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Korean J Clin Pathol. 1997 Oct;17(5):858-869. Korean. Original Article.
Son BR , Kim YK .

BACKGROUND: The precore mutant hepatits B virus (HBV) cannot produce HBeAg due to the formation of transnational stop codon at nucleotide 1896 of the HBV-DNA precore region. This mutant has been detected worldwide in acute fulminant hepatitis, carrier and chronic HBV infections. It has been controversial whether the emergence of precore mutant HBV is related to the severity of the chronic hepatitis B or not. METHODS: To determine the prevalence and clinical implication of precore mutant infection, 137 HBsAg (+) patients including 12 acute hepatitis, 59 carriers, 41 chronic hepatitis, 15 liver cirrhosis, and 10 hepatomas were examined with mutation site specific assay-polymerase chain reaction (MSSA-PCR). The specificity for the detection of mutant by MSSA-PCR method was confirmed by direct sequencing of PCR products. RESULTS: The precore mutant HBV was detected in 67 of 137 (49%) subjects : none of 12 (0%) acute hepatitis patients, 17 of 59 (29%) carriers, 31 of 41 (76%) chronic hepatitis patients, 12 of IS (80%) liver cirrhosis patients, and 6 of 10 (60%) hepatoma patients. According to the status of serum HBeAg, the emergence rate of precore mutant HBV in HBeAg(-) cases was relatively higher than in HBeAg(+) cases with blood donor and chronic hepatitis. In anti-HBe (+) patients with chronic hepatitis, the precore mutant HBV was found regardless of ALT level in all patients. Emergence rate of precore mutant HBV was abruptly increased after 30 years of age. Among HBV-DNA (-) sera by DNA probe method, the core region of HBV was amplified in 94% of sera by MSSA-PCR method. CONCLUSIONS: The presence of precore mutant HBV may be related to the duration of HBV infections and there seems to be no causal relationship between the presence of precore mutant HBV and the severity of chronic hepatitis.

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