UNDERSTANDING THE PATHOGENESIS OF HSV-ASSOCIATED ERYTHEMA MULTIFORME

Erythema multiforme (EM) is a polymorphic, often recurring eruption ca used by exposure to medication or various infections, notably herpes s implex virus (HSV). Understanding the pathogenesis of HSV-associated E M (HAEM) is essential for patient management. We suggest that HAEM res ults from the combination of viropathic effects mediated by HSV protei ns, notably DNA polymerase (Pol), and an immunological reaction to vir al antigens. Presumably, viral DNA and proteins ingested by macrophage s at HSV lesion sites undergo fragmentation and processing for present ation to T cells with HSV memory. HSV DNA is deposited on the skin, wh ere it is expressed. Activated T cells are recruited to the skin site of Pol expression, directly or indirectly resulting in the generation of an inflammatory cascade. Factors potentially involved in the incide nce of recurrences, lesion severity and anatomical localization includ e the identity of the deposited HSV genes, cutaneous capillary size, d egree of vasoconstriction and ambient temperature. Evidence in support of this interpretation is reviewed.