title: Relative functional affinity of specific anti-core IgG in different categories of hepatitis B virus infection.
abstract: While resolution of hepatitis B virus (HBV) infection occurs in most cases, a carrier state can exist in which the HBV surface antigen (HBsAg) persists. Some carriers are also positive for the HBV "e" antigen (HBeAg), indicative of high viral replication. Others are HBV "e" antibody (anti-HBe)-positive carriers in whom there appears to be a fall in the level of viral replication with the appearance of antibodies against the "e" antigen. The former group of carrier is considered to be at a higher risk of transmitting HBV infection than the latter. In order that a carrier state may occur, some degree of tolerance to the infectious agent must exist. A study of the rate of increase of specific antibody avidity following infection provides a means of assessing the maturity of the immune response to an infectious agent. Since antibodies specific for the HBV core antigen (HBcAg) are produced in almost all cases of HBV infection and the HBeAg and HBcAg share a large number of amino acids and some B- and T-cell epitopes, the increase in the avidity of antibodies against the HBV core antigen (anti-HBc) in cases of acute, resolving HBV infection and in HBV carriers has, therefore, been studied. An increase in the avidity of specific antibody, similar to that seen in other viral infections, was observed following acute, resolving infection. However, low avidity antibody persisted longer in carriers who remained positive for HBeAg, whereas in cases where there were antibodies specific for HBeAg, the anti-HBc antibody was of high avidity. Analysis of sequential sera from carriers who seroconverted from HBeAg-positive to anti-HBe-positive showed that an increase in anti-core avidity could predate seroconversion from HBeAg-positive to anti-HBe-positive status. Thus, anti-HBc avidity studies may be of diagnostic and prognostic significance.
authors.affiliation: Department of Virology, Preston Public Health Laboratory, Royal Preston Hospital, United Kingdom.
authors.forename: H I
authors.initials: HI
authors.lastname: Thomas
mesh_terms: D000208:Acute Disease; D000915:Antibody Affinity; D000917:Antibody Formation; D002353:Carrier State / Q000175:diagnosis*; D005500:Follow-Up Studies; D006509:Hepatitis B / Q000145:classification / Q000175:diagnosis* / Q000276:immunology; D006510:Hepatitis B Antibodies / Q000097:blood / Q000276:immunology*; D006512:Hepatitis B Core Antigens / Q000096:biosynthesis / Q000276:immunology*; D006513:Hepatitis B e Antigens / Q000096:biosynthesis / Q000276:immunology*; D006515:Hepatitis B virus / Q000502:physiology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology*; D012008:Recurrence; D013997:Time Factors; D014779:Virus Replication
chemical_list: D006510:Hepatitis B Antibodies; D006512:Hepatitis B Core Antigens; D006513:Hepatitis B e Antigens; D007074:Immunoglobulin G