Hepatitis C virus infection propagates through interactions between Syndecan-1 and CD81 and impacts the hepatocyte glycocalyx.
Grigorov, Boyan; Reungoat, Emma; Gentil Dit Maurin, Alice; Varbanov, Mihayl; Blaising, Julie; Michelet, Maud; Manuel, Rachel; Parent, Romain; Bartosch, Birke; Zoulim, Fabien; Ruggiero, Florence; Pécheur, Eve-Isabelle.
; 19(5)2017 05.
Artigo em Inglês | MEDLINE | ID: mdl-27930836
CLEC4M-positive and CD81-negative Huh7 cells are not susceptible to JFH-1 HCVcc infection but mediate transinfection.
Hepatoma polarization limits CD81 and hepatitis C virus dynamics.
Tandem overexpression of five human factors renders murine hepatocytes susceptible to hepatitis C virus.
Neglected but Important Role of Apolipoprotein E Exchange in Hepatitis C Virus Infection.
Hepatitis C virus utilizes VLDLR as a novel entry pathway.
A genetically humanized mouse model for hepatitis C virus infection.
Nuclear receptors control pro-viral and antiviral metabolic responses to hepatitis C virus infection.
Productive hepatitis C virus infection of stem cell-derived hepatocytes reveals a critical transition to viral permissiveness during differentiation.
N-Myc Downstream-Regulated Gene 1 Restricts Hepatitis C Virus Propagation by Regulating Lipid Droplet Biogenesis and Viral Assembly.
Apolipoprotein E, but Not Apolipoprotein B, Is Essential for Efficient Cell-to-Cell Transmission of Hepatitis C Virus.