Bhattacharyya Samit, Gesteland Per H, Korgenski Kent, Bjørnstad Ottar N, Adler Frederick R
Center for Infectious Disease Dynamics, Pennsylvania State University, University Park, PA 16802; Department of Biology, University of Utah, Salt Lake City, UT 84112;
Department of Pediatrics, School of Medicine, University of Utah, Salt Lake City, UT 84112; Department of Biomedical Informatics, University of Utah, Salt Lake City, UT 84112;
Proc Natl Acad Sci U S A. 2015 Oct 27;112(43):13396-400. doi: 10.1073/pnas.1516698112. Epub 2015 Oct 12.
Viral respiratory tract diseases pose serious public health problems. Our ability to predict and thus, be able to prepare for outbreaks is strained by the complex factors driving the prevalence and severity of these diseases. The abundance of diseases and transmission dynamics of strains are not only affected by external factors, such as weather, but also driven by interactions among viruses mediated by human behavior and immunity. To untangle the complex out-of-phase annual and biennial pattern of three common paramyxoviruses, Respiratory Syncytial Virus (RSV), Human Parainfluenza Virus (HPIV), and Human Metapneumovirus (hMPV), we adopt a theoretical approach that integrates ecological and immunological mechanisms of disease interactions. By estimating parameters from multiyear time series of laboratory-confirmed cases from the intermountain west region of the United States and using statistical inference, we show that models of immune-mediated interactions better explain the data than those based on ecological competition by convalescence. The strength of cross-protective immunity among viruses is correlated with their genetic distance in the phylogenetic tree of the paramyxovirus family.
病毒性呼吸道疾病构成了严重的公共卫生问题。驱动这些疾病流行和严重程度的复杂因素,使得我们预测并进而为疫情爆发做好准备的能力受到了限制。疾病的多样性和毒株的传播动态不仅受到诸如天气等外部因素的影响,还受到人类行为和免疫介导的病毒间相互作用的驱动。为了厘清三种常见副粘病毒,即呼吸道合胞病毒(RSV)、人副流感病毒(HPIV)和人偏肺病毒(hMPV)复杂的不同步年度和两年周期模式,我们采用了一种整合疾病相互作用的生态和免疫机制的理论方法。通过从美国西部山区实验室确诊病例的多年时间序列中估计参数,并运用统计推断,我们表明,与基于恢复期生态竞争的模型相比,免疫介导相互作用模型能更好地解释数据。病毒间交叉保护免疫的强度与其在副粘病毒科系统发育树中的遗传距离相关。