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Primary lymphocyte infection models for KSHV and its putative tumorigenesis mechanisms in B cell lymphomas

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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 various tumors in humans. KSHV primarily infects endothelial and B cells in vivo, and is associated with at least three malignancies: Kaposi’s sarcoma and two B cell lymphomas, respectively. Although KSHV readily infects endothelial cells in vitro and thus its pathogenic mechanisms have been extensively studied, B cells had been refractory to KSHV infection. As such, functions of KSHV genes have mostly been elucidated in endothelial cells in the context of viral infection but not in B cells. Whether KSHV oncogenes, defined in endothelial 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.

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    Sangmin Kang & Jinjong Myoung

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Kang, S., Myoung, J. Primary lymphocyte infection models for KSHV and its putative tumorigenesis mechanisms in B cell lymphomas. J Microbiol. 55, 319–329 (2017). https://doi.org/10.1007/s12275-017-7075-2

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