1Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS-UMR 5535, Montpellier, 34293 cedex 5, France.
2Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS-UMR 5535, Montpellier, 34293 cedex 5, France. Electronic address: firstname.lastname@example.org.
3Queen Mary University of London, The Royal London Hospital, Barts Health NHS Trust, London, UK.
4Université de Paris, Cité CRI, INSERM UMR 1149, Department of Hepatology, AP-HP Hôpital Beaujon, Clichy, France. Electronic address: email@example.com.
Hepatitis delta virus (HDV), a satellite of hepatitis B virus (HBV), possesses the smallest viral genome known to infect animals. HDV needs HBV surface protein for secretion and entry into target liver cells. However, HBV is dispensable for HDV genome amplification, as it relies almost exclusively on cellular host factors for replication. HBV/HDV co-infections affect over 12 million people worldwide and constitute the most severe form of viral hepatitis. Co-infected individuals are at higher risk of developing liver cirrhosis and hepatocellular carcinoma compared to HBV mono-infected patients. As no efficient treatment, that can cure an active HDV infection, is approved to date, there is an urgent need to develop new antiviral therapies. In this review, we detail our current fundamental knowledge of HDV lifecycle and review antiviral treatments under development against this virus, outlining their respective mechanisms-of-action. Finally, we describe the antiviral effect these compounds are showing in ongoing clinical trials, discussing their promise and potential pitfalls for managing HDV infected patients.