Thompson Robin N, Wymant Chris, Spriggs Rebecca A, Raghwani Jayna, Fraser Christophe, Lythgoe Katrina A
Department of Zoology, University of Oxford, South Parks Road, Oxford, UK.
Mathematical Institute, University of Oxford, Andrew Wiles Building, Radcliffe Observatory Quarter, Oxford, UK.
Virus Evol. 2019 Jan 30;5(1):vey038. doi: 10.1093/ve/vey038. eCollection 2019 Jan.
Understanding which HIV-1 variants are most likely to be transmitted is important for vaccine design and predicting virus evolution. Since most infections are founded by single variants, it has been suggested that selection at transmission has a key role in governing which variants are transmitted. We show that the composition of the viral population within the donor at the time of transmission is also important. To support this argument, we developed a probabilistic model describing HIV-1 transmission in an untreated population, and parameterised the model using both within-host next generation sequencing data and population-level epidemiological data on heterosexual transmission. The most basic HIV-1 transmission models cannot explain simultaneously the low probability of transmission and the non-negligible proportion of infections founded by multiple variants. In our model, transmission can only occur when environmental conditions are appropriate (e.g. abrasions are present in the genital tract of the potential recipient), allowing these observations to be reconciled. As well as reproducing features of transmission in real populations, our model demonstrates that, contrary to expectation, there is not a simple link between the number of viral variants and the number of viral particles founding each new infection. These quantities depend on the timing of transmission, and infections can be founded with small numbers of variants yet large numbers of particles. Including selection, or a bias towards early transmission (e.g. due to treatment), acts to enhance this conclusion. In addition, we find that infections initiated by multiple variants are most likely to have derived from donors with intermediate set-point viral loads, and not from individuals with high set-point viral loads as might be expected. We therefore emphasise the importance of considering viral diversity in donors, and the timings of transmissions, when trying to discern the complex factors governing single or multiple variant transmission.
了解哪些HIV-1变体最有可能传播,对于疫苗设计和预测病毒进化至关重要。由于大多数感染是由单一变体引发的,因此有人提出,传播时的选择在决定哪些变体能够传播方面起着关键作用。我们发现,传播时供体内病毒群体的组成也很重要。为支持这一观点,我们开发了一个概率模型来描述未接受治疗人群中的HIV-1传播,并使用宿主内下一代测序数据和异性传播的人群水平流行病学数据对该模型进行参数化。最基本的HIV-1传播模型无法同时解释低传播概率和由多个变体引发的感染中不可忽略的比例。在我们的模型中,只有当环境条件适宜时(例如潜在接受者的生殖道存在擦伤)传播才会发生,从而使这些观察结果能够得到协调。除了再现实际人群中传播的特征外,我们的模型还表明,与预期相反,病毒变体数量与引发每次新感染的病毒颗粒数量之间没有简单的联系。这些数量取决于传播时间,并且少量变体但大量颗粒也可能引发感染。纳入选择因素或对早期传播的偏向(例如由于治疗)会强化这一结论。此外,我们发现由多个变体引发的感染最有可能源自具有中等设定点病毒载量的供体,而不是如预期的那样源自具有高设定点病毒载量的个体。因此,我们强调在试图识别控制单一或多个变体传播的复杂因素时,考虑供体内病毒多样性和传播时间的重要性。