Humanisation of a claudin-1-specific monoclonal antibody for clinical prevention and cure of HCV infection without escape.
Fiche publication
Date publication
mars 2017
Journal
Gut
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas, Pr PESSAUX Patrick
Tous les auteurs :
Colpitts CC, Tawar RG, Mailly L, Thumann C, Heydmann L, Durand SC, Xiao F, Robinet E, Pessaux P, Zeisel MB, Baumert TF
Lien Pubmed
Résumé
HCV infection is a leading cause of chronic liver disease and a major indication for liver transplantation. Although direct-acting antivirals (DAAs) have much improved the treatment of chronic HCV infection, alternative strategies are needed for patients with treatment failure. As an essential HCV entry factor, the tight junction protein claudin-1 (CLDN1) is a promising antiviral target. However, genotype-dependent escape via CLDN6 and CLDN9 has been described in some cell lines as a possible limitation facing CLDN1-targeted therapies. Here, we evaluated the clinical potential of therapeutic strategies targeting CLDN1.
Mots clés
ANTIVIRAL THERAPY, HEPATITIS C, TIGHT JUNCTION
Référence
Gut. 2017 Mar;: