School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia.
The Kirby Institute, UNSW, Sydney, NSW, Australia.
Infect Genet Evol. 2019 Jul;71:36-41. doi: 10.1016/j.meegid.2019.02.032. Epub 2019 Mar 8.
Transfer of hepatitis C virus (HCV) infection from a donor to a new recipient is associated with a bottleneck of genetic diversity in the transmitted viral variants. Existing data suggests that one, or very few, variants emerge from this bottleneck to establish the infection (transmitted founder [T/F] variants). In HCV, very few T/F variants have been characterized due to the challenges of obtaining early infection samples and of high throughput viral genome sequencing. This study used a large, acute HCV, deep-sequenced dataset from first viremia samples collected in nine prospective cohorts across four countries, to estimate the prevalence of single T/F viruses, and to identify host and virus-related factors associated with infections initiated by a single T/F variant. The short reads generated by Illumina sequencing were used to reconstruct viral haplotypes with two haplotype reconstruction algorithms. The haplotypes were examined for random mutations (Poisson distribution) and a star-like phylogeny to identify T/F viruses. The findings were cross-validated by haplotype reconstructions across three regions of the genome (Core-E2, NS3, NS5A) to minimize the possibility of spurious overestimation of single T/F variants. Of 190 acute infection samples examined, 54 were very early acute infections (HCV antibody negative, RNA positive), and single transmitted founders were identified in 14 (26%, 95% CI: 16-39%) after cross validation across multiple regions of the genome with two haplotype reconstruction algorithms. The presence of a single T/F virus was not associated with any host or virus-related factors, notably viral genotype or spontaneous clearance. In conclusion, approximately one in four new HCV infections originates from a single T/F virus. Resolution of genomic sequences of single T/F variants is the first step in exploring unique properties of these variants in the infection of host hepatocytes.
丙型肝炎病毒(HCV)感染从供体转移到新受者与传播病毒变异体的遗传多样性瓶颈有关。现有数据表明,从这个瓶颈中出现一个或极少数变体来建立感染(传播的创始变体[T/F])。在 HCV 中,由于获得早期感染样本和高通量病毒基因组测序的挑战,很少有 T/F 变体被表征。本研究使用了来自四个国家的九个前瞻性队列中首次病毒血症样本的大量急性 HCV 深度测序数据集,来估计单一 T/F 病毒的流行率,并确定与由单一 T/F 变体引发的感染相关的宿主和病毒相关因素。Illumina 测序生成的短读序列用于使用两种单倍型重建算法来重建病毒单倍型。检查单倍型是否存在随机突变(泊松分布)和星状系统发育,以鉴定 T/F 病毒。通过跨基因组三个区域(核心-E2、NS3、NS5A)的单倍型重建对发现进行交叉验证,以最大程度地减少单个 T/F 变体的虚假高估的可能性。在检查的 190 个急性感染样本中,有 54 个是非常早期的急性感染(HCV 抗体阴性,RNA 阳性),在跨基因组多个区域使用两种单倍型重建算法进行交叉验证后,在 14 个样本中鉴定出了单一的传播创始变体(26%,95%CI:16-39%)。单一 T/F 病毒的存在与任何宿主或病毒相关因素无关,特别是病毒基因型或自发清除。总之,大约四分之一的新 HCV 感染源自单一 T/F 病毒。解析单一 T/F 变体的基因组序列是探索这些变体在感染宿主肝细胞过程中独特特性的第一步。