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J Biol Chem, Vol. 275, Issue 12, 8307-8314, March 24, 2000
From the Influenza A viruses are capable of inducing the
expression of a variety of cytokine and proapoptotic genes in infected
cells. The promoter regions of most of these genes harbor binding sites for the transcription factor NF-
Influenza Virus-induced NF-
B-dependent Gene
Expression Is Mediated by Overexpression of Viral Proteins and Involves
Oxidative Radicals and Activation of IB Kinase*
§,
,,, and
Institut für Medizinische
Strahlenkunde und Zellforschung (MSZ), Universität
Würzburg, Versbacherstr. 5, D-97078 Würzburg, Germany, the
¶ Klinik für Dermatologie und Venerologie, Universität
Rostock, Augustenstr. 20, D-18055 Rostock, Germany, the
Institut für Virologie und Immunbiologie,
Universität Würzburg, Versbacherstr. 7, D-97078
Würzburg, Germany, and the ** Institut für Klinische und
Molekulare Virologie, Universität Erlangen, Schloßgarten 4, D-91054 Erlangen, Germany
B which is an important mediator of
immune and inflammatory responses. Our present study is based on an
observation that influenza A virus infection of cells stimulates transcriptional activation of the HIV-1 long terminal repeat (LTR) which harbors two regulatory NF-B elements, and is aimed at
identifying the molecular mechanisms involved in this process. We found
that the expression of influenza virus hemagglutinin (HA), matrix
protein (M), and nucleoprotein (NP), as single factors is sufficient to transcriptionally activate the HIV-1 LTR. This process is mediated by
oxidative radicals because treatment of cells with pyrrolidine dithiocarbamate, a scavenger of such radicals, abolished the
transactivating ability. Expression of different influenza proteins
induces activation of NF-B-dependent gene expression but
not transcriptional activation of an AP-1/Ets-dependent
promoter, indicating a selectivity for NF-B transactivation.
Furthermore, influenza protein expression induces activation of IB
kinase (IKK). Accordingly coexpression of a catalytically inactive
mutant of IKK abolishes influenza protein induced activation of NF-B
as well as HIV-1 LTR-dependent reporter gene expression,
suggesting that IKK is an important intermediate within this signaling
process. Taken together, our results show that various influenza virus
proteins act as viral transactivators to modulate transcriptional
activity of B-element harboring promoters such as the HIV-LTR.
*
This work was supported by Deutsche Forschungsgemeinschaft
Grant Lu477/4-1 and the Fonds der Chemischen Industrie. This paper was
presented in part at the International Congress of Virology (ICV),
August 1999, Sydney, Australia.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Institut für
Medizinische Strahlenkunde und Zellforschung (MSZ),
Universität Würzburg, Versbacherstr. 5, D-97078
Würzburg, Germany. Tel.: 49-931-201-3851; Fax:
49-931-201-3835; E-mail: s.ludwig@mail.uni-wuerzburg.de.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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