Hepatitis A Antigens Rapid Test

Hepatitis A virus (HAV) is responsible for the worldwide occurrence of acute viral hepatitis, most prevalent in resource-poor countries, usually through contaminated food or water, causing point source outbreaks. HAV belongs to the family Picornaviridae, but it replicates very slowly and does not cause significant cellular lesions.

After HAV enters the body via fecal-oral transmission, it passes through the circulatory system and enters the target organ (liver) to multiply. Acute HAV infection has a long incubation period of about 4-6 weeks, during which a large amount of virus enters the feces. The virus can be detected in the blood both before and several weeks after the onset of clinical symptoms, a phenomenon generally referred to as viremia. At the peak of viral shedding, most patients produce hepatitis A-specific IgM, followed by IgG. The presence of anti-HAV-IgM is consistent with elevated serum ALT and AST, suggestive of liver injury. The onset of acute hepatitis A is characterized by fatigue, fever, nausea, vomiting, anorexia, abdominal pain, and jaundice. Of note, the clinical outcome of hepatitis A is usually variable, ranging from asymptomatic to fulminant hepatitis. In general, children with hepatitis A have a much milder clinical course than adults. In addition, fulminant hepatitis is a rare complication that is thought to be an important factor in the death of patients. HAV infection is generally self-limiting, with patients gradually returning to health after infection, but there are some individuals who become ill again after initial HAV infection. Recurrent hepatitis typically occurs 4 to 15 weeks after acute viral hepatitis and the clinical progression is usually milder than the initial infection.

Figure 1. Virologic, immunologic and biochemical events during the course of experimental hepatitis A virus infection in chimpanzees inoculated intravenously with human HAV, strain HLD2
(Source: Nainan OV, et al. 2006)

Hepatitis A is clinically indistinguishable from other viral hepatitis and with the help of laboratory tests can better assist the clinician in making a differential diagnosis. Anti-HAV-IgM antibodies appear a few days before or at the same time as the onset of clinical symptoms, so acute hepatitis A is diagnosed primarily by examining anti-HAV IgM. In most patients, antibody titers remain high for about 1 month and then gradually decrease to zero over about 6 months. False-positive results may occur due to specificity issues, and anti-HAV IgM may also be detected after vaccination, therefore, this analysis should be performed only when there is clinical suspicion. Anti-HAV IgG antibodies appear soon after IgM antibodies and persist for years with lifelong immunity. Their presence indicates that the patient had a past HAV infection that has normalized. HAV RNA can be detected in the feces and plasma of infected patients, as well as in contaminated water and food, but nucleic acid testing is rarely used for diagnosis. Sequencing and phylogenetic analyses are primarily used to track outbreaks and determine transmission routes.

HAV Antigens Rapid Test