known to activate the gluten-sensitive enteropathy (GSE) of coeliac disease (CD), and the non-structural E1B peptide produced during early lytic gastrointestinal infection with human adenovirus type 12 (AD12) share an identical twelve amino acid sequence. It is suggested that immunological cross reactivity between these two peptides may play an important role in the pathogenesis of CD. As a milder but histologically identical GSE is found in the majority of patients with dermatitis herpetiformis (DH), a condition also thought to be caused by dietary gluten, we postulated that AD12 may also be involved in the pathogenesis of DH. To test this we assayed sera from 40 patients with DH and 18 healthy controls for AD12-neutralizing antibodies as evidence of past viral exposure. Detectable AD12 antibodies (titre of 13 or higher) were found in only 15% (6/40) of DH patients, compared with 27.8% (5/18) controls (not significant). These findings do not support a causative role for AD12 in the pathogenesis of DH.
Key concepts: Dermatitis herpetiformis, Pathogenesis, Gluten, Antibody, Enteropathy, Coeliac disease, Immunology, Lytic cycle