Binding of Hepatitis C Virus to CD81

Author:

Pileri Piero1,Uematsu Yasushi1,Campagnoli Susanna1,Galli Giuliano1,Falugi Fabiana1,Petracca Roberto1,Weiner Amy J.1,Houghton Michael1,Rosa Domenico1,Grandi Guido1,Abrignani Sergio1

Affiliation:

1. P. Pileri, Y. Uematsu, S. Campagnoli, G. Galli, F. Falugi, R. Petracca, D. Rosa, G. Grandi, S. Abrignani, IRIS, Chiron, Siena 53100, Italy. A. J. Weiner and M. Houghton, Chiron Corporation, Emeryville, CA 94608, USA.

Abstract

Chronic hepatitis C virus (HCV) infection occurs in about 3 percent of the world's population and is a major cause of liver disease. HCV infection is also associated with cryoglobulinemia, a B lymphocyte proliferative disorder. Virus tropism is controversial, and the mechanisms of cell entry remain unknown. The HCV envelope protein E2 binds human CD81, a tetraspanin expressed on various cell types including hepatocytes and B lymphocytes. Binding of E2 was mapped to the major extracellular loop of CD81. Recombinant molecules containing this loop bound HCV and antibodies that neutralize HCV infection in vivo inhibited virus binding to CD81 in vitro.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference38 articles.

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3. J. H. Hoofnagle Hepatology 26 (suppl. 1) 15S (1997).

4. Cryoglobulinemia is a B lymphocyte proliferative disorder characterized by the presence of cryoglobulins (immunoglobulins insoluble at 4°C) in the serum. The disease is often associated with multiple organ involvement and is due to the deposition of immune complexes in small blood vessels. Three types of cryoglobulinemia can be distinguished. Type I is formed by monoclonal immunoglobulin M (IgM) and is also known as Waldenstrom's disease. Type II is formed by IgM-IgG complexes in the serum; the IgG fraction is polyclonal whereas the IgM fraction is monoclonal with rheumatoid factor activity. Type III is formed by polyclonal immunoglobulins. More than 80% of the patients with type II and type III cryoglobulinemia are infected by HCV often without liver disease [

5. Ferri C., et al., Clin. Exp. Rheumatol. 9, 95 (1991);

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