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Journal of Virology, December 2001, p. 11515-11525, Vol. 75, No. 23
Institute for Virus Research, Kyoto
University, Sakyo-ku, Kyoto 606-8507,1 and
Institute for Genetic Medicine, Hokkaido University, Kita-ku,
Sapporo 060-0815,2 Japan
Received 20 August 2001/Accepted 25 August 2001
Rat models of human T-cell leukemia virus type 1 (HTLV-1)-related
diseases such as adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis have been reported. However, these models do not completely reproduce human diseases partly because
HTLV-1 replicates poorly in rats. We investigated here the possible
reason for this. We found that the activity of Rex in rat cells is
quite low compared to that in human cells. As Rex function depends
largely on the CRM1 protein, whose human type (human CRM1 [hCRM1])
directly binds to Rex and exports it from the nucleus to the cytoplasm,
we assessed whether rat CRM1 (rCRM1) could act as well as hCRM1 as a
cofactor for Rex activity. We first cloned a cDNA encoding rCRM1 and
found that both rCRM1 and hCRM1 could bind to and export Rex protein to
the cytoplasm with similar efficiencies. However, unlike hCRM1, rCRM1
could hardly support Rex function because of its poor ability in
inducing the Rex-Rex interaction required for RNA export into the
cytoplasm. These observations suggest that the poor ability of rCRM1 to
act as a cofactor for Rex function may be responsible for the poor replication of HTLV-1 in rats.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.23.11515-11525.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Rat CRM1 Is Responsible for the Poor Activity of
Human T-Cell Leukemia Virus Type 1 Rex Protein in Rat
Cells
*
Corresponding author. Mailing address: Institute for
Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku,
Sapporo 060-0815, Japan. Phone and fax: 81-11-707-6837. E-mail:
hshida{at}imm.hokudai.ac.jp
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