Hepatitis b virus

The hepatitis B virus (HBV), is a DNA virus that consists of a core and a surface. There are numerous genotypes (A-H). Genotypes A and B respond better to interferon-alpha than genotypes C and D.

The nucleus contains a partially circular double-stranded DNA and is associated with a protein P, which has domains for polymerase, reverse transcriptase and RNAse. Genome and P protein are packed in a capsid formed from the HBc protein. The envelope contains 3 variants of the HBs protein:LHBs, MHBs, SHBs. The virus enters the hepatocytes via a bile acid co-transporter (HBV receptor) and replicates in the nuclei of infected cells. They serve to absorb the virus at its host cell and subsequently to penetrate into the cell interior.

The virus occurs worldwide. Incubation period (ICZ): 2-6 months. Hepatitis course often icteric! Acute course with healing: 90-99% lethality in fulminant hepatitis <1%. Chronically active or chronically persistent hepatitis: 1-10% of all cases in children and adults. Possible consequences: cirrhosis of the liver and primary hepatocellular carcinoma.

Note: The hepatitis B genotypes (A1, A2, B1-B4, C1-C7, D1-D7, E, G, F1-F4, H) determine the response to interferon therapy. Genotypes A and B respond better to interferon therapy than genotypes C and D. Genotype determination by genotype-specific DNA probe or sequence analysis.

Virus components in diagnostics:

HBV-DNA

Surface Antigen (HBsAg) - Protein structure

Envelope antigen (HBeAg) - protein structure, corresponds to the secretory form of HBcAg

Core antigen (HBcAg) - Protein structure

Humans are the only known reservoir of HBV. HBV used to be primarily parenterally transmitted, typically through contaminated blood or blood products. Routine testing of blood donors for hepatitis B surface antigen (HBsAg) has virtually eliminated the previously common posttransfusion transmission; however, transmission through contaminated needles is still common in drug addicts. The risk of HBV infection is generally higher in dialysis patients and oncological patients, as well as among staff in medical facilities.

Furthermore, the virus can spread through contact with mucous membranes or other body fluids (e.g. between intimate partners, both heterosexual and homosexual, and in closed psychiatric or prison settings). However, infectivity is lower than that of the hepatitis A virus, and transmission routes often remain unexplained. Sexual transmission has dominated for years in industrialised countries and is estimated to account for 65% of new infections.

Children of an infected mother have a 70 - 90% risk of acquiring hepatitis B during birth (neonatal hepatitis B virus infection). Earlier diaplacental transmission is also possible, but rather rare. Perinatal infections are almost always subclinical, but lead to chronic hepatitis B in 80-90% of cases.

To what extent insect bites play a role in transmission is not clear. Many cases of acute hepatitis B occur sporadically and without a known source of infection.

The incubation period for hepatitis B infection is 6 weeks to 6 months; inapparent or subclinical courses are common (about 6 inapparent cases to 1 manifest disease). The icterus is usually preceded by a prodromal stage with general feeling of illness, vomiting and nausea. The icteric phase lasts 2-4 weeks, the recovery stage also lasts several weeks. The hepatitis B virus causes acute and chronic hepatitis and contributes to the development of hepatocellular carcinomas. With about 350 million chronically HBV-infected people worldwide, this virus is a very important human pathogenic agent.

Supplementary laboratory parameters: liver enzymes (GPT>GOT) ↑, Bilirubin↑, AP, GGT increased only initially and decreased in the case of cholestasis, serum ants ↑, gamma-Globuline↑, liver synthesis parameters (CHE, albumin, quick value) only in the case of fulminant course.

Immunization option:Active vaccination with genetically engineered hepatitis B adsorbate vaccine: Vaccination schedule: 0-1-6 months. Recommended vaccination for all infants and toddlers. Part of the regular vaccination calendar. After a successful vaccination, i.e. Anti-HBs>100IE/l, no further booster vaccinations are generally necessary.

1. Neumeister B (2018) Hepatitis viruses. In: Neumeister B et al. (Eds) Clinical guide to laboratory diagnostics. Elsevier GmbH S. 653-656
2. Schnitzler P et al (2019) Hepadnaviridae. In: Hof H, Schlüter D, Dörries R, published by Duale Reihe Medizinische Mikrobiologie. 7th, completely revised and extended edition. Stuttgart: Thieme S 273-274