Hepatitis D virus, total antibodies (anti-HDV)

Why this test?

• For differential diagnosis of hepatitis;
• tdetect viral hepatitis D and mixed hepatitis;
• tdetect previously transmitted viral hepatitis D.

In what cases is it prescribed?

With the wave-like course of viral hepatitis B;

with rapidly progressive liver damage (fulminant hepatitis) and exacerbation of the disease in a patient with viral hepatitis B;
with chronic liver diseases (chronic viral hepatitis B, cirrhosis);

during the examination of persons whwere in contact with infected with delta hepatitis.

Test information

The hepatitis D virus is a"defective"" virus that contains a ring-shaped single-stranded RNA strand and is capable of replication only in the presence of the hepatitis B virus. HDV builds its envelope from the HBs-antigen and is unable tfully reproduce without the hepatitis B virus. According tapproximate estimates, about 5% of patients with viral hepatitis B are alsinfected with the hepatitis D virus.

There are 3 main genotypes of the virus, which differ in the severity of the course of the disease and are characteristic of certain geographical regions. The first genotype is the most common throughout the world, the second is found in East Asia, and the third - in South America. The virus is stable in an acidic environment and at high temperatures, but is destroyed by alkali.

The source of infection is a patient with acute or chronic hepatitis D or a carrier of the virus. The main route of transmission is parenteral, as with viral hepatitis B. Sexual and vertical (from mother tchild) are rare, but probable ways of spreading the infection. The group at risk of infection with the virus includes injection drug users, recipients of donor organs and patients undergoing hemodialysis. The disease develops only with acute or chronic viral hepatitis B or HBsAg carrier, i. e. with viral hepatitis D there is always a mixed infection. In case of co-infection (simultaneous infection with hepatitis B and D viruses), the disease is characterized by a shorter incubation period of 3-7 weeks.

Hepatitis begins, as a rule, acutely, with an increase in body temperature, nausea, loss of appetite and the addition of jaundice. Coinfection is characterized by a cyclic course with twperiods of increased biochemical markers of liver damage. The first increase in transaminases is associated with the cytolytic effect of the hepatitis B virus, the second - after a few weeks - is due tthe hepatitis D virus, or vice versa. Recovery is registered in 90% of patients with co-infection, fulminant hepatitis (massive necrosis of liver cells) is noted in 2-20% of cases.

Chronic hepatitis is observed in 2-7% of cases of co-infection, 80% of which lead tliver cirrhosis. When infected with the hepatitis D virus during the existing viral hepatitis B, a superinfection occurs, which is characterized by a wave-like course. At the same time, fulminant (suddenly developing) forms are noted in 10-20% of cases, chronic infection develops in 70-90% of patients, cirrhosis - in 70-80%, and complete recovery is registered only in 5-10%.

Distinguishing coinfection from superinfection is not always easy. Usually, they focus on the features of the clinical course of the disease and the presence of anti-HBc class IgM in coinfection and IgG class antibodies in superinfection. Hepatitis D infection reduces the likelihood of a successful response tantiviral therapy. In 5%, rapidly progressive liver damage ends in death.

Chronic hepatitis and cirrhosis, in turn, increase the risk of developing hepatocellular carcinoma, although a direct link between delta hepatitis and liver cancer has not been proven. With the increase of pronounced cirrhotic changes in the liver, the reproduction of the virus tends tdecrease until the complete cessation of replication.

Recipients of a donor liver infected with the hepatitis D virus have a latent form of infection. In the absence of viral hepatitis B or its inhibition by immunoprophylactic methods, viral particles multiply only within the affected hepatocytes and the infection does not spread tother areas of the liver. RNA of the virus is not detected in the blood.

Antibodies of the IgM class begin tappear from the second week of delta hepatitis and disappear 2 months after the period of exacerbation of the disease. Antibodies of the IgG class gradually replace immunoglobulins of the IgM class, 3-8 months after the onset of the disease. Their concentration gradually decreases tcomplete disappearance 1-2 years after the transfer of viral hepatitis D. With chronic persistence of the virus in the liver, high titers of total immunoglobulins remain in the blood for a long time (sometimes for many years). Tdetermine the activity of mixed infection and the degree of liver damage, it is necessary tsimultaneously study the main serological markers and biochemical indicators of liver function, as well as the results of liver biopsy.