Advances in the serodiagnosis of viral hepatitis have been dramatic, and the findings of specific viral antigens have led to further elucidation of the course of infections. The "Australia antigen," discovered in 1960, was first renamed hepatitis-associated antigen (HAA) and then, finally, hepatitis B surface antigen (HBsAg). It appears in the blood early after infection, before onset of acute illness, and persists through early convalescence. HBsAg usually disappears within 4 to 6 months after the start of clinical illness except in the case of chronic carriers.Hepatitis B 37 antigen (HBeAg) appears during the early acute phase and disappears before HBsAg is gone, although it may persist in the chronic carrier. Persons who are HBeAg-positive have higher titers of HBV and therefore are at a higher risk of transmitting the disease. HBeAg has a high correlation with DNA polymerase activity.The hepatitis B core antigen (HBcAg) is found within the nuclei of infected hepatocytes and not generally in the peripheral circulation except as an integral component of the Dane particle. The antibody to this antigen, anti-HBc, is present at the beginning of clinical illness. As long as there is ongoing HBV replication, there will be high titers of anti-HBc. During the early convalescent phase of an HBV infection, anti-HBc may be the only detectable serologic marker (window phase) if HBsAg is negative and anti-HBsAg has not appeared.