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Sequence variations in ltr and env regions of HTLV‐I do not discriminate between the virus from patients with HTLV‐I‐associated myelopathy and adult T‐cell leukemia
Author(s) -
Kinoshita Tomohiro,
Tsujimoto Atsumi,
Shimotohno Kunitada
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910470403
Subject(s) - virology , long terminal repeat , biology , myelopathy , virus , t cell leukemia , polymerase chain reaction , leukemia , nucleic acid sequence , human t lymphotropic virus 1 , peripheral blood mononuclear cell , provirus , tropical spastic paraparesis , gene , genetics , microbiology and biotechnology , gene expression , genome , neuroscience , spinal cord , in vitro
For detailed comparison of human T‐cell leukemia virus type I (HTLV‐I) in adult T‐cell leukemia (ATL) and HTLV‐I‐associated myelopathy (HAM), the nucleotide sequences of parts of the long terminal repeat (LTR) and env regions of the HTLV‐I proviruses from 12 patients with HAM, 8 patients with ATL and one with both diseases were analyzed. About 340 bp of the LTR U3 region, about 4S0 bp of the 5′ region and about 280 bp of the 3′ region of env were sequenced directly in DNAs amplified by the polymerase chain reaction (PCR) with 2 or 3 sets of primers for each region. Nucleotide insertions, deletions or point mutations were observed at 50 positions in these regions of about 1,000 nucleotides length. None of these changes was specific to either HAM or ATL, and some changes were observed in proviruses from both cases of HAM and ATL. Moreover, the sequences of proviruses isolated from pairs of cell lines established from cerebrospinal fluid (CSF) and peripheral blood mononuclear cells (PBMCs) of the 4 patients with HAM also had different sequences. These results indicate that the proviruses from HAM and ATL are indistinguishable in these sequenced regions, suggesting that these 2 diseases are caused by infection with genetically indistinguishable HTLV‐I. Therefore, the reason why these two distinct diseases, HAM and ATL, develop in HTLV‐I carriers may be based on a host factor(s) or some other factor(s) rather than variation in the virus itself.