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      The 2011 Retrovirology Prize winner Masao Matsuoka: forward looking and antisense

      editorial
      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Retrovirology
      Publisher: BioMed Central

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          Abstract

          Masao Matsuoka wins the 2011 Retrovirology Prize.

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          Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms

          Yuko Taniguchi, Kisato Nosaka, Jun-ichirou Yasunaga … (2005)
          Background Human T-cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia (ATL) after a long latent period. Among accessory genes encoded by HTLV-I, the tax gene is thought to play a central role in oncogenesis. However, Tax expression is disrupted by several mechanims including genetic changes of the tax gene, deletion/hypermethylation of 5'-LTR. To clarify the role of epigenetic changes, we analyzed DNA methylation and histone modification in the whole HTLV-I provirus genome. Results The gag, pol and env genes of HTLV-I provirus were more methylated than pX region, whereas methylation of 5'-LTR was variable and 3'-LTR was not methylated at all. In ATL cell lines, complete DNA methylation of 5'-LTR was associated with transcriptional silencing of viral genes. HTLV-I provirus was more methylated in primary ATL cells than in carrier state, indicating the association with disease progression. In seroconvertors, DNA methylation was already observed in internal sequences of provirus just after seroconversion. Taken together, it is speculated that DNA methylation first occurs in the gag, pol and env regions and then extends in the 5' and 3' directions in vivo, and when 5'-LTR becomes methylated, viral transcription is silenced. Analysis of histone modification in the HTLV-I provirus showed that the methylated provirus was associated with hypoacetylation. However, the tax gene transcript could not be detected in fresh ATL cells regardless of hyperacetylated histone H3 in 5'-LTR. The transcription rapidly recovered after in vitro culture in such ATL cells. Conclusion These results showed that epigenetic changes of provirus facilitated ATL cells to evade host immune system by suppressing viral gene transcription. In addition, this study shows the presence of another reversible mechanism that suppresses the tax gene transcription without DNA methylation and hypoacetylated histone.
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            The HBZ gene, a key player in HTLV-1 pathogenesis

            Masao Matsuoka, Patrick Green (2009)
            Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL) and is also associated with a variety of lymphocyte-mediated diseases. The HTLV-1 basic leucine zipper (HBZ) gene, found to be consistently expressed in ATL, has recently been the subject of intensive research efforts. In this review, we summarize recent findings about HBZ and discuss its roles and functions not only in the virus life cycle, but also in HTLV-1 disease pathogenesis.
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              ATF3, an HTLV-1 bZip factor binding protein, promotes proliferation of adult T-cell leukemia cells

              Keita Hagiya, Jun-ichirou Yasunaga, Yorifumi Satou … (2011)
              Background Adult T-cell leukemia (ATL) is an aggressive malignancy of CD4+ T-cells caused by human T-cell leukemia virus type 1 (HTLV-1). The HTLV-1 bZIP factor (HBZ) gene, which is encoded by the minus strand of the viral genome, is expressed as an antisense transcript in all ATL cases. By using yeast two-hybrid screening, we identified activating transcription factor 3 (ATF3) as an HBZ-interacting protein. ATF3 has been reported to be expressed in ATL cells, but its biological significance is not known. Results Immunoprecipitation analysis confirmed that ATF3 interacts with HBZ. Expression of ATF3 was upregulated in ATL cell lines and fresh ATL cases. Reporter assay revealed that ATF3 could interfere with the HTLV-1 Tax's transactivation of the 5' proviral long terminal repeat (LTR), doing so by affecting the ATF/CRE site, as well as HBZ. Suppressing ATF3 expression inhibited proliferation and strongly reduced the viability of ATL cells. As mechanisms of growth-promoting activity of ATF3, comparative expression profiling of ATF3 knockdown cells identified candidate genes that are critical for the cell cycle and cell death, including cell division cycle 2 (CDC2) and cyclin E2. ATF3 also enhanced p53 transcriptional activity, but this activity was suppressed by HBZ. Conclusions Thus, ATF3 expression has positive and negative effects on the proliferation and survival of ATL cells. HBZ impedes its negative effects, leaving ATF3 to promote proliferation of ATL cells via mechanisms including upregulation of CDC2 and cyclin E2. Both HBZ and ATF3 suppress Tax expression, which enables infected cells to escape the host immune system.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Retrovirology
                Title: Retrovirology
                Publisher: BioMed Central
                ISSN (Electronic): 1742-4690
                Publication date Collection: 2011
                Publication date (Electronic): 15 December 2011
                Volume: 8
                Page: 102
                Affiliations
                [1 ]Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, the National Institutes of Health, 9000 Rockville Pike, Bethesda 20892, MD, USA
                Article
                Publisher ID: 1742-4690-8-102
                DOI: 10.1186/1742-4690-8-102
                PMC ID: 3265421
                PubMed ID: 22171744
                SO-VID: d2acdb18-75be-478c-8d98-7006e61b67e7
                Copyright © Copyright ©2011 Jeang; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 3 December 2011
                Date accepted : 15 December 2011
                Categories
                Subject: Editorial

                ScienceOpen disciplines: Microbiology & Virology
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology

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