Transmembrane 6 superfamily member 2 gene E167K variant impacts on steatosis and liver damage in chronic hepatitis C patients

Marta Milano, Alessio Aghemo, Rosellina Margherita Mancina, Janett Fischer, Paola Dongiovanni, Stella De Nicola, Anna Ludovica Fracanzani, Roberta D'Ambrosio, Marco Maggioni, Raffaele De Francesco, Silvia Fargion, Thomas Berg, Felix Stickel, Jochen Hampe, Stefano Romeo, Massimo Colombo, Luca Valenti – 29 March 2015 – Steatosis and inherited host factors influence liver damage progression in chronic hepatitis C (CHC). The transmembrane 6 superfamily member 2 (TM6SF2) gene E167K variant increases liver fat and risk of progressive steatohepatitis by interfering with lipoprotein secretion.

Selection of a hepatitis C virus with altered entry factor requirements reveals a genetic interaction between the E1 glycoprotein and claudins

Sharon E. Hopcraft, Matthew J. Evans – 29 March 2015 – Hepatitis C virus (HCV) cell entry is a complex, multistep process requiring numerous host cell factors, including the tight junction protein claudin‐1 (CLDN1). It is not known whether CLDN1 and the HCV glycoproteins physically interact. Therefore, the focus of this work was to study genetic interactions between CLDN1 and HCV. We used CRISPR technology to generate CLDN1 knockout (KO) Huh‐7.5 cells, which could not be infected by genotype 2a Jc1 HCV unless CLDN1 expression was restored.

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