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.
journal_name
Oncogenejournal_title
Oncogeneauthors
Matsuoka Mdoi
10.1038/sj.onc.1206551subject
Has Abstractpub_date
2003-08-11 00:00:00pages
5131-40issue
33eissn
0950-9232issn
1476-5594pii
1206551journal_volume
22pub_type
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