Hepatitis B virus-infected hepatocytes promote the secretion of collagen VI to the extracellular matrix.

Fiche publication

Date publication

juillet 2025

Journal

Scientific reports

Auteurs

Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas , Dr LUPBERGER Joachim , Pr PESSAUX Patrick , Dr VERRIER Eloi

Tous les auteurs :
Virzì A, Boulahtouf Z, Moehlin J, Girard L, Meiss-Heydmann L, Bach C, Gerges E, Durand SC, Oudot MA, Roca Suarez AA, Popp O, Ramberger E, Mertins P, Felli E, Pessaux P, Schuster C, Verrier ER, Baumert TF, Lupberger J

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/40640389

Résumé

Chronic hepatitis B virus (HBV) infection is a global health problem as it is the major cause of liver fibrosis and its complications cirrhosis and hepatocellular carcinoma. The role of virus-host interactions in liver fibrosis and progression to cancer remains poorly understood. Here we show that HBV infection of permissive cells trigger pathways relevant for extracellular matrix (ECM) remodeling, which is a hallmark of liver fibrosis. We demonstrate that collagen VI (ColVI) is secreted from infected cells and induces a profibrotic phenotype in patient-derived myofibroblasts and identified HBV-induced AKT signaling as a driver of ColVI expression in HBV-infected cells. Consistently, ColVI is upregulated in the liver of HBV patients with fibrosis. Our results suggest a role of ColVI as a driver of HBV-associated liver disease and highlight the potential of ColVI as a biomarker candidate and therapeutic target in HBV-infected patients.