Immunobiology and host response to KSHV infection

Excerpt

The interplay between malignancy, infection and immunity is best illustrated by the neoplasms related to KSHV (Boshoff and Weiss, 2002): Kaposi sarcoma (KS) is approximately 100 times more common during immunosuppression and can be resolved when iatrogenic immunosuppression is stopped (Euvrard et al., 2003) and during highly active antiretroviral treatment (HAART) of HIV-1 infected individuals (Boshoff and Weiss, 2002). Primary effusion lymphoma (PEL) and plasmablastic multicentric Castleman’s disease (MCD) also occur predominantly during immunosuppression. Like other gammaherpesviruses, KSHV persists as a latent episome in B-lymphocytes (Ambroziak et al., ; Cesarman et al., ; Renne et al., 1996), without provoking host responses that would eliminate infected cells. KSHV acquired a fascinating repertoire of decoys to trick the host immune response enabling establishment of lifelong infection in humans with very few clinical manifestations. When the balance between viral infection and host immunity is disturbed, some of the molecular pathways employed by KSHV to evade host immune responses are directly involved in driving oncogenesis (Moore and Chang, 2003). KSHV is an excellent model to study the coevolution of pathogen attack and mechanisms of host counter attack.