Chronic HBV infection is mentioned when HBV is not cleared from the body within 6 months in people infected with HBV. Mostly, at this stage, the disease is silent and almost all of the patients pass into this period without being aware of it.
When liver damage increases and liver functions begin to deteriorate, symptoms such as weakness, joint and muscle pain, nausea, yellowing of the whites of the eyes and skin, swelling in the feet and abdomen occur, it is understood that they are infected with HBV as a result of a blood test performed for another reason.
Chronic HBV infection may progress with different clinical pictures such as asymptomatic HBV carrier, chronic active hepatitis that may end with liver cirrhosis, or development of liver cancer. In 15-25% of patients with chronic liver disease, the cause of death is hepatitis B virus related liver diseases (See, liver cirrhosis).
HBV When it enters the body and settles in the liver, it does not directly cause damage to the liver. As a result of the body’s immune response to the virus (the immune system’s response to the virus), liver cells are damaged. As the virus multiplies inside the liver cell, more immune response occurs, which means more liver cells are damaged.
Over time, connective tissue begins to form in place of damaged cells (fibrosis), and liver cirrhosis is the result of widespread connective tissue formation in the liver. Active replication of the virus in the liver is an important risk factor for liver damage. Liver damage is more serious in patients with high levels of virus in the blood.
Sometimes, HBV can acquire a different structure by undergoing some genetic changes during the reproduction period in the liver (viral mutation). This change may occur during the natural course of chronic HBV infection or may occur after the use of certain drugs for treatment.
This is a condition that can change the course of the liver disease and complicates the response to treatment. One of the most common mutations is the HBeAg (Hepatitis B early antigen-Hepatitis B e antigen) mutation. In non-mutated patients, HBeAg production is associated with active replication of the virus.
The formation of antibodies against HBeAg in the body (HBeAb or anti-HBe) (Hepatitis B e antibody) is accepted as an indication that the virus has stopped multiplying and the body has started to become immune to HBV, and this event is called ‘seroconversion’.
In this case, the level of HBV-DNA in the blood is low. In the presence of mutated HBV infection, although HBeAg cannot be detected in the blood and HBeAb is present, active virus proliferation continues and the HBV-DNA level in the blood is high. This condition occurs in 30 to 80% of chronic HBV infections in southeast Europe and Asia, and is usually associated with childhood HBV infection.
In practice, it may be assumed that HBeAg-negative chronic HBV muscles have erroneously seroconverted (formed antibodies to HBeAg).
Patients with seroconversion are generally called inactive carriers and it is accepted that the inflammation in the liver slows down or stops in these patients.
In contrast, patients with HBeAg-negative (and HBeAb-positive) mutant chronic HBV infection persist, albeit at a low level, of viral replication and chronic inflammation in the liver progresses. These patients continue their lives as candidates for all kinds of damage that HBV may cause in the liver.
In 2/3 of patients with chronic HBV infection living in Asia, serious complications such as liver cirrhosis and liver cancer occur in the period after HBeAb formation.
By measuring the HBV-DNA level in the blood of HBeAg negative and HBeAb formed patients, it can be understood to some extent whether the event is an active mutant virus infection or an inactive disease with seroconversion.
Although high HBV-DNA levels are usually indicative of mutant HBV infection, this rule may not always be valid. Patients with HBeAg negative mutant HBV infection do not develop any disease-related symptoms for years, and the average time it takes for liver cirrhosis to appear in these patients is around 40 years.
After the appearance of signs of cirrhosis, 25% of patients enter the stage of end-stage liver disease within 10 years.