Zhang Y, Kaplan G G
Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA.
J Virol. 1998 Jan;72(1):349-57. doi: 10.1128/JVI.72.1.349-357.1998.
To determine whether hepatitis A virus (HAV) could tolerate the insertion of exogenous sequences, we constructed full-length HAV cDNAs containing in-frame insertions at the N terminus of the polyprotein and transfected the derived T7 RNA polymerase in vitro transcripts into FRhK-4 cells. Replication of HAVvec1, a construct containing an insertion of 60 nucleotides coding for a polylinker, a 2B/2C cleavage site for HAV protease 3Cpro, and two initiation codons that restored the sequence of the N terminus of the polyprotein, was detected 2 weeks after transfection by indirect immunofluorescence analysis using anti-HAV monoclonal antibodies. Western blot analysis of HAVvec1-infected cells using anti-VP2 and anti-VP4 antibodies failed to detect the expression of the inserted sequences. Insertion of a 24-mer oligonucleotide coding for a FLAG epitope into HAVvec1 resulted in its HAV-mediated expression which was retained upon deletion of a Gln residue from the inserted 2B/2C cleavage site. Western blot analysis using anti-FLAG and anti-VP2 antibodies showed that the FLAG epitope accumulated in infected cells fused to VP0. Replacement of the FLAG epitope with an epitope of the circumsporozoite protein (CSP) of Plasmodium falciparum resulted in its stable HAV-mediated expression for at least six serial passages in FRhK-4 cells. Sedimentation analysis in sucrose density gradients showed that the CSP epitope accumulated in infected cells fused to VP0, forming 80S empty capsids which also contained native VP0. Our data suggest that the HAV internal ribosome entry site can efficiently direct dual initiation of translation of the polyprotein from AUG codons separated by 66 to 78 nucleotides and show that HAV can tolerate insertions at the N terminus of the polyprotein.
为了确定甲型肝炎病毒(HAV)是否能够耐受外源序列的插入,我们构建了全长HAV cDNA,该cDNA在多聚蛋白的N端含有读框内插入序列,并将衍生的T7 RNA聚合酶体外转录本转染到FRhK-4细胞中。通过使用抗HAV单克隆抗体的间接免疫荧光分析,在转染后2周检测到HAVvec1(一种包含编码多克隆位点的60个核苷酸插入、HAV蛋白酶3Cpro的2B/2C切割位点以及恢复多聚蛋白N端序列的两个起始密码子的构建体)的复制。使用抗VP2和抗VP4抗体对HAVvec1感染细胞进行的蛋白质印迹分析未能检测到插入序列的表达。将编码FLAG表位的24聚体寡核苷酸插入HAVvec1导致其由HAV介导的表达,该表达在从插入的2B/2C切割位点缺失一个Gln残基后仍得以保留。使用抗FLAG和抗VP2抗体的蛋白质印迹分析表明,FLAG表位在与VP0融合的感染细胞中积累。用恶性疟原虫环子孢子蛋白(CSP)的表位替换FLAG表位导致其在FRhK-4细胞中至少连续传代六次时由HAV介导的稳定表达。蔗糖密度梯度沉降分析表明,CSP表位在与VP0融合的感染细胞中积累,形成80S空衣壳,其中也含有天然VP0。我们的数据表明,HAV内部核糖体进入位点可以有效地指导多聚蛋白从相距66至78个核苷酸的AUG密码子进行双重起始翻译,并表明HAV能够耐受多聚蛋白N端的插入。