The presence of a hepatitis B virus S gene mutant was investigated in a patient being treated with thymosin α1. He was seropositive for hepatitis B e antigen throughout therapy but was intermittently seronegative for hepatitis B surface antigen (HBsAg) by an RIA. Sequence analysis revealed an S gene mutant in HBsAg-seronegative serum with two consecutive amino acid substitutions: threonine115-to-isoleucine and threonine116-to- asparagine, whereas no amino acid substitution or deletion was found in the pre-S region. A site-directed mutagenesis experiment confirmed that these mutations were responsible for the failure to detect HBsAg. In summary, an S gene mutant was identified in an HBsAg-seronegative patient. The mutations were located outside the putative 'a' determinant. The emergence of an S gene mutant during thymosin α1 treatment suggests that enhanced host immunity against HBsAg may play a role in its antiviral activity.
|Number of pages||4|
|Journal||Journal of Infectious Diseases|
|Publication status||Published - Jan 1 1998|
ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases