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Blocking HCV entry as potential antiviral therapy

Koen Vercauteren UGent, Geert Leroux-Roels UGent and Philip Meuleman UGent (2012) FUTURE VIROLOGY. 7(6). p.547-561
abstract
Infections with HCV represent a major global health problem. End-stage liver disease caused by chronic HCV infection is the most common indication for liver transplantation. Limited efficacy and severity of side effects hamper the use of pegylated interferon combined with ribavirin in a liver transplant setting. Therefore, new therapeutic options should be made available. Viral entry, the first step of the viral life cycle, represents an interesting target for therapeutic intervention. Understanding the mechanisms of viral entry is necessary to define the viral and cellular factors involved. In this review, we summarize these factors, highlight their potential as therapeutic targets and review the current (pre)clinical development of molecules that interfere with HCV entry.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
viral entry, liver transplantation, viral hepatitis, HEPATITIS-C-VIRUS, HUMAN MONOCLONAL-ANTIBODIES, B TYPE-I, HIGH-DENSITY-LIPOPROTEIN, SCAVENGER RECEPTOR-BI, PRIMARY HUMAN HEPATOCYTES, E2 ENVELOPE GLYCOPROTEIN, SERUM AMYLOID-A, NEUTRALIZING ANTIBODIES, CELL ENTRY, humanized mice, antiviral therapy
journal title
FUTURE VIROLOGY
Future Virol.
volume
7
issue
6
pages
547 - 561
Web of Science type
Review
Web of Science id
000304731400007
JCR category
VIROLOGY
JCR impact factor
0.962 (2012)
JCR rank
30/34 (2012)
JCR quartile
4 (2012)
ISSN
1746-0794
DOI
10.2217/FVL.12.47
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
3131784
handle
http://hdl.handle.net/1854/LU-3131784
date created
2013-02-14 15:46:27
date last changed
2017-06-02 12:23:05
@article{3131784,
  abstract     = {Infections with HCV represent a major global health problem. End-stage liver disease caused by chronic HCV infection is the most common indication for liver transplantation. Limited efficacy and severity of side effects hamper the use of pegylated interferon combined with ribavirin in a liver transplant setting. Therefore, new therapeutic options should be made available. Viral entry, the first step of the viral life cycle, represents an interesting target for therapeutic intervention. Understanding the mechanisms of viral entry is necessary to define the viral and cellular factors involved. In this review, we summarize these factors, highlight their potential as therapeutic targets and review the current (pre)clinical development of molecules that interfere with HCV entry.},
  author       = {Vercauteren, Koen and Leroux-Roels, Geert and Meuleman, Philip},
  issn         = {1746-0794},
  journal      = {FUTURE VIROLOGY},
  keyword      = {viral entry,liver transplantation,viral hepatitis,HEPATITIS-C-VIRUS,HUMAN MONOCLONAL-ANTIBODIES,B TYPE-I,HIGH-DENSITY-LIPOPROTEIN,SCAVENGER RECEPTOR-BI,PRIMARY HUMAN HEPATOCYTES,E2 ENVELOPE GLYCOPROTEIN,SERUM AMYLOID-A,NEUTRALIZING ANTIBODIES,CELL ENTRY,humanized mice,antiviral therapy},
  language     = {eng},
  number       = {6},
  pages        = {547--561},
  title        = {Blocking HCV entry as potential antiviral therapy},
  url          = {http://dx.doi.org/10.2217/FVL.12.47},
  volume       = {7},
  year         = {2012},
}

Chicago
Vercauteren, Koen, Geert Leroux-Roels, and Philip Meuleman. 2012. “Blocking HCV Entry as Potential Antiviral Therapy.” Future Virology 7 (6): 547–561.
APA
Vercauteren, K., Leroux-Roels, G., & Meuleman, P. (2012). Blocking HCV entry as potential antiviral therapy. FUTURE VIROLOGY, 7(6), 547–561.
Vancouver
1.
Vercauteren K, Leroux-Roels G, Meuleman P. Blocking HCV entry as potential antiviral therapy. FUTURE VIROLOGY. 2012;7(6):547–61.
MLA
Vercauteren, Koen, Geert Leroux-Roels, and Philip Meuleman. “Blocking HCV Entry as Potential Antiviral Therapy.” FUTURE VIROLOGY 7.6 (2012): 547–561. Print.