Etiology. The hepatitis A virus (Hepatitis A Virus, HAV) is a virus particle devoid of a shell, and belongs to the family Picornaviridae, a genus of Hepatovirus; The genome consists of single-stranded RNA.
Epidemiology. The source of infection for a person is a sick person. The main routes of transmission of the virus: predominantly fecal-oral route, through water and products contaminated with feces. Given the stage of viremia in the acute period of the disease, infection through the blood is possible, however, these cases are extremely rare. Epidemic cases in developed countries today are rare, associated with water, mainly viral hepatitis, and A is a “traveler’s disease.” Penetrating through the endothelium of the intestinal wall, HAV enters the lymphoid ring, then into the blood and into the liver cells, where it replicates. As the titer of anti-HAV – IgM increases and anti-HAV – IgG appears to the HAV antigen, as well as activation of cellular immunity, the virus is eliminated from the body – recovery begins. There is no persistence of this virus, so the chronic course does not develop. Vaccination effectively protects against infection, but in order to avoid over-vaccination in people older than 40 years, it is necessary to conduct a study on the level of total antibodies to HAV, since over 50% of the population is immunized at this age.
Clinical manifestations. The incubation period is 15–45 days; during epidemic outbreaks it can be reduced to 7–10 days. In most patients, HAV is asymptomatic, quite often an anicteric form, accompanied by flu-like symptoms. Chronization process does not occur, fulminant forms are rare. With age, the risk of developing a severe form of the disease increases, whereas in children, 90% of cases of HAV are asymptomatic.
Diagnostics. Laboratory diagnosis of viral hepatitis A is mainly based on the detection of serological markers (IgM immunoglobulins, IgG immunoglobulins and total antibodies). Molecular methods for the detection of the virus by PCR are not carried out in general clinical practice.
IgM is determined immediately with the appearance of jaundice and is a diagnostic marker of viral hepatitis A, which is optimally determined for the differential diagnosis of the etiology of hepatitis in the acute period of the disease. This class of antibodies lasts on average 8–12 weeks, in 4% of patients they can persist for up to 1 year. Shortly after the onset of IgM in the blood, IgGs begin to be detected, which persist for life and provide stable immunity. The presence of anti-HAV – IgG in human blood (in the absence of anti-HAV – IgM) indicates the presence of immunity to the hepatitis A virus, as a result of a previous infection or vaccination against this virus. Anti-HAV – IgG appear in serum 2 weeks after vaccination and after administration of immunoglobulins. The level of antibodies after infection is higher than after passive transmission. Anti-HAV – IgG is transmitted from mother to fetus by transplacental, and can be detected in children even over the age of 1 year.
Determining the level of total antibodies to HAV is used exclusively for epidemiological purposes or to determine pre-vaccination status. Among the common antibodies, antibodies of the IgG class predominate, with the exception of the period of acute HAV infection, when antibodies of the IgM class prevail. They are almost always present at the onset of acute hepatitis and are usually found throughout the rest of their lives (in 45% of the adult population, these antibodies are present in serum). Their presence indicates HAV’s effects. past recovery, as well as on acquired immunity to hav c. result of vaccination.