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The 11 th International Workshop on KSHV & Related Agents, Birmingham, UK Poster Session Abstract P11 KAPOSI’S SARCOMA-ASSOCIATED HERPESVIRUS (KSHV) INFECTED PRIMARY EFFUSION LYMPHOMA CELLS SHOWS A DISTINCT GENE EXPRESSION PROFILE FROM BURKITT LYMPHOMA CELLS EITHER WITH OR WITHOUT EPSTEIN-BARR VIRUS AND THE OTHER T CELL LYMPHOBLASTIC LEUKEMIA CELLS Keiji Ueda, Eriko Ohsaki, Tohru Suzuki and Masato Karayama Dept. of Infectious Disease, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 431-3192, Japan Abstract Analysis on a gene expression profile using various kinds of normal or abnormal tissues, including tumors, and cell lines etc., is very informative to know the nature of the cells, which leads to further analyses and exploring new methods to treat diseased cells. Though many reports have already published on gene expression profiles of KSHV infected tissues, either in vitro or in vivo, we will report here gene expression profiles of cultured cell lines; KSHV infected primary effusion lymphoma cell lines such as BC1, BC3, BCBL1 and TY1, Burkitt cell lines such as BJAB, Ramos, which are not infected with Epstein-Barr virus (EBV) and Daudi, Raji, Akaka, which are infected with EBV, and T lymphoblastic cell lines as Sup T1, Molt 3 and Jurkat, and HIV-1 infected MT4. What we found is that each categorized group of cell lines showed distinct gene expression profiles and Burkitt cell lines infected with or without EBV showed a similar profile. Since all PEL cell lines are infected with KSHV and BC1 is infected with both EBV and KSHV, we can not conclude that KSHV infection governs the gene expression profile but it is likely that EBV status does not affect the profile. We are further studying how a typical gene is activated in the PEL cell lines and will discuss about it. Presenting author Email: kueda@hama-med.ac.jp 108
The 11 th International Workshop on KSHV & Related Agents, Birmingham, UK Poster Session Abstract P12 THE M TYPE K15 PROTEIN OF KAPOSI'S SARCOMA-ASSOCIATED HERPESVIRUS INDUCES CELL MIGRATION, INVASION AND REGULATES MICRORNA EXPRESSION VIA ITS SH2-BINDING MOTIF Yu-Hsuan Wu 1 , Min-Fen Wu 1 , Yuan-Hau Tsai 1 , Su-Fang Lin 3 , Tyson V. Sharp 4 and Hsei- Wei Wang 1,2,5 1 Institute of Microbiology and Immunology, 2 Institute of Clinical Medicine, National Yang- Ming University; 3 Division of Clinical Research, National Health Research Institute, Taiwan; 4 School of Biomedical Sciences, University of Nottingham Medical School, Queen’s Medical Centre, Nottingham, UK; 5 Department of Teaching and Research,Taipei City Hospital, Taipei, Taiwan Abstract Kaposi’s sarcoma (KS) associated herpesvirus (KSHV) is the etiological agent of KS. In vivo KS is a tumor capable of spreading throughout the body, and pulmonary metastasis is observed clinically. In vitro KSHV induces the invasiveness of endothelial cells. However, no viral gene has yet been implicated in cell invasion. The KSHV ORF K15 is a KSHV-specific gene encoding a transmembrane protein. Two highly divergent forms of K15, the predominant (P) and minor (M) forms (K15P and K15M, respectively) have been identified in different KSHV strains. K15 resembles the LMP2A gene of Epstein-Barr virus (EBV) in their genomic locations and protein topology. Also, both K15 proteins have similar motifs to those found in EBV LMP1 protein. K15 therefore appears to be a hybrid of a distant evolutionary relative of both EBV LMP1 and 2A. Since both LMP1 and LMP2A proteins are capable of inducing cell motility and have been linked to NPC metastasis, we questioned whether K15 also possesses similar abilities. In this study, we show by the use of a K15M-specific mAb and PCR, that K15M is latently expressed in KSHV positive PEL cells. K15M localizes on lysosomal membrane and is capable of activating the NF-kB transcription factor via its SH2-binding motif. K15M induces cell migration, invasion and the expression of microRNAs miR-21 and miR-31 via this conserved motif. K15M therefore may contribute to KSHV-mediated tumor metastasis and angiogenesis. Targeting of K15 proteins or their downstream micorRNAs for therapy may represent a novel avenue of treatment for KSHV-associated neoplasia. Presenting author Email: b881625@life.nthu.edu.tw 109
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