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为探讨乙型肝炎表面抗原（ＨＢｓＡｇ）阴性乙型肝炎病毒（ＨＢＶ）感染这一特殊临床现象的分子生物学基础，对２例血清ＨＢｓＡｇ（－）／ＨＢＶＤＮＡ（＋）慢性肝炎患者ＨＢＶ的Ｓ基因全序列进行了分析，并与同时获得的１５例ＨＢｓＡｇ阳性患者序列和已发表的序列进行比较。结果发现一种新的ＨＢＶ插入变异株：１例在Ｓ基因第５１８位核苷酸前插入了６个核苷酸，从而在ＨＢｓＡｇ密码子１２２和１２３间“ａ”决定族前多编码两个氨基酸；另１例于５１８位核苷酸后插入９个核苷酸，导致在密码子１２３和１２４间增加３个氨基酸。在核苷酸水平插入部位恰好位于“ａ”编码区前的４个连续Ａ（核苷酸５１６－５１９）。我们推测Ｓ基因插入变异可能是病毒的一种免疫逃避机制。
To explore the molecular basis of this special clinical phenomenon of hepatitis B surface antigen (HBsAg) -negative hepatitis B virus (HBV) infection, two S-genes of HBV in patients with serum of HBsAg (-) / HBVDNA The complete sequence was analyzed and compared with the 15 sequences of HBsAg positive patients and the published sequences obtained simultaneously. As a result, a new HBV insertion mutant was found: 1 case had 6 nucleotides inserted before the 518th nucleotide of the S gene so as to encode two more before the “a” determinant of the HBsAg codons 122 and 123 Amino acid. The other 1 insert 9 nucleotides after 518 nucleotides, resulting in an increase of 3 amino acids between codons 123 and 124. At the nucleotide level the insertion site is exactly 4 consecutive A (nucleotides 516-519) located in front of the “a” coding region. We hypothesized that the S gene insertion mutation may be an immune evasion mechanism of the virus.