Kaposi sarcoma (KS) is an angioproliferative disease classified into classic KS, endemic KS, iatrogenic KS, and HIV-associated KS (HIV-KS), however, they share the same histological traits and are all associated with infection by the human herpesvirus 8 (HHV8; also known as KSHV). Evidence indicates that KS progression occurs upon the deregulated expression of anti-apoptotic genes (Bcl-2), oncogenes (c-myc, c-int, ras) and oncosuppressor genes (TP53), and is associated with the long-lasting expression of HHV8 latency genes (LANA, v-cyc D, v-FLIP, Kaposin). All these genes are, in fact, expressed or altered in most KS spindle cells in the nodular-late stage of KS. Bcl-2 acts as a major KS progression factor, and TP53 and c-myc may also have a role in disease progression. HHV8 latency gene products may be involved in KS progression due to their capability of promoting cell growth by direct effects or antiapoptotic effects.
