Terms used in this guidance
Chronic hepatitis B is defined as persistence of hepatitis B surface antigen (HBsAg) for 6 months or more after acute infection with hepatitis B virus (HBV).
HBV DNA level, or 'viral load', is an indicator of viral replication. Higher HBV DNA levels are usually associated with an increased risk of liver disease and hepatocellular carcinoma. HBV DNA level typically falls in response to effective antiviral treatment.
Hepatitis B surface antigen (HBsAg) is a viral protein detectable in the blood in acute and chronic hepatitis B infection.
The development of antibodies against HBsAg is known as HBsAg seroconversion. It signifies clearance of HBsAg and resolution of the chronic infection.
Hepatitis B e antigen (HBeAg) is an indicator of viral replication, although some variant forms of the virus do not express HBeAg (see 'HBeAg-negative chronic hepatitis B' below). Active infection can be described as HBeAg-positive or HBeAg-negative according to whether HBeAg is secreted.
HBeAg-negative hepatitis B is a form of the virus that does not cause infected cells to secrete HBeAg. People can be infected with the HBeAg-negative form of the virus from the beginning, or the viral mutation can emerge later in the course of infection in people initially infected with the HBeAg-positive form of the virus.
HBeAg seroconversion occurs when people infected with the HBeAg-positive form of the virus develop antibodies against the 'e' antigen. The seroconverted disease state is referred to as the 'inactive HBV carrier state' when HBeAg has been cleared, anti-HBe is present and HBV DNA is undetectable or less than 2000 IU/ml. Once seroconversion has taken place, most people remain in the inactive HBV carrier state (the immune-control phase; see figure 1). However, increasing HBV DNA and recurrent hepatitis after seroconversion indicate the emergence of the HBeAg-negative strain of the virus (the immune-escape phase; see figure 1).