H

• Hepatitis B c Antigen (HBcAg): HBcAg is an intracellular antigen synthesized within infected hepatocytes. Most of the HBcAg that is generated is assembled into the viral core (nucleocapsid). Free HBcAg does not not circulate in significant quantity in the blood, but it does circulate as part of the intact hepatitis B virion. HBcAg is not detected on serum tests.
• Hepatitis B e antigen (HBeAg) clearance: Loss of detectable HBeAg from serum, which typically signifies greater immune control of hepatitis B by the host and remission of disease activity, especially if occurs spontaneously (i.e. without treatment) and in context of decreased serum HBV DNA. HBeAg clearance usually precedes HBeAg seroconversion. In acute infection that resolves, the HBeAg is promptly cleared with subsequent development of anti-HBe antibody. This occurs more slowly in those who have chronic persistent infection.
• Hepatitis B e antigen (HBeAg) seroconversion: Loss of HBeAg and development of anti-HBe antibody. In setting of decreased HBV DNA levels and normal ALT, this is usually associated with disease remission.
• Hepatitis B surface antigen (HBsAg): HBsAg exists as the major component of the surface (envelope) of the intact hepatitis B virion and as excess viral envelope in the form of subviral lipoprotein particles (spheres and filaments). HBsAg can be detected in serum 1 to 10 weeks after acute exposure to the virus. In patients who go on to resolve their infection, HBsAg usually becomes undetectable after 4 to 6 months. Persistence of HBsAg beyond 6 months is by definition chronic hepatitis B. Clearance of this antigen with subsequent development of surface antibody (anti-HBs) is a major benchmark but occurs rarely (0.5% or less per year) in patients with chronic infection.
• Hepatitis E antigen (HBeAg): A precore protein secreted into the circulation by hepatitis B virus (HBV)-infected hepatocytes and generally considered a marker of HBV replication and infectivity. The presence of HBeAg is usually associated with high levels of HBV DNA in serum.
• Histologic response: A decline in histologic activity by at least two points on a scoring scale and no worsening fibrosis on liver biopsy compared to pre-treatment biopsy, an outcome typically measured in clinical trial rather than actual practice settings.