Vitrotest® HAV-IgM

• Solid phase: strip ELISA plate pre-coated with monoclonal anti-IgM antibodies.
• Conjugate: monoclonal antibodies to human HAV conjugated with horseradish peroxidase.
• Chromogen: ready to use TMB solution.
• Sample volume: 100 μl.
• Assay time: 2 h.

Hepatitis A is an acute infectious disease of the liver (also known as Botkin’s disease) caused by the hepatitis A virus (HAV), which belongs to the genus Hepatovirus of the family Picornaviridae. The virus has a single-stranded RNA genome and lacks a lipid envelope, which determines its high stability in the environment, in particular, it is able to remain infectious in water, soil, and on surfaces for prolonged periods and is resistant to low temperatures and the acidic environment of the stomach.

According to the World Health Organization, approximately 100 million HAV infections and 1.5 million clinically apparent cases are reported worldwide each year, of which 15,000–30,000 result in death annually. The main routes of transmission are fecal–oral, including through contaminated water and food, as well as household contact. After infection, HAV penetrates through the intestinal epithelium into the bloodstream and is transported to the liver, where it replicates in hepatocytes and Kupffer cells. Due to its cytolytic effect on liver cells, the virus is excreted with bile into the intestine and released into the environment even before clinical symptoms appear.

The incubation period of hepatitis A usually ranges from 14 to 28 days, although it may extend to 15–50 days depending on immune status, age, concomitant diseases, and other factors. In most cases, the disease is accompanied by weakness, body aches, sore throat, fever, loss of appetite, vomiting, pain, and heaviness in the right upper quadrant of the abdomen. The clinical course varies with age: in young children the infection is often asymptomatic, whereas in adults an icteric form with pronounced intoxication syndrome develops more frequently.

The immune response to HAV is characterized by the sequential appearance of specific antibodies. IgM antibodies appear in the early stages of infection, often before symptoms develop, and are the primary marker of acute infection. Their levels peak during the first weeks of illness and gradually decline over 3–6 months, sometimes persisting for up to 12 months after infection. IgG antibodies appear later and provide long-term, usually lifelong, immunity. They are also produced after vaccination against HAV, which forms the basis of specific disease prevention. The presence of IgG in the absence of IgM indicates past infection or immunization. Therefore, the determination of HAV-specific IgM antibodies by ELISA is a key tool for the early diagnosis of acute hepatitis A, which is essential for timely treatment and epidemiological control of the disease.