Previous Article | Next Article ![]()
Journal of Virology, November 2002, p. 11775-11779, Vol. 76, No. 22
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.22.11775-11779.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Institute of Microbiology, University of Ancona, 60020 Ancona,1 Università "Vita-Salute San Raffaele," IRCCS Istituto Scientifico San Raffaele, 20132 Milan, Italy,4 Research Center for Emerging Infectious Diseases and Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871,2 Department of Virology II, National Institute of Infectious Diseases, Tokyo, Japan3
Received 20 March 2002/ Accepted 8 August 2002
Hepatitis C virus (HCV) is the major causative agent of blood-borne non-A, non-B hepatitis. Although a strong humoral response is detectable within a few weeks of primary infection and during viral persistence, the role played by antibodies against HCV envelope glycoproteins in controlling viral replication is still unclear. We describe how human monoclonal anti-HCV E2 antibody fragments isolated from a chronically HCV-infected patient differ sharply in their abilities to neutralize infection of HepG2 cells by a vesicular stomatitis virus pseudotype bearing HCV envelope glycoproteins. Two clones were able to neutralize the pseudotype virus at a concentration of 10 µg/ml, while three other clones completely lacked this activity. These data can explain the lack of protection and the possibility of reinfection that occur even in the presence of a strong antiviral antibody response.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»