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Originally published In Press as doi:10.1074/jbc.C100729200 on January 7, 2002
J. Biol. Chem., Vol. 277, Issue 10, 7645-7647, March 8, 2002
ACCELERATED PUBLICATION
Antiviral Activity of Interferon- against Hepatitis B Virus
Can Be Studied in Non-hepatic Cells and Is Independent of MxA*
Andreas
Rang ,
Michael
Bruns,
Tilman
Heise, and
Hans
Will
From the Heinrich-Pette-Institut für Experimentelle Virologie
und Immunologie an der Universität Hamburg, Martinistraße
52, 20251 Hamburg, Germany
It is well established that interferon- can
induce non-cytotoxic intracellular suppression of hepatitis B virus
replication, but the mechanisms involved are unclear. Cell culture
studies to characterize these mechanisms are restricted, in part
because hepatitis B virus replicates almost exclusively in
liver-derived cells. To overcome this limitation we used a
cytomegalovirus promoter-controlled hepatitis B virus expression
system, which leads to intracellular viral replication even in
non-hepatic cell lines. In this experimental system interferon-
treatment specifically suppressed viral replication demonstrating that
antiviral activities against hepatitis B virus are not restricted to
hepatic cells. Furthermore, the interferon-inducible MxA protein was
recently reported to play a key role in the antiviral action of
interferon- against hepatitis B virus. Our data demonstrate that
interferon- also suppresses hepatitis B virus replication in
MxA-deficient HEp2 cells, indicating that MxA is not essential for
these activities. Taken together, our data imply that the experimental
approach presented can also be adapted to established cell lines which
are deficient in parts of the signal transduction pathway or other
elements located further downstream, providing important insights into
mechanisms specifically suppressing hepatitis B virus.
*
This work was supported by grants from the Bundesministerium
für Bildung und Forschung and the Deutsche
Forschungsgemeinschaft. The Heinrich-Pette-Institut für
Experimentelle Virologie und Immunologie is supported by the
Bundesministerium für Gesundheit und the Freie and Hansestadt
Hamburg.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: Bundesinstitut
für Gesundheitlichen Verbraucherschutz und
Veterinärmedizin, Thielallee 88-92, 14195 Berlin, Germany. Tel.:
49-188-8412-3716; Fax: 49-188-8412-3635; E-mail:
a.rang@bgvv.de.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.

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