Kato Hideaki, Orito Etsuro, Gish Robert G, Sugauchi Fuminaka, Suzuki Seiji, Ueda Ryuzo, Miyakawa Yuzo, Mizokami Masashi
Department of Internal Medicine and Molecular Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
J Virol. 2002 Jun;76(12):6131-7. doi: 10.1128/jvi.76.12.6131-6137.2002.
Eight hepatitis B virus (HBV) isolates of genotype G were recovered from patients and sequenced over the entire genome. Six of them had a genomic length of 3,248 bp and two had genomic lengths of 3,239 bp (USG15) and 3,113 bp (USG18) due to deletions. The 10 HBV/G isolates, including the 8 sequenced isolates as well as the original isolate (AF160501) and another isolate (B1-89), had a close sequence homology of 99.3 to 99.8% among themselves (excluding USG18 with a long deletion) but of <88.7% to any of the 68 HBV isolates of the other six genotypes with the full-length sequence known. The eight HBV/G isolates possessed an insertion of 36 bp in the core gene and two stop codons in the precore region, as did the AF160501 and B1-89 isolates. The 10 HBV/G isolates clustered on a branch separate from those bearing the other six genotypes (A through F [A-F]) in the phylogenetic tree constructed from full-length sequences of 78 HBV isolates as well as in those constructed from the core, polymerase, X, and envelope genes. Despite two stop codons in the precore region that prohibited the translation of the HBV e antigen (HBeAg), all of the eight patients with HBV/G infection possessed the HBeAg in serum. By restriction fragment length polymorphism of the surface gene, all of the eight patients were found to be coinfected with HBV of genotype A (HBV/A), which would be responsible for the expression of HBeAg in them. It is worthy of examination to determine how coinfection occurs and whether HBV/G needs HBV/A for replication.
从患者体内分离出8株G基因型乙型肝炎病毒(HBV),并对其全基因组进行测序。其中6株基因组长度为3248 bp,另外2株因缺失分别为3239 bp(USG15)和3113 bp(USG18)。这10株HBV/G分离株,包括8株测序分离株以及原始分离株(AF160501)和另一分离株(B1 - 89),彼此之间的序列同源性很高,为99.3%至99.8%(不包括有长缺失的USG18),但与其他6种已知全长序列的68株HBV分离株中的任何一株的同源性均小于88.7%。这8株HBV/G分离株在核心基因中有一个36 bp的插入,在前核心区有两个终止密码子,AF160501和B1 - 89分离株也是如此。在根据78株HBV分离株的全长序列构建的系统发育树以及根据核心、聚合酶、X和包膜基因构建的系统发育树中,这10株HBV/G分离株聚集在一个与携带其他6种基因型(A至F [A - F])的分离株不同的分支上。尽管前核心区有两个终止密码子阻止了乙型肝炎e抗原(HBeAg)的翻译,但所有8例HBV/G感染患者的血清中均存在HBeAg。通过表面基因的限制性片段长度多态性分析,发现所有8例患者均同时感染了A基因型HBV(HBV/A),这可能是导致他们体内HBeAg表达的原因。确定共感染是如何发生的以及HBV/G复制是否需要HBV/A值得研究。