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Hepatitis C virus (HCV) infection is a leading cause of liver cirrhosis and cancer. Cell entry of HCV and other pathogens is mediated by tight junction (TJ) proteins, but successful therapeutic targeting of TJ proteins has not been reported yet. Using a human liver-chimeric mouse model, we show that a monoclonal antibody specific for the TJ protein claudin-1 (ref. 7) eliminates chronic HCV infection without detectable toxicity. This antibody inhibits HCV entry, cell-cell transmission and virus-induced signaling events. Antibody treatment reduces the number of HCV-infected hepatocytes in vivo, highlighting the need for de novo infection by means of host entry factors to maintain chronic infection. In summary, we demonstrate that an antibody targeting a virus receptor can cure chronic viral infection and uncover TJ proteins as targets for antiviral therapy.

Original publication

DOI

10.1038/nbt.3179

Type

Journal article

Journal

Nat Biotechnol

Publication Date

05/2015

Volume

33

Pages

549 - 554

Keywords

Animals, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Claudin-1, Hepacivirus, Hepatitis C, Hepatocytes, Humans, Liver Cirrhosis, Mice