Department of Pathogen Molecular Biology, London School of Hygiene & Tropical Medicine, University of London, London WC1E 7HT, UK.
Institute for Structural and Molecular Biology, Department Biology, Birkbeck College University of London, London WC1E 7HX, UK.
Viruses. 2017 Dec 31;10(1):16. doi: 10.3390/v10010016.
Tissue-culture adaptation of viruses can modulate infection. Laboratory passage and bacterial artificial chromosome (BAC)mid cloning of human cytomegalovirus, HCMV, resulted in genomic deletions and rearrangements altering genes encoding the virus entry complex, which affected cellular tropism, virulence, and vaccine development. Here, we analyse these effects on the reference genome for related betaherpesviruses, Roseolovirus, human herpesvirus 6A (HHV-6A) strain U1102. This virus is also naturally "cloned" by germline subtelomeric chromosomal-integration in approximately 1% of human populations, and accurate references are key to understanding pathological relationships between exogenous and endogenous virus. Using whole genome next-generation deep-sequencing Illumina-based methods, we compared the original isolate to tissue-culture passaged and the BACmid-cloned virus. This re-defined the reference genome showing 32 corrections and 5 polymorphisms. Furthermore, minor variant analyses of passaged and BACmid virus identified emerging populations of a further 32 single nucleotide polymorphisms (SNPs) in 10 loci, half non-synonymous indicating cell-culture selection. Analyses of the BAC-virus genome showed deletion of the BAC cassette via loxP recombination removing green fluorescent protein (GFP)-based selection. As shown for HCMV culture effects, select HHV-6A SNPs mapped to genes encoding mediators of virus cellular entry, including virus envelope glycoprotein genes gB and the gH/gL complex. Comparative models suggest stabilisation of the post-fusion conformation. These SNPs are essential to consider in vaccine-design, antimicrobial-resistance, and pathogenesis.
病毒的组织培养适应可以调节感染。人类巨细胞病毒(HCMV)的实验室传代和细菌人工染色体(BAC)中间克隆导致基因组缺失和重排,改变了编码病毒进入复合物的基因,从而影响细胞嗜性、毒力和疫苗开发。在这里,我们分析了这些对相关β疱疹病毒、玫瑰疹病毒、人类疱疹病毒 6A(HHV-6A)株 U1102 的参考基因组的影响。这种病毒也自然通过生殖系端粒染色体整合在大约 1%的人类中“克隆”,准确的参考是理解外源性和内源性病毒之间病理关系的关键。使用全基因组下一代深度测序 Illumina 方法,我们将原始分离株与组织培养传代和 BACmid 克隆病毒进行了比较。这重新定义了参考基因组,显示了 32 个校正和 5 个多态性。此外,传代和 BACmid 病毒的次要变异分析在 10 个基因座中鉴定出了另外 32 个单核苷酸多态性(SNP)的新兴群体,其中一半是非同义的,表明细胞培养选择。对 BAC 病毒基因组的分析表明,通过 loxP 重组删除了 BAC 盒,去除了基于绿色荧光蛋白(GFP)的选择。正如 HCMV 培养效应所示,选择的 HHV-6A SNP 映射到编码病毒细胞进入介质的基因上,包括病毒包膜糖蛋白基因 gB 和 gH/gL 复合物。比较模型表明融合后构象的稳定性增加。在疫苗设计、抗菌药物耐药性和发病机制中,这些 SNP 是必不可少的考虑因素。