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HBeAg-Negative/Anti-HBe-Positive Chronic Hepatitis B: A 40-Year-Old History
Ferruccio Bonino 1 , Piero Colombatto 2 , Maurizia R Brunetto 1 2
Affiliations
Affiliations
1
Institute of Biostructure and Bioimaging, National Research Council, Via De Amicis 95, 80145 Naples, Italy.
2
Hepatology Unit and Laboratory of Molecular Genetics and Pathology of Hepatitis Viruses, Reference Center of the Tuscany Region for Chronic Liver Disease and Cancer, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy.
PMID: 36016312 PMCID: PMC9416321 DOI: 10.3390/v14081691
Free PMC article
Abstract
Hepatitis B "e" antigen (HBeAg) negative chronic hepatitis B (CHB), 40 years since discovery in the Mediterranean area, has become the most prevalent form of HBV-induced liver disease worldwide and a major health care burden caused by HBV infection. A great deal of knowledge accumulated over the last decades provides consistent evidence on the bimodal dynamics of the expression of structural and non-structural forms of the viral core proteins which associate with different virologic and clinic-pathologic outcomes of HBV infection. In absence of serum HBeAg, the presence and persistence of HBV replication causes and maintains virus-related liver injury. Thus, in clinical practice it is mandatory to screen HBV carriers with HBeAg-negative infection for the early diagnosis of HBeAg-negative CHB since antiviral therapy can cure HBV-induced liver disease when started at early stages.
Keywords: HBV; HBV-DNA; HBeAg; HBeAg defective HBV mutants; anti-HBe; chronic hepatitis B.
Conflict of interest statement
F.B.: Advisory Board and Speakers Bureau for Abbott, DiaPro, DiaSorin, Echosens, Fujirebio, and Roche. M.R.B.: Advisory Board and Speakers’ Bureau AbbVie, Gilead, Janssen, EISAI-MSD, Roche.
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