Abstract
Human T-cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia (ATL) in about 5% of carriers after a long latent period. After its infection, HTLV-I promotes the clonal proliferation of HTLV-I infected cells in vivo by actions of encoded viral proteins, including Tax. However, leukemic cells frequently lack the expression of Tax by the genetic and epigenetic changes of HTLV-I provirus, suggesting that Tax is not always necessary after transformation. Alternatively, ATL cells without Tax protein could escape from the host immune system since Tax is the major target of cytotoxic lymphocytes. During the latent period, alterations of host genome accumulate, finally leading to onset of ATL.
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Acknowledgements
I thank the members of the Matsuoka laboratory for experimental contribution and helpful discussion. This work was supported by a grant-in-aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan.
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Matsuoka, M. Human T-cell leukemia virus type I and adult T-cell leukemia. Oncogene 22, 5131–5140 (2003). https://doi.org/10.1038/sj.onc.1206551
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