Takayanagi M, Kakumu S, Ishikawa T, Higashi Y, Yoshioka K, Wakita T
Third Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Virology. 1993 Sep;196(1):138-45. doi: 10.1006/viro.1993.1462.
We analyzed entire pre-C/C and pre-S/S coding genes of hepatitis B virus (HBV) in serial serum samples from four chronic HBV carriers with 4-5 years of follow-up. Two patients with chronic active hepatitis became seronegative for HB e antigen (HBeAg), but the hepatitis did not subside, while the other two were persistent asymptomatic carriers with normal aminotransferase values. DNAs amplified by PCR were cloned and sequenced (subtype adr). After HBeAg became negative, one patient had 96-183 bp deletions in 4/6 clones for C gene. In addition, both patients had 129-183 bp deletions in 3/6 and 2/5 clones for pre-S1 gene, respectively. Divergence rate of deduced amino acid for both pre-C/C and pre-S/S regions from the adr subtype was significantly higher in patients with chronic hepatitis than in asymptomatic carriers. Furthermore, the divergence rate for pre-S/S region was usually greater in asymptomatic carriers as well as chronic hepatitis patients compared with that for pre-C/C region. However, no significant difference was found in the rate of amino acid divergence for the entire HBV genes between the serial samples in all patients studied here. These results suggest that active hepatitis induces variation of HBV gene and defective virus is often selected along with the disappearance of HBeAg. In addition, the fact that patients with active liver disease possess greater numbers of mutant clones than asymptomatic carriers suggests that viral mutants are being immune-selected.
我们对4名慢性乙肝病毒(HBV)携带者连续4至5年的血清样本中的整个乙肝病毒前C/C区和前S/S编码基因进行了分析。两名慢性活动性肝炎患者的乙肝e抗原(HBeAg)转为血清学阴性,但肝炎并未消退,而另外两名患者是转氨酶值正常的持续性无症状携带者。通过聚合酶链反应(PCR)扩增的DNA被克隆并测序(adr亚型)。HBeAg转阴后,一名患者的C基因在4/6个克隆中有96至183bp的缺失。此外,两名患者的前S1基因分别在3/6和2/5个克隆中有129至183bp的缺失。慢性肝炎患者前C/C区和前S/S区推导氨基酸与adr亚型的差异率显著高于无症状携带者。此外,与前C/C区相比,无症状携带者以及慢性肝炎患者前S/S区的差异率通常更大。然而,在本文研究的所有患者的系列样本中,整个HBV基因的氨基酸差异率未发现显著差异。这些结果表明,活动性肝炎会诱导HBV基因变异,并且缺陷病毒常伴随HBeAg的消失而被选择。此外,活动性肝病患者比无症状携带者拥有更多突变克隆这一事实表明病毒突变体正在被免疫选择。