Etiology and Antigenic Structure
The causative agent of the disease is the Hepatitis B virus (HBV). Its complete infectious form is called the Dane particle. It has a diameter of 42–45 nm and consists of a nucleocapsid, as well as inner and outer lipoprotein envelopes.
The virus has a complex antigenic structure, knowledge of which is essential for accurate diagnosis:
- HBsAg (surface or "Australian" antigen) — forms the outer envelope. It contains pre-S1 and pre-S2 proteins, which are responsible for virion attachment to the cell and its penetration inside.
- HBcAg (core antigen) — possesses high immunogenicity and protein kinase activity (phosphorylates proteins). It ensures an adequate immune response during a cyclic course of the disease.
- HBeAg (infectivity antigen) — closely associated with HBcAg. It is a critical marker of active virus replication and high activity of the DNA polymerase enzyme.
- HBxAg — the least studied component. It activates viral protein synthesis and presumably triggers malignant transformation of liver cells.
Fthe virus is prone to mutational variability, which often causes an acyclic course of the disease. In addition to the "wild" (normal) strain, mutant forms exist. For example, the "Senegal" variant lacks detectable antibodies to HBcAg, while the HBVe (-) variant lacks HBeAg.
Epidemiology and Risk Groups
The primary mechanism of transmission is parenteral. The virus is present in blood, semen, saliva, vaginal secretions, menstrual blood, and breast milk. Patients with chronic hepatitis B pose the highest epidemiological risk.
Approximately 4 million new cases of acute hepatitis B are registered worldwide each year. According to WHO data, there are over 350 million virus carriers, and about 1 million people die annually from complications of chronic infection.
Susceptibility to the virus is extremely high, especially in infants under one year of age. Main risk groups include:
- Healthcare workers in contact with biological materials (surgeons, obstetrician-gynecologists, laboratory technicians, pathologists).
- Hemodialysis patients and recipients of frequent blood transfusions.
- People who inject drugs.
- Individuals with multiple sexual partners, a history of STIs, and men who have sex with men.
- Children born to infected mothers.
In endemic regions (developing countries in Asia and Africa), up to 10% of the population is infected. Infection often occurs in childhood there, and up to 25% of such patients eventually die from liver cancer.
Pathogenesis and Clinical Forms
The hepatitis B virus itself does not possess direct cytotoxicity — it does not destroy hepatocytes directly. Tissue damage occurs due to immune mechanisms: cross-sensitization arises, in which the immune system attacks its own cells due to similarities between hepatocyte and viral antigens.
Upon entering the body, the virus circulates in the blood (primary viremia), and then accumulates in the liver (in hepatocytes and Kupffer cells) and organs of the mononuclear phagocyte system (bone marrow, spleen, lymph nodes). If the primary immune response is adequate, the virus is eliminated, which in 70% of cases proceeds in an anicteric form. With an insufficient response, the infection generalizes.
Interaction of the virus with the cell can follow two pathways:
- Replicative form — the virus actively multiplies without integrating into the genetic apparatus of the hepatocyte.
- Integrative form — a fragment or the entire viral genome is integrated into the human cell DNA. This is a key mechanism in the development of persistent forms of infection and primary hepatocellular carcinoma (HCC).
Serological Diagnostics
Determining the stage of the disease is based on detecting specific antigens and antibodies in the patient's blood.
- Markers of active ongoing infection: HBsAg, HBeAg, specific viral DNA, the DNA polymerase enzyme, and IgM class antibodies to the core antigen (anti-HBc IgM) are detected.
- Markers of resolved infection (recovery): protective anti-HBs and anti-HBc IgG antibodies appear in the blood.
- Sign of potential chronicity: prolonged persistence of HBsAg and HBeAg in the bloodstream.