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DOI: 10.1017/S1462399408000756; 14 July 2008
Caroline Bussmann, Wen-Ming Peng, Thomas Bieber and Natalija Novak (2008) Molecular pathogenesis and clinical implications of eczema herpeticum. Expert Rev. Mol. Med. Vol. 10, e21, DOI: 10.1017/S1462399408000756

Molecular pathogenesis and clinical implications of eczema herpeticum

Caroline Bussmann a1, Wen-Ming Peng a1, Thomas Bieber a1 and Natalija Novak a1 c1

a1 Department of Dermatology and Allergology, University of Bonn, Bonn, Germany.

c1 Corresponding author: Natalija Novak, Department of Dermatology and Allergology, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. Tel: +49 228 287 15370; Fax: +49 228 287 14333; E-mail: Natalija.Novak@ukb.uni-bonn.de

A subgroup of patients with atopic dermatitis develops one or more episodes of a severe viral skin infection caused by herpes simplex virus superimposed on eczematous skin lesions. This condition is named atopic dermatitis complicated by eczema herpeticum. Characteristic features of patients developing eczema herpeticum include an early age of onset of atopic dermatitis with a persistent and severe course into adulthood, predilection for eczematous skin lesions in the head and neck area, elevated total serum IgE levels and increased allergen sensitisation. Deficiencies at the level of both the innate and the adaptive immune system, which have been identified in atopic dermatitis, are much more pronounced in this subgroup. Predisposing cellular factors include a reduced number of plasmacytoid dendritic cells in the epidermis and a modified capacity of these cells to produce type I interferons after allergen challenge. In addition, lower levels of antimicrobial peptides in the skin of atopic dermatitis patients, resulting in part from a Th2-prone micromilieu, contribute to the lack of an effective defence against viral attack. In this review, we summarise the current knowledge of the molecular pathogenesis of eczema herpeticum.

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