De novo infection in a renal transplant recipient caused by novel mutants of hepatitis B virus despite the presence of protective anti-hepatitis B surface antibody.
A renal transplant recipient became persistently positive for hepatitis B virus (HBV) despite preexisting anti-hepatitis B surface (HBs) antibodies. The antigenicity and immunogenicity of wild-type (wt) and mutant HBs antigens (Ags) were compared. In contrast to wt HBsAg, genetic vaccination with mutant HBsAgs did not induce anti-HBs. Thus, mutations within HBsAg may enable HBV to escape immunological control.
Lu
Mengji
M
Institut für Virologie, Universitätsklinikum Essen, Essen, Germany. mengji.lu@uni-essen.de
Lorentz
Thomas
T
D000328:Adult; D000818:Animals; D006508:Hepatitis Antibodies / Q000276:immunology*; D006509:Hepatitis B / Q000276:immunology* / Q000821:virology*; D006514:Hepatitis B Surface Antigens / Q000235:genetics* / Q000276:immunology*; D017325:Hepatitis B Vaccines / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology / Q000502:physiology*; D006801:Humans; D007668:Kidney; D016030:Kidney Transplantation; D051379:Mice; D009154:Mutation
D006508:Hepatitis Antibodies; D006514:Hepatitis B Surface Antigens; D017325:Hepatitis B Vaccines