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AIM:HBsAg is the most important serological marker foracute or chronic hepatitis B.Nevertheless,there were reportsof HBsAg-negative infection caused by hepatitis B virus inrecent years.We had a patient with crytogenic cirrhosis whowas negative for HBsAg,positive for anti-HBs and HBeAg.This paper was to explore the pathogenic and molecularbasis of the unusual serological pattern.METHODS:HBV serologic markers were qualitatively andquantitatively determined.HBV DNA in serum wasqualitatively tested using routine Polymerase chain reaction(PCR),and the viral level was determined with real-timefluorescence quantitative PCR.HBsAg gene was amplifiedand cloned.Four clones were sequenced.The new genomicsequences were compared with GenBank on the DNA levelas well as the protein level.RESULTS:The qualitative results of serological markerswere HBsAg(-),anti-HBs(+),HBeAg(+),anti-HBe(-) andanti-HBc(+).The quantitative results of serological markerwere HBsAg (S/N):0.77 (cut off of S/N:≥2.00),HBeAg (S/N):56.43 (cut off S/N:≥2.10),anti-HBc (S/C_o):2.03 (cutoff of S/C_o:≤1.00).The viral level was as high as 1.54×10~9copies/ml.Sequencing of the HBsAg gene clones revealeda unique point mutation at nucleotide 336 (C to A),whichresulted in a novel stop codon at aa 61.The novel HBsAggene stop mutation had not been described.CONCLUSION:The lack of detection of HBsAg in thepresence of high viral levels of replication may be caused bythe existence of viral genomes harboring point mutationswhich resulted in stop codon upstream of the“a”determinantin HBsAg gene.
AIM: HBsAg is the most important serological marker foracute or chronic hepatitis B. Nevertheless, there were reports of HBsAg-negative infection caused by hepatitis B virus in recent years. We had a patient with cryogenic gyrhosis whowas negative for HBsAg, positive for anti-HBs and HBeAg.This paper was to explore the pathogenic and molecularbasis of the unusual serological pattern. METHODS: HBV serologic markers were qualitatively andquantitatively determined. HBV DNA in serum was quantitatively qualified tested by routine Polymerase chain reaction (PCR), and the viral level was determined with real -timefluorescence quantitative PCR. HBsAg gene was amplified and cloned.Four clones were sequenced. The new genomic sequences were compared with GenBank on the DNA levelas well as the protein level .RESULTS: The qualitative results of serological markerswere HBsAg (-), anti-HBs ( The quantitative results of serological markerwere HBsAg (S / N): 0.77 (cut off of S / N: ≥2.00), HBeAg (+), anti-HBe /N):56.43 (cut off S / N: ≥2.10), anti-HBc (S / C_o): 2.03 (cutoff of S / C_o: ≤1.00) .The viral level was as high as 1.54 × 10 ~ 9copies / ml. Sequencing of the HBsAg gene clones revealeda unique point mutation at nucleotide 336 (C to A), which was solved in a novel stop codon at aa 61. The novel HBsAggene stop mutation had not been described. CONCLUSION: The lack of detection of HBsAg in thepresence of high viral levels of replication may be caused by the existence of viral genomes harboring point mutationswhich resulted in stop codon upstream of the “” "determinantin HBsAg gene.