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논문 기본 정보

저자정보
(The Wistar Institute)
저널정보
한국미생물학회 한국미생물학회 학술대회논문집 2013년도 International Meeting of the Microbiological Society of Korea
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    초록·키워드

    The human gammaherpesviruses, Epstein-Barr Virus (EBV) and Kaposi’s Sarcoma Associated Herpesvirus (KSHV) can establish long-term latent infections that drive cellular proliferation and carcinogenesis. Viral genomes and gene products are consistently detected in cancers of various lymphoid and epithelial cell origin. EBV is associated with endemic forms of nasopharyngeal carcinoma and Burkitt’s lymphoma, and sporadic forms of gastric carcinoma, Hodgkin’s disease, B-cell lymphoma, NK-T cell lymphoma, and lymphoproliferative diseases of the immunosuppressed. KSHV is associated with all forms of KS, pleural effusion lymphomas, and Castlemen’s disease. The pathogenesis depends on the ability of the viral genomes to establish and maintain a latent infection in long-term proliferating cells. Our lab has focused on the molecular chromosome biology of the latent viral genomes. Both EBV and KSHV persist in B-lymphocytes as multicopy, chromatin-associated episomes. They enter cells as nucleosome-free, linear DNA but rapidly acquire a chromatin structure that is competent for transcription, replication, and mitotic chromosome segregation mediated by host cell machinery. The mechanisms that control this epigenetic process are not completely understood, but essential for viral persistence, and potential novel targets for therapeutic intervention. Both viruses maintain their genomes through a centromere-like maintenance element that is bound by a viral encoded maintenance protein. EBV encoded EBNA1 and KSHV encoded LANA are DNA binding proteins with similar structural and functional properties. EBNA1 and LANA bind to multiple, repetitive elements and block replication fork ... 전체 초록 보기

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      UCI(KEPA) : I410-ECN-0101-2017-475-001058368