ArticleClinical and molecular hepatology2014
Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers.
Article in Clinical and molecular hepatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Near extinction of the HBV quasispecies driven by the hard selective sweep in chronic hepatitis B.mBio · 2025Article
- Role of S protein transmembrane domain mutations in the development of occult hepatitis B virus infection.Emerging microbes & infections · 2022Article
- Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity.PloS one · 2017Article
- Article
- Genetic variation of occult hepatitis B virus infection.World journal of gastroenterology · 2016Review
- Occult hepatitis B virus infection: influence of S protein variants.Virology journal · 2016Article
- Occult hepatitis B virus infection: clearance or disguise?Clinical and molecular hepatology · 2014Article
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7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsOccult HBV infection can persist following HBsAg loss and be transmitted, but the virological features are not well defined.
methodsHere we investigated 25 Korean patients who lost HBsAg during follow up, either spontaneously or subsequent to therapy.
resultsWhereas subtype adr (genotype C) was found in 96% of HBsAg positive patients, 75 % of patients who lost HBsAg spontaneously were seemed to be infected with the ayw subtype with sequence similar to genotype D. Mutations in the major hydrophilic region (MHR) of HBsAg were found in 7 patients who lost HBsAg spontaneously. The mutations include T123S, M125I/N, C139R, D144E, V177A, L192F, and W196L, some of which have not been reported before. Functional analysis via transfection experiments indicate that the C139R and D144E mutations drastically reduced HBsAg antigenicity, while the Y225del mutation found in one interferon-treated patient impaired HBsAg secretion.
conclusionsLack of detectable HBsAg in patient serum could be explained by low level of ccc DNA in liver tissue, low antigenicity of the surface protein, or its secretion defect.
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