Beneduce F, Pisani G, Divizia M, Panà A, Morace G
Laboratory of Virology, Istituto Superiore di Sanitá, Rome, Italy.
Virus Res. 1995 May;36(2-3):299-309. doi: 10.1016/0168-1702(95)00009-f.
The molecular basis of the cytopathic effect induced in cell culture by some hepatitis A virus (HAV) strains and variants has not been determined. In order to assess the molecular mechanism(s) underlying this particular phenotype the genome of an Italian cytopathic isolate (strain FG) was sequenced from cDNAs obtained by RT-PCR. Sequence analysis revealed the presence of mutations common to either adapted or cytopathic variants of HAV. In particular, amino acid deletions in proteins VP1 and 3A were detected. Expression of protein 3A in E. coli showed that the N-terminal deletion renders this protein toxic to bacteria.
某些甲型肝炎病毒（HAV）毒株和变异体在细胞培养中诱导产生细胞病变效应的分子基础尚未明确。为了评估这种特殊表型背后的分子机制，对一株意大利细胞病变分离株（FG株）的基因组进行了测序，这些基因组来自通过逆转录聚合酶链反应（RT-PCR）获得的互补脱氧核糖核酸（cDNA）。序列分析揭示了HAV适应性或细胞病变变异体共有的突变。特别是，检测到了病毒蛋白VP1和3A中的氨基酸缺失。蛋白质3A在大肠杆菌中的表达表明，N端缺失使该蛋白对细菌具有毒性。
