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C100729200v1
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Papers In Press, published online ahead of print January 7, 2002
J. Biol. Chem, 10.1074/jbc.C100729200
Submitted on December 14, 2001
Revised on January 7, 2002
Accepted on January 4, 2002

Antiviral Activity of Interferon-alpha 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

FG 213, Bundesinstitut f. gesundheitlichen Verbraucherschutz und Veterniärmedizin, Berlin D-14195

Corresponding Author: a.rang{at}bgvv.de

It is well established that interferon-alpha 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 CMV-promoter controlled hepatitis B virus expression system, which leads to intracellular viral replication even in non-hepatic cell lines. In this experimental system interferon-alpha 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-alpha against hepatitis B virus. Our data demonstrate that interferon-alpha 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.


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