Recently, a new hepatitis B virus (HBV) mutant with HBe antigen-negative phenotype has been characterized, in which one TATA box-like motif of the precore/core promoter had degenerated: most frequently by both A → T and G → A mutations at positions 1762 and 1764, respectively. The clinical significance of this mutant is as yet unknown. In our present study, the T A mutant was sought in sera from HBV-infected blood donors and chronic liver disease patients by directly sequencing a PCR-amplified region of HBV DNA. Also, because the A mutation generates a 3AI cleavage site (GTC → GTC), we digested the PCR products with 3AI to see if cleavage would occur at this specific site. Our results mostly corroborated the earlier report but we found a higher-than-predicted frequency of HBe antigen-positive blood donors positive for the mutant (22%). The titres of HBe antigen in these mutant-positive sera were slightly decreased compared to the titres in wild-type HBV infection. In addition, these blood donors had relatively high (though within the normal range) serum alanine aminotransferase (ALT) levels, suggesting that the T A mutation could be used as a sensitive laboratory marker for insidious hepatitis in these otherwise ‘asymptomatic’ carriers. The 3AI assay, which is much more convenient than sequencing, was shown to be useful for the detection of the T A mutant in an extensive number of clinical samples.


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