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Journal of Clinical Microbiology, June 2004, p. 2861-2865, Vol. 42, No. 6
0095-1137/04/$08.00+0 DOI: 10.1128/JCM.42.6.2861-2865.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Academic Department of Medicine, Hippokration General Hospital, Athens, Greece,1 Department of Medicine, Imperial College London, Faculty of Medicine, St. Mary's Campus, London, United Kingdom2
Received 4 December 2003/ Returned for modification 26 January 2004/ Accepted 17 February 2004
A patient with agammaglobulinemia developed acute hepatitis that progressed to chronic liver disease with high levels of hepatitis B virus (HBV) DNA in the absence of detectable HBsAg. Sequencing of the a determinant region of HBsAg revealed multiple amino acid substitutions that, unusually, also included a substitution at position 122 that defines subtype specificity. All of these mutations had a profound effect on the antigenicity of this region, which led to the complete failure of variant detection by commercially available routine diagnostic assays or laboratory-based monoclonal antibody assays.
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