Different environmental factors have been implicated in the pathogenesis of pemphigus vulgaris (PV), including drugs, diet, bums, X-rays, ultraviolet radiation, neoplasms, and infections. Several reports described the manifestation or aggravation of PV due to herpes simplex virus (HSV), varicella-zoster virus, Epstein-Baff virus, cytornegalovirus and human herpesvirus-8 infections. In the present study, we correlated secondary HSVI infection in 3 PV patients on immunosuppressive treatment with the titers of IgG autoantibodies against desmoglein I (DSG I) and 3 (DSG3) over a follow-up period of at least 18 months. In these patients, the detection of HSV I and clinical flare-up of PV did not correlate with a significant increase of DSG-specific IgG. Thus, secondary cutaneous HSV infections should be considered in patients with chronic PV with atypical sudden relapses or resistance to sufficient immunosuppressive treatment who do not show an increase of DSG-