Abstract

Kaposi’s sarcoma-associated herpesvirus (KSHV) is the latest addition to the human herpesvirus family. Unlike alpha- and beta-herpesvirus subfamily members, gamma-herpesviruses, including Epstein-Barr virus (EBV) and KSHV, cause vari-ous tumors in humans. KSHV primarily infects endothelial and B cells in vivo, and is associated with at least three malig-nancies: Kaposi’s sarcoma and two B cell lymphomas, res-pectively. Although KSHV readily infects endothelial cells in vitro and thus its pathogenic mechanisms have been exten-sively studied, B cells had been refractory to KSHV infection. As such, functions of KSHV genes have mostly been eluci-dated in endothelial cells in the context of viral infection but not in B cells. Whether KSHV oncogenes, defined in endo-thelial cells, play the same roles in the tumorigenesis of B cells remains an open question. Only recently, through a few ground-breaking studies, B cell infection models have been established. In this review, those models will be compared and contrasted and putative mechanisms of KSHV-induced B cell transformation will be discussed.

• Keywords: KSHV; B cell; infection model; lymphoma