School of Biological Sciences, Georgia Institute of Technology, Atlanta, Georgia, USA.
Interdisciplinary Graduate Program in Quantitative Biosciences, Georgia Institute of Technology, Atlanta, Georgia, USA.
mBio. 2024 Aug 14;15(8):e0137624. doi: 10.1128/mbio.01376-24. Epub 2024 Jul 19.
Viral impacts on microbial populations depend on interaction phenotypes-including viral traits spanning the adsorption rate, latent period, and burst size. The latent period is a key viral trait in lytic infections. Defined as the time from viral adsorption to viral progeny release, the latent period of bacteriophage is conventionally inferred via one-step growth curves in which the accumulation of free virus is measured over time in a population of infected cells. Developed more than 80 years ago, one-step growth curves do not account for cellular-level variability in the timing of lysis, potentially biasing inference of viral traits. Here, we use nonlinear dynamical models to understand how individual-level variation of the latent period impacts virus-host dynamics. Our modeling approach shows that inference of the latent period via one-step growth curves is systematically biased-generating estimates of shorter latent periods than the underlying population-level mean. The bias arises because variability in lysis timing at the cellular level leads to a fraction of early burst events, which are interpreted, artefactually, as an earlier mean time of viral release. We develop a computational framework to estimate latent period variability from joint measurements of host and free virus populations. Our computational framework recovers both the mean and variance of the latent period within simulated infections including realistic measurement noise. This work suggests that reframing the latent period as a distribution to account for variability in the population will improve the study of viral traits and their role in shaping microbial populations.IMPORTANCEQuantifying viral traits-including the adsorption rate, burst size, and latent period-is critical to characterize viral infection dynamics and develop predictive models of viral impacts across scales from cells to ecosystems. Here, we revisit the gold standard of viral trait estimation-the one-step growth curve-to assess the extent to which assumptions at the core of viral infection dynamics lead to ongoing and systematic biases in inferences of viral traits. We show that latent period estimates obtained via one-step growth curves systematically underestimate the mean latent period and, in turn, overestimate the rate of viral killing at population scales. By explicitly incorporating trait variability into a dynamical inference framework that leverages both virus and host time series, we provide a practical route to improve estimates of the mean and variance of viral traits across diverse virus-microbe systems.
病毒对微生物种群的影响取决于相互作用表型,包括跨越吸附率、潜伏期和爆发大小的病毒特征。潜伏期是裂解感染中关键的病毒特征。定义为从病毒吸附到病毒后代释放的时间,噬菌体的潜伏期通常通过一步生长曲线推断得出,其中通过在感染细胞的群体中随时间测量游离病毒的积累来测量。一步生长曲线是 80 多年前开发的,它没有考虑到裂解时间在细胞水平上的变化,这可能会影响病毒特征的推断。在这里,我们使用非线性动力学模型来了解潜伏期的个体水平变化如何影响病毒-宿主动力学。我们的建模方法表明,通过一步生长曲线推断潜伏期会产生系统偏差,即产生比群体水平平均潜伏期更短的估计值。这种偏差是由于细胞水平上裂解时间的变化导致了早期爆发事件的一部分,这些事件被人为地解释为病毒释放的早期平均时间。我们开发了一种计算框架,从宿主和游离病毒群体的联合测量中估计潜伏期的变异性。我们的计算框架在包括真实测量噪声的模拟感染中恢复了潜伏期的平均值和方差。这项工作表明,将潜伏期重新定义为一个分布,以解释种群的变异性,将提高对病毒特征及其在塑造微生物种群中的作用的研究。
重要性
量化病毒特征,包括吸附率、爆发大小和潜伏期,对于描述病毒感染动力学以及在从细胞到生态系统的各个尺度上开发病毒影响的预测模型至关重要。在这里,我们重新审视病毒特征估计的黄金标准——一步生长曲线,以评估病毒感染动力学核心假设在多大程度上导致了对病毒特征推断的持续和系统偏差。我们表明,通过一步生长曲线获得的潜伏期估计值系统地低估了平均潜伏期,进而在群体尺度上高估了病毒杀伤率。通过明确将特征变异性纳入一个利用病毒和宿主时间序列的动力学推断框架,我们提供了一种实用的方法来改善跨各种病毒-微生物系统的病毒特征的平均值和方差的估计。