Department of Mathematics, Marshall University, Huntington, West Virginia, United States of America.
PLoS One. 2013 Apr 23;8(4):e60343. doi: 10.1371/journal.pone.0060343. Print 2013.
A striking characteristic of the past four influenza pandemic outbreaks in the United States has been the multiple waves of infections. However, the mechanisms responsible for the multiple waves of influenza or other acute infectious diseases are uncertain. Understanding these mechanisms could provide knowledge for health authorities to develop and implement prevention and control strategies.
We exhibit five distinct mechanisms, each of which can generate two waves of infections for an acute infectious disease. The first two mechanisms capture changes in virus transmissibility and behavioral changes. The third mechanism involves population heterogeneity (e.g., demography, geography), where each wave spreads through one sub-population. The fourth mechanism is virus mutation which causes delayed susceptibility of individuals. The fifth mechanism is waning immunity. Each mechanism is incorporated into separate mathematical models, and outbreaks are then simulated. We use the models to examine the effects of the initial number of infected individuals (e.g., border control at the beginning of the outbreak) and the timing of and amount of available vaccinations.
Four models, individually or in any combination, reproduce the two waves of the 2009 H1N1 pandemic in the United States, both qualitatively and quantitatively. One model reproduces the two waves only qualitatively. All models indicate that significantly reducing or delaying the initial numbers of infected individuals would have little impact on the attack rate. Instead, this reduction or delay results in a single wave as opposed to two waves. Furthermore, four of these models also indicate that a vaccination program started earlier than October 2009 (when the H1N1 vaccine was initially distributed) could have eliminated the second wave of infection, while more vaccine available starting in October would not have eliminated the second wave.
美国过去四次流感大流行的一个显著特征是多次感染浪潮。然而，导致流感或其他急性传染病多次浪潮的机制尚不清楚。了解这些机制可以为卫生当局提供知识，以制定和实施预防和控制策略。
我们展示了五个不同的机制，每个机制都可以为急性传染病产生两波感染。前两个机制捕捉了病毒传染性的变化和行为变化。第三个机制涉及人口异质性（例如，人口统计学，地理），其中每一波传播通过一个亚人群。第四个机制是病毒突变，导致个体易感性延迟。第五个机制是免疫力下降。每个机制都被纳入单独的数学模型中，然后进行爆发模拟。我们使用这些模型来研究初始感染人数（例如，疫情爆发初期的边境控制）以及可获得的疫苗接种时间和数量的影响。
四个模型，单独或组合使用，都可以定性和定量地再现 2009 年美国 H1N1 大流行的两次浪潮。一个模型仅定性地再现了两次浪潮。所有模型都表明，显著减少或延迟初始感染人数对攻击率的影响不大。相反，这种减少或延迟导致单次浪潮而不是两次浪潮。此外，这四个模型中的四个还表明，早于 2009 年 10 月（即首次分发 H1N1 疫苗时）开始的疫苗接种计划本可以消除第二次感染浪潮，而 10 月开始提供更多疫苗并不会消除第二次感染浪潮。
