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JVI Accepts, published online ahead of print on 7 February 2007
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J. Virol. doi:10.1128/JVI.02622-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

SULFATED HOMOLOGUES OF HEPARIN INHIBIT HEPATITIS C VIRUS ENTRY INTO MAMMALIAN CELLS

Arnab Basu, Tatsuo Kanda, Aster Beyene, Kousuke Saito, Keith Meyer, and Ranjit Ray*

Departments, of Internal Medicine, Pathology, and Molecular Microbiology & Immunology, Saint Louis University, St. Louis, Missouri, USA

* To whom correspondence should be addressed. Email: rayr{at}slu.edu.


  Abstract

The entry mechanism for hepatitis C virus (HCV) through interactions between the envelope glycoproteins and specific cell surface receptors remains unclear at this time. We have previously shown with the vesicular stomatitis virus (VSV)/HCV pseudotype model that the hypervariable region 1 (HVR1) of HCV E2 envelope glycoprotein helps in binding with glycosaminoglycans (GAGs) present on the cell surface. In this study, we have examined the binding of HCV envelope glycoproteins with chemically modified derivatives of heparin. Furthermore, we have determined the functional relevance of the interaction of heparin derivatives with HCV envelope glycoproteins for infectivity using human immunodeficiency virus (HIV)/HCV pseudotype, VSV/HCV pseudotype, and cell culture grown HCV genotype 1a. Taken together, our results suggested that the HCV envelope glycoproteins rely upon O-sulfated esters of a heparin homologue to facilitate entry into mammalian cells.




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