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 diagnostics:
- 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) has high immunogenicity and protein kinase activity (phosphorylates proteins). It ensures an adequate immune response during the cyclic course of the disease.
- HBeAg (infectivity antigen) is closely associated with HBcAg. It is a crucial marker of active viral replication and high activity of the DNA polymerase enzyme.
- HBxAg is the least studied component. It activates viral protein synthesis and, presumably, triggers malignant transformation of liver cells.
The virus is prone to mutational variability, which is often the cause of an acyclic course of the disease. In addition to the "wild-type" (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 greatest epidemiological hazard.
Approximately 4 million new cases of acute hepatitis B are registered worldwide each year. According to WHO data, there are more than 350 million virus carriers, and about 1 million people die annually from the consequences of chronic infection.
Susceptibility to the virus is extremely high, especially in infants under one year of age. The main risk groups include:
- Medical personnel handling 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 of Asia and Africa), up to 10% of the population is infected. Transmission there often occurs in childhood, 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 develops, where 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 proceeds in anicteric form in 70% of cases. With an insufficient response, the infection generalizes.
The interaction of the virus with the cell can follow two pathways:
- Replicative form — the virus actively replicates 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 the key mechanism for the development of persistent forms of infection and primary hepatocellular carcinoma (HCC).
Serological diagnostics
Determining the stage of the disease is based on identifying 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.
Briefly: answers to topical questions
What morphological changes in hepatocytes are characteristic of acute viral hepatitis B?
Acute viral hepatitis B is characterized by dystrophic changes, necrosis, and apoptosis of hepatocytes. The following morphological features are observed:
- Dystrophy — focal protein (hydropic and ballooning) as well as fatty dystrophy.
- Necrosis — spotty (spotty necrosis), confluent (in zone 3 of the acinus), periportal, centrilobular, bridging, submassive, and massive.
- Apoptosis — formation of apoptotic bodies (Councilman bodies).
- Polymorphism — moderate polymorphism and the appearance of regenerating cells.
Additionally, cholestasis (cholestasis) may be observed in the liver tissue.
What transmission routes are characteristic of the hepatitis B virus?
The hepatitis B virus is characterized by a parenteral transmission mechanism. The following routes of infection are distinguished:
- Parenteral — via blood, its products, and body secretions; possible during injections and blood transfusions.
- Sexual.
- Vertical — transmission of infection from an infected mother; infection can occur transplacentally and intrapartum, most commonly manifesting in the third trimester of pregnancy.
What extrahepatic systemic manifestations are characteristic of viral hepatitis B?
Viral hepatitis B is characterized by immunologically mediated extrahepatic manifestations. These include:
- Vascular manifestations — vasculitis, polyarteritis nodosa.
- Articular manifestations — polyarthritis, arthralgia.
- Renal manifestations — glomerulonephritis.
- Neurological manifestations — peripheral polyneuropathy.
- Skin manifestations — urticarialike exanthema, maculopapular rash.
These manifestations are driven by immune complex reactions and delayed-type hypersensitivity reactions, and they can mask the underlying liver pathology.
What macroscopic changes in the liver are observed in the fulminant form of hepatitis B (massive progressive necrosis)?
In the fulminant form of viral hepatitis, leading to rapid hepatocyte destruction and massive progressive liver necrosis, the macroscopic picture of yellow atrophy is described:
- the liver is reduced in size;
- the capsule is wrinkled due to the reduction in parenchymal volume;
- the consistency is flabby, and the tissue "collapses" and fails to hold its shape;
- on cross-section, the liver tissue is mottled, predominantly yellow in color.
What outcomes and complications are possible in chronic viral hepatitis B?
The following outcomes and complications are possible in chronic viral hepatitis B:
- Restoration of hepatic tissue structure.
- Liver cirrhosis — possible in severe courses of chronic hepatitis.
- Hepatocellular carcinoma — an etiological link with HCC development has been proven for hepatitis B virus; viral genome integration is considered a mechanism for the development of primary hepatocellular carcinoma.
How to remember the antigens: S (Surface) — Outside (surface), C (Core) — Core (nuclear), E (rEplication) — rEplication (activity), X — unknown (X-factor, cancer).
Class and exam questions
Does the hepatitis B virus destroy liver cells directly?
No, the virus lacks direct cytotoxicity. Hepatocyte death occurs due to an attack by the host's own immune system reacting to viral proteins.
What is a Dane particle?
This is a complete, infectious hepatitis B virion with a diameter of 42–45 nm. It consists of a nucleocapsid and two lipoprotein envelopes.
Which marker indicates active viral replication?
The main marker of active replication and high activity of the DNA polymerase enzyme is HBeAg (infectivity antigen).
What is the danger of the integrative form of infection?
In this form, viral DNA integrates into the hepatocyte genome, leading to an acyclic (chronic) course of the disease and a high risk of developing primary liver cancer.
What else to study on this topic
- Mechanisms of HBV mutational variability ("Senegal" strain and HBVe-negative variant)
- Detailed characteristics of pre-S1 and pre-S2 proteins and their role in adsorption
- The role of the mononuclear phagocyte system in the pathogenesis of hepatitis B
- Formation of post-infection immunity in convalescents
- Association of viral hepatitis B with the development of liver cirrhosis
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