Journal of Microbiology

Review

[Minireview] Primary lymphocyte infection models for KSHV and its putative tumorigenesis mechanisms in B cell lymphomas: Sangmin Kang , Jinjong Myoung; J. Microbiol. 2017;55(5):319-329. Published online April 29, 2017; DOI: https://doi.org/10.1007/s12275-017-7075-2

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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.

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Journal Article

Latent Kaposi’s sarcoma-associated herpesvirus infection in bladder cancer cells promotes drug resistance by reducing reactive oxygen species: Suhyuk Lee , Jaehyuk Jang , Hyungtaek Jeon , Jisu Lee , Seung-Min Yoo , Jinsung Park , Myung-Shin Lee; J. Microbiol. 2016;54(11):782-788. Published online October 29, 2016; DOI: https://doi.org/10.1007/s12275-016-6388-x

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Abstract

Kaposi’s sarcoma-associated herpesvirus (KSHV) is the major etiologic agent of Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman’s disease. Recent studies have indicated that KSHV can be detected at high frequency in patient-derived bladder cancer tissue and might be associated with the pathogenesis of bladder cancer. Bladder cancer is the second most common cancer of the genitourinary tract, and it has a high rate of recurrence. Because drug resistance is closely related to chemotherapy failure and cancer recurrence, we investigated whether KSHV infection is associated with drug resistance of bladder cancer cells. Some KSHV-infected bladder cancer cell lines showed resistance to an anti-cancer drug, cisplatin, possibly as a result of downregulation of reactive oxygen species. Additionally, drug resistance acquired from KSHV infection could partly be overcome by HDAC1 inhibitors. Taken together, the data suggest the possible role of KSHV in chemo-resistant bladder cancer, and indicate the therapeutic potential of HDAC1 inhibitors in drug-resistant bladder cancers associated with KSHV infection.

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Primary lymphocyte infection models for KSHV and its putative tumorigenesis mechanisms in B cell lymphomas
Sangmin Kang, Jinjong Myoung
Journal of Microbiology.2017; 55(5): 319. CrossRef
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Research Support, Non-U.S. Gov't

KSHV Infection of B-Cell Lymphoma Using a Modified KSHV BAC36 and Coculturing System: Hyosun Cho , Hyojeung Kang; J. Microbiol. 2012;50(2):285-292. Published online April 27, 2012; DOI: https://doi.org/10.1007/s12275-012-1495-9

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Abstract: Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of two B cell lymphoproliferative diseases, namely primary effusion lymphoma (PEL) and multicentric Castleman’s disease (MCD). KSHV infection of B cell lymphoma in vitro has been a long-standing battle in advancing human KSHV biology. In this study, a modified form of KSHV BAC36 named BAC36A significantly increased the fidelity of gene-targeted site-directed mutagenesis in the KSHV genome. This modification eliminates tedious screening steps required to obtain mutant clones when a KSHV BAC36 reverse genetic system is used. Coculturing B-cell lymphoma BJAB cells with KSHV BAC36A stably transfected 293T cells enabled us to infect BJAB cells with a KSHV virion derived from the KSHV BAC36A. The coculture system produced substantial amounts of KSHV infection to BJAB, meaning that KSHV virions were released from 293T cells and then infected neighboring BJAB cells. Owing to our success with the KSHV BAC36A and coculture system, we propose a new genetic system for the study of KSHV gene expression and regulation in B-cell lymphoma.

Journal Article

Notch Signal Transduction Induces a Novel Profile of Kaposi’s Sarcoma-Associated Herpesvirus Gene Expression: Heesoon Chang; J. Microbiol. 2006;44(2):217-225.; DOI: https://doi.org/2362 [pii]

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Abstract: Kaposi’s sarcoma-associated herpesvirus (KSHV) RTA transcription factor is recruited to its responsive elements through interaction with RBP-Jк that is a downstream transcription factor of the Notch signaling pathway that is important in development and cell fate determination. This suggests that KSHV RTA mimics cellular Notch signal transduction to activate viral lytic gene expression. Here, I demonstrated that unlike other B lymphoma cells, KSHV-infected primary effusion lymphoma BCBL1 cells displayed the constitutive activation of ligand-mediated Notch signal transduction, evidenced by the Jagged ligand expression and the complete proteolytic process of Notch receptor I. In order to investigate the effect of Notch signal transduction on KSHV gene expression, human Notch intracellular (hNIC) domain that constitutively activates RBP-Jк transcription factor activity was expressed in BCBL1 cells, TRExBCBL1-hNIC, in a tetracycline inducible manner. Gene expression profiling showed that like RTA, hNIC robustly induced expression of a number of viral genes including K5 immune modulatory gene resulting in downregulation of MHC I and CD54 surface expression. Finally, the genetic analysis of KSHV genome demonstrated that the hNIC-mediated expression of K5 during viral latency consequently conferred the downregulation of MHC I and CD54 surface expression. These results indicate that cellular Notch signal transduction provides a novel expression profiling of KSHV immune deregulatory gene that consequently confers the escape of host immune surveillance during viral latency.

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