Hepatic infections. Part II. The effect of acute and chronic hepatitis B antigenaemia on the reaction to antibodies to sheep red cells (microbial antigens) and human T-activated cells (exposed autologous tissue antigens).
Using the agglutination of sheep red cells by human antibodies as an indicator of microbial antibody activity, a highly significant association was found between the response to the e antigen of the hepatitis B virus and the formation of strong antibody levels to microbial substances (chi 2(1) = 33). This kind of association was not found among chronic carriers of the hepatitis B virus who do not produce antibodies to the e antigen (chi 2(1) = 3,7). In the presence of e antigen activity, patients with acute virus B hepatitis almost always show significantly reduced levels of antibodies to microbial substances (chi 2(1) = 20). The findings indirectly reveal that e activity is associated with the inability of the liver to trap bacterial antigens. Circumstantial evidence further suggests that the e factor may bear antigens on its immunoglobulin-like structure very similar to microbial cell wall components. Accepting that human antibodies to the T (Thomsen-Friedenreich) antigen represent reactions to cryptantigenic membrane structure of autologous tissues, it was significant to record that increased anti-t activity is always demonstrated when virus B infections progress from the acute to the chronic carrier stage (chi 2(1) = 73). The most intense anti-T activity is commonly found in subjects who produce antibodies to the hepatitis B surface antigen (chi 2(1) = 138). In the presence of e antigen the amount of anti-T in circulation is always significantly depressed. Since this type of depression is not seen in patients with acute virus B hepatitis who lack the e antigen, we suspect that the reduced anti-T levels in e antigen-positive patients are linked with the in vivo exposure of T receptors by microbial neuraminidase.
D000208:Acute Disease; D000372:Agglutination Tests; D000373:Agglutinins / Q000276:immunology; D000818:Animals; D000914:Antibodies, Viral / Q000276:immunology*; D001782:Blood Donors; D002908:Chronic Disease; D003429:Cross Reactions; D004912:Erythrocytes / Q000276:immunology*; D006510:Hepatitis B Antibodies / Q000276:immunology*; D006514:Hepatitis B Surface Antigens / Q000276:immunology*; D006525:Hepatitis, Viral, Human / Q000276:immunology*; D006649:Histocompatibility Antigens / Q000276:immunology; D006801:Humans; D008213:Lymphocyte Activation; D012756:Sheep / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D000373:Agglutinins; D000914:Antibodies, Viral; D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D006649:Histocompatibility Antigens