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NATURAL HISTORY OF CHRONIC HBV INFECTION

The natural history of chronic HBV infection is characterized by four distinct phases. These phases are dependent on a complex interaction between host, viral and environmental factors, and the age at infection particularly.

The immune tolerance phase occurs when the infection is contracted early in childhood, but is absent in individuals who acquire the infection later in life. This is due to the immaturity of children’s immune system, and as a result, the virus is tolerated. This phase usually persists for a few decades, and is characterized by hepatitis B e antigen (HBeAg) positivity, very high viral load (>20,000 IU/ml), normal alanine aminotransferase (ALT) levels and minimal level liver injury. It is associated with a low risk of progression to advanced liver disease.

The immune clearance phase occurs most commonly in the third or fourth decades of life, but the triggering mechanism for this phase is not well understood. During this phase, an immune-mediated cytotoxic response is initiated against the infected liver cells resulting in fluctuating HBV DNA and ALT levels. These recurring immune-mediated attacks can result in inflammatory liver damage and lead to liver fibrosis and cirrhosis. The immune attack is, however, insufficient to eradicate the virus or the infected hepatocytes. An important outcome of this phase is the seroconversion of HBeAg to HBe antibody (anti-HBe), which is associated with lower level viremia.

Patients in the immune control phase (low replicative phase) have also been described as ‘inactive carriers’ of the infection. During this long phase, liver inflammation is minimal, HBV DNA is undetectable or at a low level (<2000 IU/ml) and liver function tests are normal.

The immune escape or replicative phase occurs in around 30% of individuals, and is characterized by negative HBeAg, positive anti-HBe and detectable viral load (HBV DNA >2000 IU/ml). Reactivation after HBeAg seroconversion is referred to HBeAg-negative chronic hepatitis. The natural course of patients with HBeAg negative disease is characterized by fluctuations in clinical status, and biochemical and viral load parameters caused by recurrent hepatic flares.

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