Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
PLoS One. 2012;7(12):e51439. doi: 10.1371/journal.pone.0051439. Epub 2012 Dec 7.
Human respiratory syncytial virus (RSV) is an important cause of severe lower respiratory tract infections in infants and the elderly. In the vast majority of cases, however, RSV infections run mild and symptoms resemble those of a common cold. The immunological, clinical, and epidemiological profile of severe RSV infections suggests a disease caused by a virus with typical seasonal transmission behavior, lacking clear-cut virulence factors, but instead causing disease by modifying the host's immune response in a way that stimulates pathogenesis. Yet, the interplay between RSV-evoked immune responses and epidemic behavior, and how this affects the genomic evolutionary dynamics of the virus, remains poorly understood. Here, we present a comprehensive collection of 33 novel RSV subgroup A genomes from strains sampled over the last decade, and provide the first measurement of RSV-A genomic diversity through time in a phylodynamic framework. In addition, we map amino acid substitutions per protein to determine mutational hotspots in specific domains. Using Bayesian genealogical inference, we estimated the genomic evolutionary rate to be 6.47 × 10(-4) (credible interval: 5.56 × 10(-4), 7.38 × 10(-4)) substitutions/site/year, considerably slower than previous estimates based on G gene sequences only. The G gene is however marked by elevated substitution rates compared to other RSV genes, which can be attributed to relaxed selective constraints. In line with this, site-specific selection analyses identify the G gene as the major target of diversifying selection. Importantly, statistical analysis demonstrates that the immune driven positive selection does not leave a measurable imprint on the genome phylogeny, implying that RSV lineage replacement mainly follows nonselective epidemiological processes. The roughly 50 years of RSV-A genomic evolution are characterized by a constant population size through time and general co-circulation of lineages over many epidemic seasons - a conclusion that might be taken into account when developing future therapeutic and preventive strategies.
人类呼吸道合胞病毒(RSV)是导致婴儿和老年人严重下呼吸道感染的重要原因。然而,在绝大多数情况下,RSV 感染症状较轻,类似于普通感冒。严重 RSV 感染的免疫、临床和流行病学特征表明,这种疾病是由一种具有典型季节性传播行为的病毒引起的,缺乏明确的毒力因子,但通过改变宿主的免疫反应来刺激发病机制。然而,RSV 引起的免疫反应和流行行为之间的相互作用,以及这如何影响病毒的基因组进化动态,仍然知之甚少。在这里,我们提供了过去十年中采集的 33 株新的 RSV-A 亚组基因组的综合数据集,并在系统发育框架中首次测量了 RSV-A 基因组随时间的多样性。此外,我们将每个蛋白的氨基酸替换映射到特定结构域中的突变热点。使用贝叶斯系统发育推断,我们估计基因组进化率为 6.47×10(-4)(置信区间:5.56×10(-4),7.38×10(-4))替换/位点/年,明显慢于以前仅基于 G 基因序列的估计。然而,G 基因的替换率明显高于其他 RSV 基因,这可以归因于选择压力的放松。与此一致的是,基于特定位点的选择分析表明 G 基因是多样化选择的主要目标。重要的是,统计分析表明,免疫驱动的正选择不会在基因组系统发育树上留下可测量的印记,这意味着 RSV 谱系更替主要遵循非选择性的流行病学过程。RSV-A 基因组大约 50 年的进化历史表明,其种群大小随时间保持不变,并且许多流行季节中都会共同循环多种谱系,这一结论可能在制定未来的治疗和预防策略时被考虑在内。