Effects of hepatitis C virus envelope glycoprotein unfolded protein response activation on translation and transcription

Effects of hepatitis C virus envelope glycoprotein unfolded protein response activation on... The hepatitis C virus (HCV) envelope glycoproteins have been shown to cause ER stress and induce the unfolded protein response (UPR). Using a bicistronic reporter, we show that the envelope glycoproteins repressed both cap-dependent and HCV IRES-mediated translation in HeLa cells but displayed a differential repression of cap-dependent translation in Huh-7 cells. In contrast, the envelope glycoproteins repressed E2F transcriptional activity in both HeLa and Huh-7 cells and caused increased accumulation of the underphosphorylated retinoblastoma protein. Expression of the envelope glycoproteins induced eIF2α phosphorylation, suggesting a role of the UPR in regulating translation and E2F transcriptional activity. The envelope glycoproteins also enhanced transcriptional activity from the COX-2 promoter and endogenous COX-2 expression in HeLa cells, but not in Huh-7 cells. Together, these results suggest that the envelope glycoproteins may assume more functional roles in viral replication and host cell interactions. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Effects of hepatitis C virus envelope glycoprotein unfolded protein response activation on translation and transcription

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Publisher
Springer Journals
Copyright
Copyright © 2009 by Springer-Verlag
Subject
Biomedicine; Infectious Diseases; Medical Microbiology ; Virology
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-009-0495-5
Publisher site
See Article on Publisher Site

Abstract

The hepatitis C virus (HCV) envelope glycoproteins have been shown to cause ER stress and induce the unfolded protein response (UPR). Using a bicistronic reporter, we show that the envelope glycoproteins repressed both cap-dependent and HCV IRES-mediated translation in HeLa cells but displayed a differential repression of cap-dependent translation in Huh-7 cells. In contrast, the envelope glycoproteins repressed E2F transcriptional activity in both HeLa and Huh-7 cells and caused increased accumulation of the underphosphorylated retinoblastoma protein. Expression of the envelope glycoproteins induced eIF2α phosphorylation, suggesting a role of the UPR in regulating translation and E2F transcriptional activity. The envelope glycoproteins also enhanced transcriptional activity from the COX-2 promoter and endogenous COX-2 expression in HeLa cells, but not in Huh-7 cells. Together, these results suggest that the envelope glycoproteins may assume more functional roles in viral replication and host cell interactions.

Journal

Archives of VirologySpringer Journals

Published: Oct 1, 2009

References

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