Hepatitis A is caused by an RNA virus that belongs to the Picornavirus family. HAV infection usually develops in an acute form.

Transmission occurs mainly via the fecal-oral route, consuming contaminated food (raw or undercooked seafood, berries, vegetables) or water, or through contact with infected persons. In recent years, sexual transmission has also been described. Travel to areas with high endemicity represents a critical risk factor.

From a pathogenetic point of view, viral replication occurs in the cytoplasm of hepatocytes. Liver injury is the result of the host’s immune response to HAV.

The incubation period of hepatitis A infection averages 28 days (15–50 days). More than 70% of HAV-infected adults present with symptomatic illness, which begins with the sudden onset of nausea, vomiting, anorexia, fever, malaise, and abdominal pain. From a biochemical-clinical point of view, hepatitis A is characterized by increased serum ALT, serum bilirubin (typically ≤10 mg/dL), and alkaline phosphatase (up to 400 U/L) levels. Increases in serum ALT generally precede elevations in bilirubin. Serum aminotransferase peaks approximately 1 month after exposure to the virus and then progressively declines. Serum bilirubin concentration usually declines within 2 weeks of the peak. Other laboratory changes include increases in acute phase proteins and markers of inflammation.

Full biochemical-clinical recovery is observed within 2–3 months in 85% of patients and complete recovery within 6 months in almost all patients. HAV infection does not become chronic, and individuals cannot reinfect it.

The diagnosis of acute HAV infection is based on identifying serum anti-HAV IgM antibodies IgM is detectable from symptoms beginning, peaks during the convalescent phase of the disease, and remains detectable for 3–6 months. Detection of serum IgM antibodies without clinical symptoms may reflect a previous hepatitis A infection with pro longed IgM persistence, a false-positive result, or an asymptomatic infection (which is more common in children younger than 6 years of age than in older children or adults).

Serum IgG antibodies appear early in the convalescent phase of the disease, remain detectable for decades, and are associated with lifelong protective immunity. Detection of anti-HAV IgG in the absence of anti-HAV IgM indicates prior infection or vaccination.