1 Odum School of Ecology, University of Georgia , Athens, GA 30602 , USA.
2 Department of Infectious Diseases, University of Georgia , Athens, GA 30602 , USA.
Philos Trans R Soc Lond B Biol Sci. 2019 Jun 24;374(1775):20180270. doi: 10.1098/rstb.2018.0270.
Measles, an acute viral disease, continues to be an important cause of childhood mortality worldwide. Infection with the measles virus is thought to be associated with a transient but profound period of immune suppression. Recently, it has been claimed that measles-induced immune manipulation lasts for about 30 months and results in increased susceptibility to other co-circulating infectious diseases and more severe disease outcomes upon infection. We tested this hypothesis using model-based inference applied to parallel historical records of measles and whooping cough mortality and morbidity. Specifically, we used maximum likelihood to fit a mechanistic transmission model to incidence data from three different eras, spanning mortality records from 1904 to 1912 and 1922 to 1932 and morbidity records from 1946 to 1956. Our aim was to quantify the timing, severity and pathogenesis impacts of measles-induced immune modulation and their consequences for whooping cough epidemiology across a temporal gradient of measles transmission. We identified an increase in susceptibility to whooping cough following recent measles infection by approximately 85-, 10- and 36-fold for the three eras, respectively, although the duration of this effect was variable. Overall, while the immune impacts of measles may be strong and clearly evident at the individual level, their epidemiological signature in these data appears both modest and inconsistent. This article is part of the theme issue 'Modelling infectious disease outbreaks in humans, animals and plants: approaches and important themes'. This issue is linked with the subsequent theme issue 'Modelling infectious disease outbreaks in humans, animals and plants: epidemic forecasting and control'.
麻疹是一种急性病毒性疾病，仍然是全世界儿童死亡的一个重要原因。感染麻疹病毒被认为与短暂但深刻的免疫抑制期有关。最近，有人声称麻疹引起的免疫操纵持续约 30 个月，导致对其他同时传播的传染病的易感性增加，并在感染时导致更严重的疾病后果。我们使用基于模型的推断方法检验了这一假说，该方法适用于麻疹和百日咳死亡率和发病率的平行历史记录。具体来说，我们使用最大似然法拟合了一个机制传播模型，该模型适用于三个不同时期的发病率数据，涵盖了 1904 年至 1912 年和 1922 年至 1932 年的死亡率记录，以及 1946 年至 1956 年的发病率记录。我们的目的是量化麻疹引起的免疫调节的时间、严重程度和发病机制影响，以及它们在麻疹传播的时间梯度上对百日咳流行病学的影响。我们发现，在三个时期中，最近感染麻疹后对百日咳的易感性分别增加了约 85 倍、10 倍和 36 倍，尽管这种效应的持续时间是可变的。总的来说，虽然麻疹的免疫影响在个体水平上可能很强且明显，但它们在这些数据中的流行病学特征既适度又不一致。本文是主题为“模拟人类、动物和植物中的传染病爆发：方法和重要主题”的一部分。该主题与后续主题“模拟人类、动物和植物中的传染病爆发：流行预测和控制”相关联。
