Manipulation of apoptosis by herpes viruses (Kaposi's sarcoma pathogenesis).

Abstract

The initial description of Kaposi’s sarcoma can be traced back to 1872, when a Hungarian dermatologist, Moritz Kaposi, published a case of skin cancer with clinical presentation of so-called pigmented sarcomas. This disease was designated Kaposi’s sarcoma (KS) in 1891. There are four distinct epidemiological forms of KS: classic KS occurring predominantly in Europe and the Mediterranean; endemic KS of the human immunodeficiency virus (HIV-1) negative patients in Africa; posttransplant or iatrogenic KS; and HIV-associated KS. The speculation of a viral etiology for KS was confirmed by the discovery of KSHV from HIV-associated KS lesions in 1994 (Chang et al. 1994). Subsequent epidemiological studies have demonstrated that KSHV DNA is present in all forms of KS tumors, suggesting that KSHV is the etiology agent for the development of KS (Sarid et al. 1999). In addition to KS, KSHV also associates with primary effusion lymphoma (PEL) and an immunoblast variant of Castleman’s disease (CD), which are of B cell origin (Cesarman et al. 1995; Soulier et al. 1995).