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World J Gastroenterol. Mar 28, 2011; 17(12): 1543-1548
Published online Mar 28, 2011. doi: 10.3748/wjg.v17.i12.1543
Pathogenesis of occult chronic hepatitis B virus infection
Rocio Aller de la Fuente, María L Gutiérrez, Javier Garcia-Samaniego, Conrado Fernández-Rodriguez, Jose Luis Lledó, Gregorio Castellano
Rocio Aller de la Fuente, Gastroenterology, Hospital Clinico Universitario Valladolid, Institute of endocrinology and Nutrition, Medical School, University of Valladolid, 47003 Valladolid, Spain
María L Gutiérrez, Service of Gastroenterology, Hospital Universitario Fundación Alcorcón, Av Budapest-1, 28922 Alcorcón, Madrid, Spain
Javier Garcia-Samaniego, Gastroenterology Department, Hospital Carlos III, c/ Sinesio Delgado, 28029 Madrid, Spain
Conrado Fernández-Rodriguez, Service of Gastroenterology, Hospital Universitario Fundación Alcorcón, Av Budapest-1, 28922 Alcorcón, Madrid, Spain
Jose Luis Lledó, Service of Gastroenterology, Hospital Universitario Fundación Alcorcón, Av Budapest-1, 28922 Alcorcón, Madrid, Spain
Gregorio Castellano, Hospital Universitario 12 de Octubre, Av de Andalucia 28041, 28039 Madrid, Spain
Author contributions: Aller de la Fuente R and Gutiérrez ML contributed towards the conception and design of the review; García-Samniego J, Fernández-Rodríguez C, Lledó JL and Castellano G contributed equally to the supportive work and supervision.
Correspondence to: Dr. Rocio Aller de la Fuente, Gastroenterology Department, Hospital Clinico Universitario Valladolid, Institute of Endocrinology and Nutrition, Medical School, University of Valladolid, Avenida Ramón y Cajal s/n., 47003 Valladolid, Spain. roaller@yahoo.es
Telephone: +34-983-420000 Fax: +34-983-420000
Received: August 6, 2010
Revised: January 22, 2011
Accepted: January 29, 2011
Published online: March 28, 2011
Abstract

Occult hepatitis B infection (OBI) is characterized by hepatitis B virus (HBV) DNA in serum in the absence of hepatitis B surface antigen (HBsAg) presenting HBsAg-negative and anti-HBc positive serological patterns. Occult HBV status is associated in some cases with mutant viruses undetectable by HBsAg assays; but more frequently it is due to a strong suppression of viral replication and gene expression. OBI is an entity with world-wide diffusion. The failure to detect HBsAg, despite the persistence of the viral DNA, is due in most cases to the strong suppression of viral replication and gene expression that characterizes this “occult” HBV infection; although the mechanisms responsible for suppression of HBV are not well understood. The majority of OBI cases are secondary to overt HBV infection and represent a residual low viremia level suppressed by a strong immune response together with histological derangements which occurred during acute or chronic HBV infection. Much evidence suggests that it can favour the progression of liver fibrosis and the development of hepatocellular carcinoma.

Keywords: Occult hepatitis B virus infection, Hepatitis B virus-DNA, Anti-HBc alone, Hepatitis B virus, Hepadnaviral hepatitis, Occult viral persistence, Primary occult infection, Secondary occult infection, Virus reactivation