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The human T-cell leukemia virus type I (HTLV-I) is the causative
agent of an aggressive T-cell malignancy in humans. While the virus
appears to maintain a state of latency in most infected cells, high
level virion production is an essential step in the HTLV-I life cycle.
The virally-encoded Tax protein, a potent activator of gene expression,
is believed to control the switch from latency to replication. Tax
stimulation of HTLV-I transcription is mediated through cellular
activating transcription factor/cAMP response element binding proteins,
which bind the three 21-base pair (bp) repeat viral enhancer elements.
In this report, we show that viral latency may result from a highly
unstable interaction between CREB and the HTLV-I 21-bp repeats,
resulting in rapid dissociation of CREB from the viral promoter. In the
presence Tax, the dissociation rate of CREB from a 21-bp repeat element
is decreased. This stabilization is highly specific, requiring the
amino-terminal region of CREB and appropriate 21-bp repeat sequences.
We suggest that Tax stabilization of CREB binding to the viral promoter
leads to an increase in gene expression, possibly providing the switch
from latency to high level replication of the virus.
Volume 270,
Number 21,
Issue of May 26, pp. 12814-12822, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
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