Specific immunotherapy proposed for hepatitis B virus infection.
Immune response to hepatitis B surface antigen (HBsAg), coinciding with removal of HBsAg from the circulation, has been shown to be a cell-mediated response assessed by leukocyte migration inhibition assay. Immune response to HBsAg is a T-cell dependent phenomenon in the nude mouse model. Immunological tolerance in man appears to stem from the absence of cellular and humoral immune response to HBsAg, causing a chronic carrier state which serves as an epidemiological reservior for the transmission of viral hepatitis type B. Specific immunotherapy in hepatitis may consist of adoptive transfer of immunity to HBsAg. It is proposed to be accomplished by administration of anti-HBs, transfer factor or 'immune-RNA'. The efficacy and safety of 'immune-RNA' administration to chronic carriers can be validated by leukocyte migration inhibition techniques in vitro and in HBsAg positive chimpanzees in vivo.
D000818:Animals; D000917:Antibody Formation; D006168:Guinea Pigs; D006509:Hepatitis B / Q000276:immunology / Q000628:therapy*; D006510:Hepatitis B Antibodies / Q000008:administration & dosage; D006511:Hepatitis B Antigens; D006801:Humans; D007111:Immunity, Cellular; D007112:Immunity, Maternally-Acquired; D007167:Immunotherapy / Q000379:methods*; D007962:Leukocytes / Q000276:immunology; D051379:Mice; D002679:Pan troglodytes / Q000276:immunology; D012313:RNA / Q000276:immunology; D014165:Transfer Factor
D006510:Hepatitis B Antibodies; D006511:Hepatitis B Antigens; D014165:Transfer Factor; D012313:RNA