Hepatitis B virus, IgM antibodies to “cor” antigen (anti-Hbcor)
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Why this test?
To evaluate the serological profile;
To find out the stage of the disease and the degree of contagiousness;
To confirm the disease and clarify its form (acute, chronic, carrier);
To monitor the course of chronic hepatitis B; to evaluate the effectiveness of antiviral therapy.
In what cases is it prescribed?
When the surface antigen of the hepatitis B virus (HBsAg) is detected in the patient;
In case of suspicion of infection with the hepatitis B virus and questionable results of serological tests; with mixed hepatitis (combined viral hepatitis B and C);
During dynamic observation of a patient with hepatitis B (determining the stage of the process during a joint examination for other specific markers of infection).
Hepatitis B virus (HBV) is an infectious disease that causes serious liver damage. Most often, hepatitis B turns into a chronic form, its course becomes protracted and provokes the occurrence of cirrhosis and liver cancer. The hepatitis B virus (Hepadnaviridae) contains double-stranded DNA surrounded by a 27-nm nucleocapsid containing the HBcAg antigen and an outer envelope containing the HBsAg antigen. This antigen is detected in the blood 6 weeks before the appearance of symptoms of the disease and can be detected for a long time both in their presence and in their absence (with chronic hepatitis and carriage). In the early stages of the disease, it is present in 90-95% of patients.
The peculiarity of the hepatitis B virus is that it enters the blood directly and circulates in it during the entire period of the disease. In some patients, the virus remains in the blood for a lifetime. For this reason, the source of infection can be not only those who are sick with hepatitis in its acute form, but also those who have already suffered from this disease, as well as people who do not have the disease, but they are carriers of the virus.
Complete recovery is recorded in 92-95% of patients with acute hepatitis B, and only 5-8% of them experience the transition of the disease to a chronic form. Hepatitis B is treated exclusively in hospital conditions. This disease, in the case of a long course, is a risk factor for the development of primary hepatocellular carcinoma (liver cancer). In the vital activity of the hepatitis B virus, two phases are distinguished: the replication phase and the integration phase. In the replication phase, reproduction (reproduction) of the virus takes place. The DNA of the virus penetrates into the nucleus of the hepatocyte, where with the help of DNA polymerase, a nucleocapsid is synthesized containing the DNA of the virus, antigens HBcAg, HBeAg, which are the main target of the immune system. The nucleocapsid then migrates from the nucleus to the cytoplasm, where the outer envelope proteins (HBsAg) are replicated, and thus a complete virion is assembled.
At the same time, the excess of HBsAg, not used for the assembly of the virus, enters the blood through the intercellular space. Complete assembly (replication) of the virus ends with the presentation of its soluble nucleocapsid antigen - HBeAg on the hepatocyte membrane, where it is recognized by immunocytes. The HBcAg antigen cannot be determined by serological methods because it is not present in the blood in free form.
The presence of antibodies (anti-HBc) to this antigen in the blood, which are produced due to its high immunogenicity, is determined. Markers of the replication phase of the hepatitis B virus are: detection of HBeAg and anti-HBc (Ig M) antigens in the blood. In 7-12% of patients with chronic viral hepatitis B, there may be a spontaneous transition from the replication phase to the non-replicative phase (at the same time, HBeAg disappears from the blood and anti-HBe appears). It is the replication phase that determines the severity of liver damage and the contagiousness of the patient.
In the integration phase, the hepatitis B virus fragment carrying the HBsAg gene is integrated (embedded) into the genome (DNA) of the hepatocyte, followed by the formation of mainly HBsAg. At the same time, virus replication stops, but the genetic apparatus of hepatocytes continues to synthesize HBsAg in large quantities. Viral DNA can be integrated not only into hepatocytes, but also into cells of the pancreas, salivary glands, leukocytes, spermatozoa, and kidney cells.
