HAV is a non-enveloped RNA virus belonging to the picornavirus family, with 4 genotypes belonging to one serotype. This agent is transmitted almost exclusively by the fecal-oral route.
It is an outbreak prone disease with an incubation period of around 4 weeks. Person to person spread of HAV is enhanced by poor personal hygiene and overcrowding. Excretion in the stool occurs for only 7-14 days after the onset of the clinical illness and is diagnostic of an acute HAV infection.
No carrier state has been identified. Inactivated attenuated vaccine, which is safe, immunogenic and effective, is available.
The incubation period for HAV ranges from 15-45 days. The prodromal symptoms of acute viral hepatitis are systemic and quite variable. Constitutional symptoms of low grade fever, anorexia, nausea and vomiting, fatigue, malaise, arthralgias, myalgias, headache, photophobia, pharyngitis, cough and coryza may precede onset of jaundice by 1-2 weeks.
Dark urine and clay colored stools may be noticed by the patient from 1-5 days before the onset of clinical jaundice. With the onset of clinical jaundice, the constitutional prodromal symptoms usually diminish. The liver becomes enlarged and tender and may be associated with right upper quadrant pain and discomfort. During recovery phase the constitutional symptoms disappear, but usually some liver enlargement and abnormalities in liver biochemical tests are still evident.
HAV has an incubation period of ~4 weeks. Its replication is limited to the liver, but the virus is present in liver, bile, stools and blood during late incubation period and acute pre-icteric / pre-symptomatic phase of illness.
In acute hepatitis with clinical jaundice, the serum bilirubin levels are above 2.5mg/dL and serum alanine aminotransferase (ALT) is more than 10 times the upper limit of normal.
Detection of anti- HAV antibody in serum/plasma is important in diagnosis of infection, as HAV is present in blood transiently during the incubation period.
IgM antibodies against HAV are generally detectable 5-10 days before onset of symptoms and can persist for up to 6 months. Anti-HAV IgM antibodies indicate acute infection. IgG antibodies against HAV becomes the predominant antibody during convalescence and remains detectable indefinitely.
Anti-HAV total antibodies (IgG and IgM) or specific IgG (but anti-HAV IgM negative) indicate immunity to hepatitis A either because of past infection or vaccination.
The serum aminotransferases, aspartate aminotransferase (AST) and ALT increase to a variable degree during prodromal phase of illness and precede the rise in bilirubin levels. Yellowish discoloration of sclera (jaundice) and skin is usually visible when serum bilirubin value is above 2.5 mg/dL.
There is no role for antiviral drugs in therapy for HAV infection. Virtually all previously healthy patients with hepatitis A recover completely with no clinical sequelae. The case fatality is very-very low (~0.1%) but is increased in advanced age and in the presence of underlying debilitating diseases. Infection in the community is best prevented by improving social conditions especially overcrowding and poor sanitation.