HTLV-1 Infection and Its Associated Diseases
1Department of Immunology, Graduate School and Faculty of Medicine, University of the Ryukyus, Okinawa 903-0215, Japan
2Department of Microbiology and Immunology, Drexel Institute for Biotechnology and Virology Research, Drexel University College of Medicine, Doylestown, PA 18902, USA
3Department of Molecular Medicine and Hematology, Molecular Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan
4Department of Immunology, Faculty of Medicine, Imperial College, London W2 1PG, UK
HTLV-1 Infection and Its Associated Diseases
Description
It has been more than 30 years since human T-cell leukemia virus type 1 (HTLV-1) was discovered as the first human retrovirus associated with a human cancer called adult T-cell leukemia/lymphoma (ATLL). Interestingly, HTLV-1 also causes a chronic inflammatory neurologic disorder called HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 is now estimated to infect up to 10 million people worldwide: endemic areas include southwestern Japan, the Caribbean basin, Central and South America, localized areas of Iran, Melanesia, and equatorial regions of Africa. Although only approximately 2%–3% develop ATLL and another 0.25%–3.8% develop HAM/TSP, both ATLL and HAM/TSP are still highly intractable to conventional therapeutics. Therefore, further research to enhance our understanding of the pathogenesis and treatment of HTLV-1 associated diseases is of crucial importance. A topic of intense investigation for HTLV-1-mediated leukemogenesis has been focused on the HTLV-1 encoded viral oncoprotein Tax, which activates many cellular target genes through binding to groups of transcription factors and coactivators and is necessary and sufficient for cellular transformation. However, recent reports indicate that another regulatory protein, HTLV-1 basic leucine zipper factor (HBZ), which is encoded on the antisense viral transcript and inhibits Tax-mediated viral gene expression, has a critical role in the development of ATL and HAM/TSP. Important progress has also been made in the treatment of ATL, such as combination therapy with zidovudine and interferon-alpha, immunotherapy with anti-IL-2 receptor or anti-CC chemokine receptor 4 monoclonal antibodies, and allogeneic bone marrow or stem cell transplantation. Potential topics include, but are not limited to:
- Molecular pathogenesis of ATL
- Animal models of HTLV-1 infection
- Clinical trials for ATL
- Treatment for ATL
- ATL and microRNAs
- HAM/TSP pathogenesis
- Host immune response against HTLV-1 infection
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