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Mol Cell Biol, July 1998, p. 3796-3802, Vol. 18, No. 7
Department of Biology, University of
California at San Diego, La Jolla, California
92093,1 and
Department of Pathology,
State University of New York at Stony Brook, Stony Brook, New York
117942
Received 25 November 1997/Returned for modification 29 December
1997/Accepted 12 March 1998
Interferon establishes an antiviral state in numerous cell types
through the induction of a set of immediate-early response genes.
Activation of these genes is mediated by phosphorylation of latent
transcription factors of the STAT family. We found that infection
of primary foreskin fibroblasts with human cytomegalovirus (HCMV)
causes selective transcriptional activation of the
alpha/beta-interferon-responsive ISG54 gene. However, no activation or
nuclear translocation of STAT proteins was detected. Activation of
ISG54 occurs independent of protein synthesis but is prevented
by protein tyrosine kinase inhibitors. Further analysis revealed that
HCMV infection induced the DNA binding of a novel complex, tentatively
called cytomegalovirus-induced interferon-stimulated response element
binding factor (CIF). CIF is composed, at least in part, of the
recently identified interferon regulatory factor 3 (IRF3), but it
does not contain the STAT1 and STAT2 proteins that
participate in the formation of interferon-stimulated gene factor 3. IRF3, which has previously been shown to possess no
intrinsic transcriptional activation potential, interacts with the
transcriptional coactivator CREB binding protein, but
not with p300, to form CIF. Activating interferon-stimulated genes without the need for prior synthesis of interferons might provide the
host cell with a potential shortcut in the activation of its antiviral
defense.
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Cytomegalovirus Activates Interferon Immediate-Early Response
Gene Expression and an Interferon Regulatory Factor 3-Containing
Interferon-Stimulated Response Element-Binding Complex
*
Corresponding author. Mailing address: University of
California, San Diego, Department of Biology, Bonner Hall 3138, 9500 Gilman Dr., La Jolla, CA 92093-0322. Phone: (619) 822-1108. Fax: (619)
822-1106. E-mail: midavid{at}ucsd.edu.
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