General features:
• It is an DNA virus from the Hepadnavirus family. The incubation period is 30-180 (average 80) days.
• The risk of becoming chronic is directly proportional to the early receipt of the virus.
• There is a risk of 90% of perinatal infection, 20-50% of infection at 1-5 years of age, and 1-5% of infection acquired in adulthood.
Transmission routes:
• Vertical transmission: The risk of infection in the baby born to an HBeAg (+) mother is 90%.
• Horizontal transfer: The most common way of lateral transfer in adults is sexual intercourse and intravenous drug addiction.
• Transfusion by transfusion: It is very rare today as blood products are routinely screened.
Clinical features:
• Most of the cases are asymptomatic.
• In symptomatic cases, the clinic is typical acute viral hepatitis.
• The best indicator of prognosis is prothrombin time.
• The majority of cases with acute hepatitis B in adulthood recover fully by developing immunity.
• 0.1%-1% of cases with acute hepatitis B may progress with liver failure in the form of fulminant hepatitis, and they have a high mortality risk.
HBV Extrahepatic findings
Gianotti Crosty syndrome (maculopapular rash)
Serum sickness-like syndrome
Arthritis
Polyarteritis nodosa
Mixed cryoglobulinemia
aplastic anemia
membranous glomerulonephritis
Diagnosis
hepatitis B surface antigen HBsAG and its antibody Anti-HBs:
The first antigen detected in the blood is HBsAg.
After HBsAg becomes negative, anti-HBs emerges and shows natural immunity.
Hepatitis B core antigen HBcAg:
It is an antigen found only in infected hepatocytes; not detected in serum.
Anti-HBc IgM:
It is the best indicator of acute hepatitis.
The period between the disappearance of HBsAg and the formation of anti-HBs in the course of acute hepatitis B is called the window period. During this period, HBsAg and anti-HBs are negative, while anti-HBc IgM is positive.
Anti-HBc IgG:
Indicates that you have been exposed to the hepatitis B virus at some point in your life.
HBeAg:
HBV is an indicator of replication and infectivity.
With a mutation occurring in the precore region of the virus, HBeAg cannot be synthesized and is found negative despite replication. This is called a precore mutant virus (recognized by negative HBeAg while HBV DNA is high in serum).
• Anti-HBe:
It is the antibody synthesized against HBeAg and suppresses the infectivity.
• HBV DNA:
It is the most important determinant of viral replication.
