Human herpesvirus 7 (HHV-7) was discovered in 1989 as a new member of the beta-herpesvirus subfamily. Primary infection occurs early in life and manifests as exanthema subitum, or other febrile illnesses mimicking measles and rubella. Thus, HHV-7 has to be considered as a causative agent in a variety of macular-papular rashes in children. In addition, HHV-7 was found in some cases of other inflammatory skin disorders, such as psoriasis. There are controversial data on the detection of HHV-7 in pityriasis rosea, but so far there is not enough evidence for a pathogenetic association of HHV-7 with this exanthematic skin disease. Although HHV-7 can be found in some cases of Hodgkin's disease, there are no data supporting a direct causative role in this lymphoma type nor in other nodal or primary cutaneous lymphomas. In various epidemiologic forms of Kaposi's sarcoma, infection of monocytic cells with HHV-7 was demonstrated, which may indirectly influence tumor biology. In the context of immunosuppression, HHV-7 has recently been identified as an emerging pathogen in transplant recipients and may exacerbate graft rejection in renal transplant recipients. The ability of HHV-7 to induce cytokine production in infected cells could make HHV-7 an important pathogenetic co-factor in inflammatory and neoplastic disorders. Moreover, the restricted cellular tropism of HHV-7 may render this virus an interesting vector for gene therapy. Thirteen years after the discovery of HHV-7, there has been considerable progress in characterizing its genetic structure, virus-induced effects on infected host cells and in the development of diagnostic tools. Nevertheless, the role of HHV-7 in various skin diseases and the clinical manifestations of reactivation of HHV-7 infection have still to be defined.