Hepatitis A continues to be one of the most frequently reported vaccine-preventable diseases in the world, despite the licensure of hepatitis A vaccine in 1995. Widespread vaccination of appropriate susceptible populations would substantially lower disease incidence and potentially eliminate indigenous transmission of hepatitis A virus (HAV) infection. HAV, a 27-nm RNA agent classified as a picornavirus, can produce either asymptomatic or symptomatic infection in humans after an average incubation period of 28 days (range, 15-50 days). The illness caused by HAV infection typically has an abrupt onset of symptoms that can include fever, malaise, anorexia, nausea, abdominal discomfort, dark urine, and jaundice. The likelihood of having symptoms with HAV infection is related to the person’s age. In children less than 6 years of age, most (70%) infections are asymptomatic; if illness does occur, it is not usually accompanied by jaundice. Among older children and adults, infection is usually symptomatic, with jaundice occurring in greater than 70% of patients. Signs and symptoms usually last less than 2 months, although 10%-15% of symptomatic persons have prolonged or relapsing disease lasting up to 6 months. In infected persons, HAV replicates in the liver, is excreted in bile, and is shed in the stool. Peak infectivity of infected persons occurs during the 2-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus in stool is highest. The concentration of virus in stool declines after jaundice appears. Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness. Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness. Viremia occurs soon after infection and persists through the period of liver enzyme elevation. Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. Serologic testing to detect immunoglobulin M (IgM) antibody to the capsid proteins of HAV (IgM anti-HAV) is required to confirm a diagnosis of acute HAV infection. In most persons, IgM anti-HAV becomes detectable 5-10 days before the onset of symptoms and can persist for up to 6 months after infection. Immunoglobulin G (IgG) anti-HAV, which appears early in the course of infection, remains detectable for the person’s lifetime and confers lifelong protection against the disease. Commercial diagnostic tests are available for the detection of IgM and total (IgM and IgG) anti-HAV in serum. HAV RNA can be detected in the blood and stool of most persons during the acute phase of infection by using nucleic acid amplification methods, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates.

The assay is based on the principle of “IgM capture” where IgM class antibodies in the sample are first captured by the solid phase coated with anti hIgM antibody.

Ordering Information:

• 1. Cassette Cat No.: AN3024C
• 2. Dipstick Cat No.: AN3024S

Helpful Documents:

• 1. Instruction for use
• 2. MSDS