Molecular Mechanisms of Epstein-Barr virus-mediated carcinogeneis
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- IWAKIRI Dai
- Institute for Genetic Medicine Hokkaido University
Bibliographic Information
- Other Title
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- EBウイルスによる発癌の分子機構
- EB ウイルス ニ ヨル ハツガン ノ ブンシ キコウ
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Abstract
Epstein-Barr virus (EBV), a ubiquitous human double stranded DNA virus, is associated with a variety of malignancies including Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma (NPC) and gastric carcinoma (GC). These EBV-associated cancers are characterized by the proliferation of monoclonal EBV-infected cells, and viral gene expression in these cells is limited to a subset of latent genes, indicating that EBV latent genes contribute to carcinogenesis. Here I describe the mechanisms of carcinogenesis by EBV, focusing on the function of two EBV latent gens, latent membrane protein 2A (LMP2A) and EBV-encoded small RNA (EBER). LMP2A, which is known to mimic the B cell receptor (BCR) signaling, has been reported to contribute to malignant lymphoma development through the modulation of immune signals. Also, it has been demonstrated that LMP2A-mediated intracellular signaling plays significant roles in epithelial carcinogenesis. On the other hand, it has been demonstrated that EBER, which is expected to form double stranded RNA (dsRNA) structure, triggers a signal transduction from host viral RNA sensors RIG-I and TLR3. Activation of innate immune signals by EBER has been reported to contribute to the pathogenesis of EBV-associated disseases, including cancers.
Journal
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- Uirusu
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Uirusu 64 (1), 49-56, 2014
The Japanese Society for Virology
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Keywords
Details 詳細情報について
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- CRID
- 1390001205078946048
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- NII Article ID
- 130004922978
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- NII Book ID
- AN00018808
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- ISSN
- 18843433
- 00426857
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- NDL BIB ID
- 025647291
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- PubMed
- 25765980
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- Text Lang
- ja
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed