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Review
. 2011 Mar 28;17(12):1543-8.
doi: 10.3748/wjg.v17.i12.1543.

Pathogenesis of occult chronic hepatitis B virus infection

Affiliations
Review

Pathogenesis of occult chronic hepatitis B virus infection

Rocio Aller de la Fuente et al. World J Gastroenterol. .

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

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References

    1. Lee WM. Hepatitis B virus infection. N Engl J Med. 1997;337:1733–1745. - PubMed
    1. Bréchot C, Hadchouel M, Scotto J, Fonck M, Potet F, Vyas GN, Tiollais P. State of hepatitis B virus DNA in hepatocytes of patients with hepatitis B surface antigen-positive and -negative liver diseases. Proc Natl Acad Sci USA. 1981;78:3906–3910. - PMC - PubMed
    1. Thiers V, Nakajima E, Kremsdorf D, Mack D, Schellekens H, Driss F, Goudeau A, Wands J, Sninsky J, Tiollais P. Transmission of hepatitis B from hepatitis-B-seronegative subjects. Lancet. 1988;2:1273–1276. - PubMed
    1. Wang JT, Wang TH, Sheu JC, Shih LN, Lin JT, Chen DS. Detection of hepatitis B virus DNA by polymerase chain reaction in plasma of volunteer blood donors negative for hepatitis B surface antigen. J Infect Dis. 1991;163:397–399. - PubMed
    1. Loriot MA, Marcellin P, Bismuth E, Martinot-Peignoux M, Boyer N, Degott C, Erlinger S, Benhamou JP. Demonstration of hepatitis B virus DNA by polymerase chain reaction in the serum and the liver after spontaneous or therapeutically induced HBeAg to anti-HBe or HBsAg to anti-HBs seroconversion in patients with chronic hepatitis B. Hepatology. 1992;15:32–36. - PubMed

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