Ontology type: schema:ScholarlyArticle Open Access: True
2015-05
AUTHORSLaurent Mailly, Fei Xiao, Joachim Lupberger, Garrick K Wilson, Philippe Aubert, François H T Duong, Diego Calabrese, Céline Leboeuf, Isabel Fofana, Christine Thumann, Simonetta Bandiera, Marc Lütgehetmann, Tassilo Volz, Christopher Davis, Helen J Harris, Christopher J Mee, Erika Girardi, Béatrice Chane-Woon-Ming, Maria Ericsson, Nicola Fletcher, Ralf Bartenschlager, Patrick Pessaux, Koen Vercauteren, Philip Meuleman, Pascal Villa, Lars Kaderali, Sébastien Pfeffer, Markus H Heim, Michel Neunlist, Mirjam B Zeisel, Maura Dandri, Jane A McKeating, Eric Robinet, Thomas F Baumert
ABSTRACTHepatitis 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. More... »
PAGES549-554
http://scigraph.springernature.com/pub.10.1038/nbt.3179
DOIhttp://dx.doi.org/10.1038/nbt.3179
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/25798937
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