Author information
1
Inserm, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, 67000, Strasbourg, France.
2
Université de Strasbourg, 67000, Strasbourg, France.
3
Pôle Hépato-digestif, Institut Hospitalo-universitaire, Hôpitaux Universitaires de Strasbourg, 67000, Strasbourg, France.
4
Institut Universitaire de France, Paris, France.
Abstract
Chronic hepatitis B virus (HBV) infection is a major cause of advanced liver disease and hepatocellular carcinoma (HCC) world-wide (1). Current antiviral treatments control HBV replication and reduce progressive liver disease. However, viral cure is rarely achieved and patients still remain at risk for HCC (1). The pathogenesis of HBV-induced HCC is thought to be multifactorial with both direct and indirect mechanisms (2): HBV-related HCCs can also arise in non-cirrhotic livers, supporting the notion that HBV plays a direct role in liver transformation by triggering both common and etiology specific oncogenic pathways in addition to stimulating the host immune response and driving liver chronic necro-inflammation.