Structure and Molecular Virology
Francesco Negro
Divisions of Clinical Pathology and Gastroenterology and Hepatology, University Hospital, Geneva, Switzerland
Search for more papers by this authorFrancesco Negro
Divisions of Clinical Pathology and Gastroenterology and Hepatology, University Hospital, Geneva, Switzerland
Search for more papers by this authorHoward C. Thomas BSc, PhD, FRCP, FRCPath, FMedSci
Emeritus Professor of Hepatology, Department of Medicine, Imperial College London, London, UK
Search for more papers by this authorAnna S.F. Lok MD
Alice Lohrman Andrews Research Professor in Hepatology, Director of Clinical Hepatology, Professor of Internal Medicine, Associate Chair for Clinical Research, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI, USA
Search for more papers by this authorStephen A. Locarnini MBBS, BSc(Hons), PhD, FRCPath
Head, Research & Molecular Development, Victorian Infectious Diseases Reference Laboratory, Melbourne, VIC, Australia
Search for more papers by this authorArie J. Zuckerman MD, DSc, FRCP, FRCPath, FMedSci
Emeritus Professor of Medical Microbiology, Formerly Principal and Dean, Royal Free Hospital School of Medicine
Search for more papers by this authorSummary
Hepatitis D virus (HDV) is a defective RNA infectious agent needing the presence of hepatitis B virus (HBV) to complete its life cycle. HDV is present worldwide, but the distribution pattern is not uniform. Different viral strains are classified into eight genotypes found in specific geographical areas and often associated with severe disease outcome. The HDV particle is composed of an envelope, provided by the helper HBV, surrounding the 1.7 kB RNA genome and the HDV antigen. Replication occurs in the hepatocyte nucleus via a rolling-circle mechanism that leads to a full-length, complementary RNA as replication intermediate. Since HDV does not possess the encoding capability for a RNA polymerase, replication is brought about by cellular polymerases.
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