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The latency pattern of Epstein–Barr virus infection and viral IL-10 expression in cutaneous natural killer/T-cell lymphomas
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  • Published: 03 April 2001

The latency pattern of Epstein–Barr virus infection and viral IL-10 expression in cutaneous natural killer/T-cell lymphomas

  • Z-G Xu1,
  • K Iwatsuki2,
  • N Oyama1,
  • M Ohtsuka1,
  • M Satoh1,
  • S Kikuchi1,
  • H Akiba1 &
  • …
  • F Kaneko1 

British Journal of Cancer volume 84, pages 920–925 (2001)Cite this article

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Abstract

The nasal type, extranodal natural killer or T(NK/T)-cell lymphoma is usually associated with latent Epstein–Barr virus (EBV) infection. In order to elucidate the EBV gene expression patterns in vivo, we examined eight patients with cutaneous EBV-related NK/T-cell lymphomas, including six patients with a NK-cell phenotype and two patients with a T-cell phenotype. The implication of EBV in the skin lesions was determined by the presence of EBV-DNA, EBV-encoded nuclear RNA (EBER) and a clonality of EBV-DNA fragments containing the terminal repeats. Transcripts of EBV-encoded genes were screened by reverse transcription- polymerase chain reaction (RT-PCR), and confirmed by Southern blot hybridization. The expression of EBV-related antigens was examined by immunostaining using paraffin-embedded tissue sections and cell pellets of EBV-positive cell lines. Our study demonstrated that all samples from the patients contained EBV nuclear antigen (EBNA)-1 mRNA which was transcribed using the Q promoter, whereas both the Q promoter and another upstream promoter (Cp/Wp) were used in EBV-positive cell lines, B95.8, Raji and Jiyoye. Latent membrane protein-1 (LMP-1) mRNA was detected in seven of eight patients and all cell lines, whereas EBNA-2 transcripts were found only in the cell lines. Immunostaining showed no LMP-1, EBNA-2 or ZEBRA antigens in the paraffin-embedded tissue sections, although they were positive in the cell line cells. Latent BHRF1 transcripts encoding bcl-2 homologue and BCRF1 transcripts encoding viral interleukin (vIL)-10 were detected in one and two of eight patients, respectively. A patient with NK-cell lymphoma expressing both transcripts died of rapid progression of the illness. Our results indicate that the restricted expression of the latency-associated EBV genes and the production of vIL-10 and bcl-2 homologue may favour tumour growth, evading the host immune surveillance. © 2001 Cancer Research Campaign

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  • 16 November 2011

    This paper was modified 12 months after initial publication to switch to Creative Commons licence terms, as noted at publication

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Authors and Affiliations

  1. Department of Dermatology, Fukushima Medical University School of Medicine, Hikarigaoka, 1, 960-1295, Fukushima, Japan

    Z-G Xu, N Oyama, M Ohtsuka, M Satoh, S Kikuchi, H Akiba & F Kaneko

  2. Department of Dermatology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools, 2-5-1 Shikata-cho, Okayama, 700-8558, Japan

    K Iwatsuki

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Correspondence to: K Iwatsuki; Email: keijiiwa@fmu.ac.jp

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From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

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Xu, ZG., Iwatsuki, K., Oyama, N. et al. The latency pattern of Epstein–Barr virus infection and viral IL-10 expression in cutaneous natural killer/T-cell lymphomas. Br J Cancer 84, 920–925 (2001). https://doi.org/10.1054/bjoc.2000.1687

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  • Received: 04 April 2000

  • Revised: 06 December 2000

  • Accepted: 07 December 2000

  • Published: 03 April 2001

  • Issue date: 06 April 2001

  • DOI: https://doi.org/10.1054/bjoc.2000.1687

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Keywords

  • Epstein–Barr virus
  • NK/T-cell lymphomas
  • latency
  • viral IL-10
  • bcl-2 homologue
  • LMP
  • EBNA

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