Details

Autor(en) / Beteiligte

• Bell, Sally J
• Locarnini, Stephen A
• Thompson, Alexander J. V
• Hayden, Frederick G
• Richman, Douglas D
• Whitley, Richard J

Titel

Hepatitis B Virus

Ist Teil von

• Clinical Virology, 2009, p.673-707

Ort / Verlag

Washington, DC: ASM Press

Erscheinungsjahr

2009

Quelle

Wiley Online Library All Obooks

Beschreibungen/Notizen

• The goal of chemoprevention for chronic hepatitis B (CHB) must be to improve the quality and the outcomes of care for patients with CHB. This chapter focuses on the human hepatitis B virus (HBV). HBV is an enveloped, 3.2‐kb double‐stranded DNA virus which may be classified into eight major genotypes (A to H) based on a nucleotide diversity of 8% or more. HBV infection is usually diagnosed using specific serologic assays. During the course of infection, the viral proteins HBsAg, HBcAg, and HBeAg stimulate the immune system to produce the corresponding antibodies anti‐HBs, anti‐HBc, and anti‐HBe. Once HBV DNA becomes detectable, replication increases exponentially to peak at levels of >10 12 copies/ml in serum. In adult‐acquired acute HBV infection, in which the host is able to control the virus, viral replication then declines, preceding the onset of clinical hepatitis. The risk of fulminant hepatic failure (FHF) may be higher in patients acutely infected with basal core promoter (BCP) or precore variants, coinfected with other hepatitis viruses, or with underlying liver disease. The major complications of CHB are cirrhosis, hepatic decompensation, and HCC. The current challenge in CHB is to identify patients at risk for progressive liver disease, so that therapy may be offered early to alter the natural history. The major risk factors for progression to cirrhosis are viral load, the presence of fibrosis on liver biopsy, and elevated serum alanine aminotransferase (ALT).