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J Virol, April 1998, p. 2600-2606, Vol. 72, No. 4
Zentrum für Molekulare Biologie (ZMBH),
Universität Heidelberg, 69120 Heidelberg, Germany
Received 5 September 1997/Accepted 12 December 1997
The effect of glucagon on the establishment of hepadnavirus
infection was studied in vitro with the duck hepatitis B virus (DHBV)
model. The presence of the peptide hormone throughout infection or
starting up to 8 h after virus uptake resulted in a dose-dependent reduction in the levels of intra- and extracellular viral gene products
and of secreted virions. Treatment with forskolin or dibutyryl-cyclic
AMP, two drugs that also stimulate the cyclic AMP (cAMP) signal
transduction pathway, resulted in comparable inhibition, suggesting
that the inhibitor effect is related to changes in the activity of
protein kinase A. In persistently infected hepatocytes, only a slight,
but continuous, decrease in viral replication was observed upon
prolonged drug treatment. Time course analysis, including detection of
DHBV covalently closed circular (ccc) DNA templates, revealed that
glucagon acts late during the establishment of infection, at a time
when the virus is already internalized, but before detectable ccc DNA
accumulation in the nucleus. These data suggest that nuclear import
(and reimport) of DHBV DNA genomes from cytosolic capsids is subject to
cAMP-mediated regulation by cellular factors responding to changes in
the state of the host cell.
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Glucagon Treatment Interferes with an Early Step of
Duck Hepatitis B Virus Infection

and
*
Corresponding author. Mailing address: ZMBH, University
of Heidelberg, Im Neuenheimer Feld 282, 69120 Heidelberg, Germany. Phone: 49 6221 54 68 85. Fax: 49 6221 54 58 93. E-mail:
hshd{at}zmbh.uni-heidelberg.de.
Present address: Max-Planck-Institut für Immunbiologie, 79108 Freiburg, Germany.
Present address: Bayer AG, 42096 Wuppertal, Germany.
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