Human T-cell leukemia virus type I and adult T-cell leukemia

Human T-cell leukemia virus type I and adult T-cell leukemia
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DOI:
10.1038/sj.onc.1206551
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发表时间:
2003-08-11
期刊:
影响因子:
8
通讯作者:
Matsuoka, M
Matsuoka, M
中科院分区:
医学1区
文献类型:
--
作者:
Matsuoka, M

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人类T细胞白血病病毒I型(HTLV-I)在约5%的携带者中潜伏期较长,可导致成人T细胞白血病(ATL)。HTLV-I感染HTLV-I后,通过编码包括Tax在内的病毒蛋白的作用,在体内促进HTLV-I感染细胞的克隆性增殖。然而,由于HTLV-I前病毒的遗传和表观遗传变化,白血病细胞经常缺乏Tax的表达,这表明Tax在转化后并不总是必要的。另外,由于TAX是细胞毒性淋巴细胞的主要靶点,因此没有TAX蛋白的ATL细胞可以逃离宿主免疫系统。在潜伏期内,宿主基因组的改变累积,最终导致ATL的发病。
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.