Mailly, LaurentXiao, FeiLupberger, JoachimWilson, Garrick K.Aubert, PhilippeDuong, François H. T.Calabrese, DiegoLeboeuf, CélineFofana, IsabelThumann, ChristineBandiera, SimonettaLütgehetmann, MarcVolz, TassiloDavis, ChristopherHarris, Helen J.Mee, Christopher J.Girardi, ErikaChane-Woon-Ming, BéatriceEricsson, MariaFletcher, NicolaBartenschlager, RalfPessaux, PatrickVercauteren, KoenMeuleman, PhilipVilla, PascalKaderali, LarsPfeffer, SébastienHeim, Markus H.Neunlist, MichelZeisel, Mirjam B.Dandri, MauraMcKeating, Jane A.Robinet, EricBaumert, Thomas F.2015-12-042015Mailly, L., F. Xiao, J. Lupberger, G. K. Wilson, P. Aubert, F. H. T. Duong, D. Calabrese, et al. 2015. “Clearance of persistent hepatitis C virus infection using a claudin-1-targeting monoclonal antibody.” Nature biotechnology 33 (5): 549-554. doi:10.1038/nbt.3179. http://dx.doi.org/10.1038/nbt.3179.1087-0156http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845271Hepatitis C virus (HCV) infection is a leading cause of liver cirrhosis and cancer1. Cell entry of HCV2 and other pathogens3-5 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 model6 we show that a monoclonal antibody specific for TJ protein claudin-17 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 via 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.en-USJournal Article2015-12-0410.1038/nbt.3179