Virion structure and unique genome
The hepatitis B virus is spherical in shape. Externally, it is covered by a lipoprotein envelope, underneath which lies an icosahedral core (nucleocapsid) consisting of 180 protein subunits.
The HBV genome has an unusual structure. It is a double-stranded circular DNA whose strands are asymmetric:
- Minus strand — complete, carries genetic information (contains 4 genes: P, C, S, X) and is covalently linked to the DNA polymerase enzyme.
- Plus strand — shortened by 1/3 of its length.
Upon entering the cell, viral DNA polymerase extends the plus strand, converting the genome into a complete double-stranded structure.
Viral antigen profile
Viral antigens play a key role in diagnostics and understanding the stage of the disease:
- HBsAg (surface). Located in the virion envelope, consists of glycoproteins (preS1, preS2, S). Historically known as the “Australia antigen”. It can circulate in the blood both as part of whole virions and as empty subviral particles. Stimulates the production of protective virus-neutralizing antibodies (anti-HBs).
- HBcAg (core). Internal nucleocapsid protein. In free form, it is not detectable in the blood; it can only be identified in liver biopsy specimens.
- HBeAg. A derivative of the HBc antigen. Its appearance in the blood is a precise marker of active viral replication and high patient infectivity.
- HBxAg. A transactivator protein. Its accumulation is associated with the risk of developing hepatocellular carcinoma (liver cancer) because it blocks the p53 cellular protein, which suppresses tumor growth.
Life cycle and forms of infection
The incubation period lasts from 3 to 6 months. The virus enters the hepatocyte via endocytosis, using serum albumin as a bridge between cell receptors and the preS2 antigen.
Further development can follow two pathways:
- Integrative infection (viral carriage). Viral DNA integrates into the cell chromosome (provirus). Only HBsAg is synthesized. This particular form increases the risk of malignant transformation (cancer).
- Productive infection. Active assembly of new virions takes place. A feature of this process: pregenomic RNA is synthesized on the DNA minus-strand template, and then viral DNA polymerase creates a new DNA minus strand based on it via reverse transcription. This is accompanied by the release of HBe antigen into the blood.
Immunopathogenesis and outcomes
Hepatitis B virus itself lacks cytopathic action — it does not destroy infected hepatocytes. Liver damage is exclusively immune-mediated.
Viral peptides in complex with class I MHC appear on the membrane of the infected cell. Cytotoxic CD8+ T lymphocytes recognize this “tag” and destroy the cell. Massive lysis of hepatocytes leads to inflammation and the development of jaundice.
Outcomes of infection:
- Recovery with the formation of lifelong immunity (virus elimination is ensured by anti-HBs and cellular response).
- Chronification (in 5–10% of cases in adults and 50–90% of cases when infected during the first year of life).
- Fulminant form (about 1% of cases, accompanied by high mortality).
Epidemiology and prevention
The infection is widespread globally. The reservoir consists of over 400 million virus carriers and sick individuals.
Routes of transmission:
- Parenteral (medical procedures, blood transfusion, tattoos).
- Natural (sexual, contact-household via razors and toothbrushes, vertical transmission from mother to child).
For specific prophylaxis, a recombinant engineered vaccine containing purified HBs antigen is used. Newborns are vaccinated in the first 24 hours of life. Immunity persists for at least 7 years.
To memorize the clinical role of antigens: “S” (Surface) — Outside (protective antibodies), “C” (Core) — Hidden (only in the liver), “E” (Emission) — Leaving/Replicating (marker of infectivity), “X” — X-factor (liver cancer).
Class and exam questions
Why is hepatitis B virus called reverse-transcribing?
During replication in the cytoplasm, viral DNA polymerase (reverse transcriptase) synthesizes a new DNA strand using the intermediate pregenomic RNA template.
How does the virus itself destroy liver cells?
The virus does not have a direct cytopathic effect. Hepatocytes die due to an attack by their own cytotoxic CD8+ T lymphocytes, which recognize viral antigens on the surface of infected cells.
Can HBc antigen be detected in a routine blood test?
No, in free form it is not found in the blood. It is detected only inside hepatocytes during liver biopsy examination.
What does the appearance of anti-HBe in the blood indicate?
This is the process of seroconversion (disappearance of HBe antigen and appearance of antibodies against it). It indicates the activation of T-helper cells and is a favorable prognostic sign.
What else to study on this topic
- Detailed mechanism of virion assembly in the cytoplasm and the role of pregenomic RNA
- Decoding serological profiles: interpretation of markers in acute and chronic phases
- Molecular mechanism of HBx antigen binding to the p53 protein and carcinogenesis
- Mechanisms of viral immune evasion and reasons for the high frequency of chronification in infants
- Function of inactivated subviral particles in the bloodstream
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