title: [Natural history and clinical manifestations of chronic hepatitis B virus].
abstract: Hepatitis B virus (HBV) infection is a serious public health problem worldwide. In the last few decades, major advances have been achieved that have contributed to greater understanding of the natural history and clinical manifestations of this infection. The fluctuation between viral replication and the host's immune response has implications in the pathogenesis and progression of the hepatic lesion. In immunocompetent adults, most HBV infections resolve spontaneously in contrast with progression to chronic infection in most infants. Patients with chronic hepatitis due to HBV or chronic hepatitis B can present at four phases: 1) the immune tolerance phase, 2) HBeAg-positive chronic hepatitis B, 3) inactive HBsAg carrier state, and 4) HBeAg-negative chronic hepatitis. HBeAg-positive or -negative chronic hepatitis can progress to cirrhosis, liver failure and hepatocellular carcinoma. Progression to these complications is more frequent in HBeAg-negative forms, associated with mutations that affect the pre-core region and maintain active viral replication. Risk factors are HBV-DNA positive serum levels, an increase in serum transaminase levels and some genotypes. These factors highlight the need to evaluate and monitor all HBV carriers to identify those who could benefit from early antiviral treatment, thus avoiding progression to more advanced forms of liver disease. These measures could improve prevention and treatment of hepatitis B.
authors.affiliation: Clínica Universitária de Gastrenterologia, Faculdade de Medicina de Lisboa e Hospital de Santa Maria, Lisboa, Portugal. hsm.cm@mail.telepac.pt
authors.forename: Miguel
authors.initials: M
authors.lastname: Carneiro de Moura
authors.forename: Rui
authors.initials: R
authors.lastname: Marinho
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use; D002353:Carrier State; D004279:DNA, Viral / Q000097:blood / Q000235:genetics; D018450:Disease Progression; D005838:Genotype; D005921:Glomerulonephritis / Q000209:etiology; D006509:Hepatitis B / Q000150:complications / Q000188:drug therapy / Q000453:epidemiology; D006513:Hepatitis B e Antigens / Q000032:analysis / Q000502:physiology; D006515:Hepatitis B virus / Q000235:genetics* / Q000502:physiology; D019694:Hepatitis B, Chronic / Q000150:complications / Q000453:epidemiology* / Q000276:immunology / Q000517:prevention & control / Q000821:virology; D006801:Humans; D007121:Immunocompetence; D007223:Infant; D008103:Liver Cirrhosis / Q000209:etiology / Q000517:prevention & control; D010488:Polyarteritis Nodosa / Q000209:etiology; D011693:Purpura / Q000209:etiology; D019562:Viral Load; D014779:Virus Replication
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006513:Hepatitis B e Antigens