Epidemiology and Pathogenesis
The source of infection is most often individuals with asymptomatic or subclinical forms of the disease. About 80% of all cases occur in children under 15 years of age, with a traditional seasonal peak in the summer and autumn months.
The infectious process develops sequentially:
- Entry: The virus enters via the gastrointestinal tract, enters the bloodstream, and is transported to the liver.
- Attachment: The pathogen binds to specific hepatocyte receptors and enters the cells for replication.
- Excretion: New virions return to the intestine via the bile canaliculi and are excreted into the environment.
- Injury: The virus itself has no direct cytopathic effect. Hepatocellular damage is primarily mediated by immune mechanisms, including interferons, natural killer (NK) cells, and antibodies.
Clinical Manifestations and Disease Forms
Symptomatic infection includes four consecutive periods: incubation (2 to 26 weeks), prodromal (pre-icteric with non-specific symptoms), icteric (manifest jaundice), and convalescence.
Clinical presentations are diverse:
- Typical course: Mild, cyclical, accompanied by mild jaundice, dark urine (choluria), and pale stools (acholia).
- Non-specific syndromes: Toxic, flu-like, dyspeptic, and astheno-vegetative.
- Clinical-morphological forms: Anicteric and subclinical variants predominate in most individuals. Rarely (0.1% of cases), a fulminant form develops with massive hepatic necrosis.
Pathology and Diagnostics
During the peak of the disease, characteristic morphological changes are identified in liver tissue:
- Degeneration: Pronounced hydropic degeneration of hepatocytes.
- Inflammation: Lymphomacrophagic infiltrates localized predominantly in the periportal zones of lobules and portal tracts.
- Alteration: Coagulative and liquefactive necrosis, alongside the formation of apoptotic bodies.
- Outcomes: Focal intralobular sclerosis and fibrosis of portal tracts may form at the sites of damaged cells.
To confirm the diagnosis, laboratory methods are used: detection of specific anti-HAV IgM antibodies via enzyme-linked immunosorbent assay (ELISA) and viral RNA detection using molecular methods.
Complications, Outcomes, and Prevention
In 90% of cases, the disease resolves favorably with complete recovery and the development of lifelong post-infection immunity mediated by anti-HAV IgG.
Remaining patients may experience residual phenomena:
- Astheno-vegetative (post-hepatitis) syndrome;
- Hepatic sclerosis and biliary tract disorders (dyskinesia, cholecystitis), with liver function tests remaining within normal limits;
- Relapses, exacerbations, and concomitant biliary tract conditions.
Preventive measures include sanitary and hygienic measures, passive immunization with donor immunoglobulin for close contacts, and active vaccination using inactivated monovalent or combined vaccines.