Definition and epidemiological significance
Viral hepatitis B is an anthroponotic infectious disease with contact and vertical transmission mechanisms, characterized by cyclic parenchymal hepatitis, jaundice, and a potential for chronicity. Its anthroponotic nature means that the exclusive reservoir of infection is humans.
According to WHO data, approximately 820,000 people died from hepatitis B in 2019. More than 2 billion people worldwide have serological evidence of past or current infection. Meanwhile, less than half of children globally receive vaccination, which has an efficacy and safety profile of about 95%.
Sources and transmission routes
The source of infection includes patients with acute and chronic forms, as well as virus carriers. The virus is found in blood, semen, saliva, tears, urine, feces, vaginal secretions, cerebrospinal fluid, and cord blood, but blood and semen present the greatest epidemiological hazard due to the high concentration of the pathogen.
The transmission mechanism is parenteral. The following routes are distinguished:
- Natural: sexual (unprotected sexual intercourse), household, perinatal (from mother to fetus).
- Artificial non-medical: intravenous drug use, manicures, pedicures, tattoos, and piercings with contaminated instruments (80–100% infection risk).
- Artificial medical: blood and blood component transfusion, hemodialysis, organ transplantation.
Vertical (transplacental) transmission depends on the gestational age: in the 1st–2nd trimesters, the risk is 3–6%, reaching 100% in the 3rd trimester if the mother is HBsAg- and HBeAg-positive.
Clinical presentation of acute hepatitis B
The disease is divided into acute (up to 6 months) and chronic (more than 6 months). Duration is determined by the persistence of HBsAg in the blood. Acute hepatitis B proceeds through four periods.
- Incubation period — up to 6 months, averaging about 80 days.
- Pre-icteric period — from 7 days to 3 months. Asthenovegetative syndrome (80%) predominates: weakness, fatigue, sleep disturbances, headache; dyspeptic syndrome (40%): decreased appetite, nausea, heaviness in the right upper quadrant. Characteristic features include hepatomegaly (80%), splenomegaly (20%), and dark urine (100%). Laboratory findings: ALT and AST elevation more than 10-fold, elevated total bilirubin at the expense of the conjugated fraction.
- Icteric period — about 6 weeks. The condition does not improve, with worsening weakness and anorexia. ALT/AST are elevated 50–60 fold, albumin and prothrombin index decrease, hemorrhagic syndrome and fever are possible. Blood tests show leukopenia with lymphocytosis.
- Convalescence period — from 3 months to a year or more; gradual recovery of clinical and biochemical parameters.
The typical icteric form occurs in only 20–30% of cases. Anicteric, mild, and inapparent subclinical forms are registered much more frequently, manifesting as non-specific weakness, bitter taste in the mouth, and heaviness in the right upper quadrant, which complicates timely diagnosis.
Serological markers and their interpretation
Laboratory diagnostics are based on ELISA (antigens and antibodies) and PCR (viral DNA).
- HBsAg — surface antigen, the first marker of infection; appears during the incubation period. Persistence for more than 6 months indicates chronicity. Paradoxically, in severe cases, its level can be very low.
- HBeAg — a marker of active replication and high infectivity; circulates only together with HBsAg. Persistence for more than 3 months indicates chronicity.
- HBcAg — not detected in the blood, found only in hepatocytes during biopsy.
- Anti-HBc IgM — the main marker of acute hepatitis B, appears at the onset of jaundice, circulates for up to 5 months; the only marker in the "window period".
- Anti-HBc IgG — persists for life, indicates contact with the virus.
- Anti-HBe — a sign of the onset of convalescence or low replication in the chronic form; indicates viral elimination.
- Anti-HBs — protective antibodies, a marker of recovery and post-vaccination immunity; appear 3–4 months after HBsAg clearance.
There are mutually exclusive markers: HBsAg and anti-HBs, HBeAg and anti-HBe cannot be detected simultaneously—their concurrent detection requires re-testing. The most reliable method is the detection of viral DNA by PCR, which allows evaluation of the virus genotype, viral load, and treatment efficacy.
Algorithm for interpreting the serological profile
- Acute hepatitis B: positive anti-HBc IgM (100%).
- Chronic hepatitis B: HBsAg+, anti-HBc IgG+, viral DNA+; anti-HBs are absent.
- Past infection: anti-HBs+, anti-HBc IgG+, viral DNA is negative.
- Post-vaccination immunity: isolated positive anti-HBs (the vaccine contains only purified HBsAg).
- Virus carrier state: HBsAg+, anti-HBc IgG+ in the absence of clinical and biochemical signs of hepatitis.
Principles of treatment
Treatment of acute hepatitis B is carried out in an infectious diseases hospital with mandatory admission. In 90–95% of cases, spontaneous viral elimination occurs, so specific antiviral therapy is not always required. When indicated, nucleoside and nucleotide analogues are used: lamivudine, entecavir, telbivudine, tenofovir — one drug at a standard dose once daily.
Duration of therapy is at least 3 months, until seroconversion is achieved (disappearance of HBeAg and appearance of anti-HBe), along with a reduction of HBsAg and viral load to undetectable levels.
Key points
- Hepatitis B is an anthroponotic infection with a parenteral transmission mechanism; blood and semen pose the greatest hazard.
- Chronicity is diagnosed when HBsAg or viral DNA persists for more than 6 months.
- Anicteric and subclinical forms are tens of times more common than the typical icteric form.
- Anti-HBc IgM is the main marker of acute infection and the only marker of the "window period".
- HBeAg reflects active replication and high infectivity of the patient.
- Anti-HBs is a marker of recovery and post-vaccination immunity.
- PCR detection of HBV DNA is the most reliable method of diagnosis and treatment monitoring.
- Therapy with nucleoside analogues (entecavir, tenofovir, etc.) is carried out until seroconversion and suppression of viral load.