As RNA virus mutation occurs during replication within host cells, we hypothesized that viral evolution during acute infections in healthy hosts reflects host immune pressure. We therefore investigated the within-host diversification of human respiratory syncytial virus (RSV), a highly prevalent cause of acute respiratory infections. We evaluated healthy adults experimentally infected with an identical inoculum and infants hospitalized with naturally acquired infections. In aggregate, viral diversification in adults peaked at day 3, with overrepresentation of diversity in the matrix protein 2 (M2) and non-structural protein 2 (NS2) genes. In one subject, delayed viral clearance was accompanied by a late peak of diversity at day 10 in known and predicted B and T cell epitopes. In contrast, infant infections showed much less viral diversity. Our findings suggest multiple overlapping mechanisms for early control of acute viral infections, which may differ between age groups and host immune responses.

由于在宿主细胞内复制期间发生RNA病毒突变，因此我们假设健康宿主在急性感染期间的病毒进化反映了宿主的免疫压力。因此，我们研究了人类呼吸道合胞病毒（RSV）的宿主内部多样性，RSV是急性呼吸道感染的高度普遍原因。我们评估了通过实验实验感染相同接种物的健康成人和因自然感染而住院的婴儿。总的来说，成人的病毒多样化在第3天达到高峰，其中基质蛋白2（M2）和非结构蛋白2（NS2）基因的多样性过高。在一个受试者中，在已知和预测的B和T细胞表位中，病毒清除延迟伴随着在第10天的多样性晚期峰。相反，婴儿感染表现出的病毒多样性要低得多。