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Pediatrics · Chapter 12. Infectious and parasitic diseases

Acute viral hepatitis A

Hepatitis A

Acute viral hepatitis A is an acute cyclic infection caused by a hepatotropic RNA-containing virus. The disease is characterized by enteral transmission, the development of a transient cytolysis syndrome, and always has a favorable outcome without progressing to a chronic form.

PathogenHepatovirus RNA virus, highly resistant to chlorine and freezing
ChronificationNever progresses to a chronic form
IncubationAverage 2–4 weeks (10 to 45 days)
SpecificityReplication occurs strictly in the cytoplasm of hepatocytes
3 min readFor medical studentsUpdated Sep 20, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Pathogen and epidemiology

The pathogen belongs to the family Picornaviridae, genus Hepatovirus. It is a monotypic RNA-containing virus that possesses phenomenal stability in the external environment: it survives freezing down to -21 °C, is resistant to chlorine (persisting calmly in treated tap water), and is only completely inactivated by ultra-deep freezing (-85 °C).

Hepatitis A is a strict anthroponosis, with only an infected human acting as the source. Transmission occurs via the fecal-oral mechanism (through contaminated water, food, or unwashed hands). It is important to note that vertical transmission (from mother to fetus) is excluded, as the virus does not cross the placenta.

The disease exhibits pronounced autumn seasonality and most commonly affects children aged 5–14 years (accounting for over 60% of cases). The population susceptibility index is extremely high, and local outbreaks in childcare settings are frequently registered.

How the disease develops (pathogenesis)

Having entered the body via the enteral route, the virus primarily replicates in the small intestine epithelium and lymphoid tissue. Then it enters the systemic bloodstream (short-term viremia) and reaches its main target—the liver. Replication occurs directly in the cytoplasm of hepatocytes.

Massive destruction of liver cells (cytolysis syndrome) is caused by two factors:

  1. Direct cytopathic effect of the virus itself.
  2. Immune-mediated lysis (T-cell cytolysis). The virus induces the synthesis of interferon, which activates NK cells and T lymphocytes that destroy infected cells.

As a result of cytolysis, liver transaminases enter the bloodstream. Disruption of pigment metabolism leads to classic clinical markers: urine acquires a "beer color," stool becomes discolored, and the skin and sclerae turn yellow.

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Clinical periods (typical form)

The disease proceeds strictly cyclically and goes through five stages:

  • Incubation period (10–45 days). There are no external symptoms, but the viral antigen is already present in the blood and high enzyme activity is recorded (preclinical cytolysis).
  • Preicteric (prodromal) period (3–10 days). Acute onset with fever of 38–39 °C, dyspepsia, and dull pain in the right upper quadrant due to hepatomegaly. By the end of the period, urine darkens and stool becomes acholic.
  • Icteric period (7–14 days). Key feature: the appearance of jaundice is accompanied by a dramatic improvement in the child's condition and the subsidence of intoxication. Icterus spreads from top to bottom (sclerae → face → trunk → limbs). The liver is firm and rounded, and splenomegaly appears. A complete blood count (CBC) shows leukopenia with lymphocytosis. By days 7–10, the jaundice begins to subside, and a diuretic crisis (polyuria) occurs.
  • Posticteric period. Children feel healthy, but hepatomegaly and biochemical markers of cytolysis resolve slowly.
  • Convalescence period. Takes from 2–3 months to a year for complete recovery.

Diagnostics and management

The diagnosis is confirmed serologically. The main marker of the acute phase is the detection of Anti-HAV IgM antibodies in the blood by ELISA. The detection of IgG (Anti-HAV IgG) indicates a past infection and established immunity.

In mild forms and good living conditions, the patient is treated at home; hospitalization is not mandatory.

Basis of therapy:

  • Regimen and diet: semi-bed rest to reduce the metabolic load on the liver, therapeutic diet table No. 5.
  • Pharmacotherapy: enterosorbents, herbal choleretics, multivitamins, and alkaline mineral waters are prescribed.
  • For protracted courses: ursodeoxycholic acid (UDCA) preparations are used during the convalescence stage.
How to memorize

The rule of "Jaundice heals": in viral hepatitis A, the transition to the icteric period is paradoxically accompanied by the relief of intoxication and a dramatic improvement in well-being.

Class and exam questions

During what period is a hepatitis A patient most contagious?

The patient is most contagious (actively shedding the virus) during the final days of the incubation period and throughout the entire preicteric period. By days 4–5 after the appearance of jaundice, virus shedding stops.

Is the transition of hepatitis A to a chronic form possible?

No, a fundamental feature of viral hepatitis A is that it never becomes chronic. The disease ends in complete morphological recovery, although it can act as a trigger for autoimmune hepatitis in individuals with genetic T-suppressor defects.

Why are urine tests and ALT monitoring prescribed to contacts in the focus?

Biochemical shifts (rise in transaminases) and the appearance of bile pigments in the urine occur even during the incubation period, prior to the development of symptoms. This allows infected children to be identified at the preclinical stage.

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What else to study on this topic

  • Severity criteria for typical forms (mild, moderate, severe, fulminant)
  • Clinical features of atypical forms (anicteric, subclinical, cholestatic)
  • Measures in the infection focus: rules for imposing a 35-day quarantine
  • Specific immunization: schedules for using inactivated vaccines

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