The integration phase is accompanied by the development of clinical and morphological remission. In this phase, in most cases, a state of immunological tolerance to the virus is formed, which leads to the fading of the activity of the process and the HBsAg carrier. Integration makes the virus inaccessible to immune control. Serological markers of the integration phase: the presence in the blood of only HBsAg or in combination with anti-HBc (IgG); absence of DNA virus in the blood; seroconversion of HBeAg to anti-HBe (that is, the disappearance of HBeAg from the blood and the appearance of anti-HBe). Patients who have been infected and have antibodies to the virus cannot be re-infected with hepatitis B. In some cases, full recovery does not occur and the person becomes a chronic virus carrier.
Viral carriage may be asymptomatic, but in some cases chronic active hepatitis B develops. The key risk factor for active viral carriage is the age at which a person was infected: for infants, the risk level exceeds 50%, while for adults it remains at the level of 5-10% . Studies show that men are more likely to become carriers than women. HBsAg - surface antigen of hepatitis B virus Hepatitis B virus surface antigen (HВsAg) is a protein that is present on the surface of the virus. It is found in the blood in acute and chronic hepatitis B. The earliest marker.
It reaches a maximum by the 4-6th week of the disease. It is stored for up to 6 months in case of acute hepatitis, more than 6 months - when the disease becomes chronic.
HBeAg - nuclear e-antigen of the hepatitis B virus Antigen located in the core of the virus. It appears in the blood at the same time as HBsAg and persists for 3-6 weeks. HBeAg appears in the blood of a patient with acute hepatitis B at the same time as HBsAg or after it and remains in the blood for 3-6 weeks. Indicates active reproduction and a high risk of transmission of the virus at a hundred contact, as well as perinatally. The infectivity of HBeAg-positive serum is 3-5 times higher than HBsAg-positive.
The detection of HBeAg in the blood for more than 8-10 weeks indicates the transition of the disease into a chronic form. In the absence of replicative activity of the virus during chronic infection, HBeAg is not detected. Its appearance indicates reactivation of the virus, which most often occurs against the background of immunosuppression. In the treatment of viral hepatitis B, the disappearance of HBeAg and the appearance of antibodies to the HBe antigen indicate the effectiveness of therapy.
anti-HBc (Ig M) - specific antibodies of the IgM class to the nuclear 'core' antigen of the virus. They begin to be produced even before clinical manifestations, indicating active replication of the virus. They appear in the blood after 3-5 weeks, persist for 2-5 months and disappear during the recovery period.
anti-HBc - total antibodies (IgM + IgG) to the core antigen of the hepatitis B virus An important diagnostic marker, especially with a negative HBsAg value. Antibodies of the IgM class are produced after 3-5 weeks. Antibodies of the IgG class begin to be produced from the 4th to the 6th month and can be preserved for life. They confirm the body's contact with the virus.
anti-HBs - total antibodies to the surface antigen of the hepatitis B virus They appear slowly, reaching a maximum after 6-12 months. They indicate a previous infection or the presence of post-vaccination antibodies. Detection of these antibodies indicates recovery and development of immunity. Detection of antibodies in a high titer in the first weeks of the disease may be associated with the development of hyperimmune variants of fulminant hepatitis B.
anti-HBe - antibodies to the e-antigen of the hepatitis B virus They appear in 8-16 weeks after infection in 90% of patients. They indicate the end of the acute period of the disease and the beginning of the convalescence period. They can be stored up to 5 years after the disease. HBV (DNA) - DNA of the hepatitis B virus A marker of the presence and replication of the virus. The DNA of the virus can be determined qualitatively or quantitatively by the PCR method. Thanks to the qualitative method, the presence of the hepatitis B virus in the body and its active reproduction is confirmed. This is especially important in complex diagnostic cases. When infected with mutant strains of the virus, the results of the test for specific antigens HBsAg and HBeAg may be negative, but the risk of spreading the virus and developing the disease in the infected person remains.
Qualitative determination of viral DNA plays an important role in the early detection of hepatitis B in people at high risk of infection. The genetic material of the virus is detected in the blood several weeks earlier than HBsAg. A positive PCR result for a period of more than 6 months indicates a chronic infection. Determining the viral load (the amount of DNA of the virus in the blood) makes it possible to estimate the probability of the disease becoming chronic. Elevated levels of liver transaminases with a positive PCR result are indicators of the need for therapy. During the treatment of viral hepatitis B, the disappearance of the DNA of the virus indicates the effectiveness of the treatment.