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Sequence heterogeneity of HTLV‐I proviral DNA in the central nervous system of patients with HTLV‐I–associated myelopathy
Author(s) -
Kira Junichi,
Koyanagi Yoshio,
Yamada Takeshi,
Itoyama Yasuto,
Tateishi Jun,
Akizuki Shinichiro,
Kishikawa Masao,
Baba Eishi,
Nakamura Minoru,
Suzuki Jun,
Nakamura Tatsufumi,
Nakamura Naomi,
Yamamoto Naoki,
Goto Ikuo
Publication year - 1994
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410360206
Subject(s) - tropical spastic paraparesis , open reading frame , virology , polymerase chain reaction , biology , nucleic acid sequence , myelopathy , microbiology and biotechnology , gene , virus , genetics , peptide sequence , spinal cord , neuroscience
The nucleotide sequence of human T‐lymphotropic virus type I (HTLV‐I) in central nervous system tissue was determined in 3 autopsy cases with HTLV‐I–associated myelopathy (HAM)/tropical spastic paraparesis (TSP) and 1 seropositive carrier without HAM/TSP but with multiple sclerosis. All HAM/TSP samples (3 spinal cords and 2 brains) and the sample from the seropositive carrier without HAM/TSP (brain) were positive for HTLV‐I env (5146–6681), pX5′ (6549–7494), and pX3′ (7354–8276) regions by the two‐step polymerase chain reaction method. A nucleotide sequence analysis of the pX5′ and pX3′ polymerase chain reaction products from nucleotides 6631 to 8259 revealed heterogeneity of the HTLV‐I genome in all cases. It is notable that 13 of 50 clones derived from the pX3′ polymerase chain reaction products were defective in the tax open reading frame while 7 were defective in the rex open reading frame in the HAM/TSP samples. All 17 clones from 1 HAM/TSP case were defective in the pX open reading frame II. One nucleotide insertion at 7784 creating a frame shift in both tax and rex was seen in all 3 HAM/TSP cases but not in the HTLV‐I carrier without HAM/TSP. The pX‐defective mutants found frequently in the central nervous system may contribute to the neural damage, since the pX gene products are essential for the transactivation of various cellular genes as well as for viral replication.