Hepatitis D virus (HDV), also known as hepatitis delta virus, is a defective, hepatotropic pathogenic agent. The life cycle of HDV requires the hepatitis B surface antigen (HBsAg) provided by hepatitis B virus (HBV).1 Like HBV, HDV is transmitted by the parenteral route through infectious body fluids; intravenous drug users are at highest risk for infection because of contaminated syringes.2,3 Key features of the infection are its unique biologic characteristics and ominous medical effect. Clinical studies have shown that chronic hepatitis D is the most severe and progressive form of viral hepatitis in humans.2 The infection is ubiquitous, yet 40 years after it was identified, the prevalence remains undetermined in many parts of the world. In three recent meta-analyses, the number of HDV-infected persons worldwide ranged from 12 million to 72 million, underscoring the heterogeneity of current epidemiologic data.3 Valid therapies to cure hepatitis D are an urgent need, and new therapeutic strategies are in development.

Liens