Department of Ecology and Evolution, Biological Sciences Division, University of Chicago, Chicago, IL 60637.
Department of Ecology and Evolution, Biological Sciences Division, University of Chicago, Chicago, IL 60637;
Proc Natl Acad Sci U S A. 2021 Mar 2;118(9). doi: 10.1073/pnas.2019716118.
The contributions of asymptomatic infections to herd immunity and community transmission are key to the resurgence and control of COVID-19, but are difficult to estimate using current models that ignore changes in testing capacity. Using a model that incorporates daily testing information fit to the case and serology data from New York City, we show that the proportion of symptomatic cases is low, ranging from 13 to 18%, and that the reproductive number may be larger than often assumed. Asymptomatic infections contribute substantially to herd immunity, and to community transmission together with presymptomatic ones. If asymptomatic infections transmit at similar rates as symptomatic ones, the overall reproductive number across all classes is larger than often assumed, with estimates ranging from 3.2 to 4.4. If they transmit poorly, then symptomatic cases have a larger reproductive number ranging from 3.9 to 8.1. Even in this regime, presymptomatic and asymptomatic cases together comprise at least 50% of the force of infection at the outbreak peak. We find no regimes in which all infection subpopulations have reproductive numbers lower than three. These findings elucidate the uncertainty that current case and serology data cannot resolve, despite consideration of different model structures. They also emphasize how temporal data on testing can reduce and better define this uncertainty, as we move forward through longer surveillance and second epidemic waves. Complementary information is required to determine the transmissibility of asymptomatic cases, which we discuss. Regardless, current assumptions about the basic reproductive number of severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) should be reconsidered.
无症状感染对群体免疫和社区传播的贡献是 COVID-19 疫情反弹和控制的关键,但目前的模型忽略了检测能力的变化,因此难以估计。我们使用一种将每日检测信息纳入其中并与纽约市的病例和血清学数据拟合的模型,表明无症状病例的比例较低,范围在 13%至 18%之间,而且繁殖数可能比通常假设的要大。无症状感染对群体免疫以及与症状前感染一起对社区传播有重大贡献。如果无症状感染的传播率与有症状感染相似,那么所有类别中的总体繁殖数大于通常假设的,估计值在 3.2 到 4.4 之间。如果它们传播不佳,那么有症状的病例的繁殖数更大,范围从 3.9 到 8.1。即使在这种情况下,症状前和无症状病例一起构成了疫情高峰期感染力的至少 50%。我们没有发现所有感染亚群的繁殖数都低于 3 的情况。这些发现阐明了当前病例和血清学数据无法解决的不确定性,尽管考虑了不同的模型结构。它们还强调了随着更长时间的监测和第二波疫情的到来,关于检测的时间数据如何能够减少和更好地定义这种不确定性。我们需要确定无症状病例的传染性的补充信息,我们将对此进行讨论。无论如何,目前关于严重急性呼吸系统综合征冠状病毒 2 (SARS-Cov-2)基本繁殖数的假设都应该重新考虑。