论文标题
传染病和社会意识的传播是聚类网络上的寄生虫传播
Spread of infectious disease and social awareness as parasitic contagions on clustered networks
论文作者
论文摘要
具有丰富的模型历史,用于诸如流感之类的生物传播与相关信息(例如流感疫苗接种运动)的传播。关于网络上相互作用传播的传播的最新工作表明,这些相互作用的传染病可以与网络结构具有反直觉相互作用。在这里,我们概括了其中一个框架,以应对意识和疾病传播的三个重要特征:第一,我们对高度集群,cliquish网络的动态进行建模,以模仿工作场所和家庭的作用;第二,意识传染性通过降低意识或接种人不太可能被感染的传播率来影响生物传播的传播。第三,生物传染还会影响意识传染的传播,但通过提高其传播率,而感染者更容易接受,并且更有可能共享与该疾病有关的信息。在这些条件下,我们发现,增加网络聚类的增加(已知会阻碍疾病传播)实际上可以使它们在有意识的模型中维持更大的疾病流行病。这种违反直觉的结果与传统的观点背道而驰,这表明随机网络是合理的,因为它们提供了最差的场景预测。为了进一步研究这一结果,我们提供了一个基于两步分支过程(即预期的三级感染的数量)的封闭形式标准,以识别参数空间中不同区域的净效应和共同感染的净效应。总而言之,我们的结果再次强调了超越疾病建模中的随机网络的需求,并说明了即使在复杂的相互作用模型中也是可能的分析类型。
There is a rich history of models for the interaction of a biological contagion like influenza with the spread of related information such as an influenza vaccination campaign. Recent work on the spread of interacting contagions on networks has highlighted that these interacting contagions can have counter-intuitive interplay with network structure. Here we generalize one of these frameworks to tackle three important features of the spread of awareness and disease: one, we model the dynamics on highly clustered, cliquish, networks to mimic the role of workplaces and households; two, the awareness contagion affects the spread of the biological contagion by reducing its transmission rate where an aware or vaccinated individual is less likely to be infected; and three, the biological contagion also affects the spread of the awareness contagion but by increasing its transmission rate where an infected individual is more receptive and more likely to share information related to the disease. Under these conditions, we find that increasing network clustering, which is known to hinder disease spread, can actually allow them to sustain larger epidemics of the disease in models with awareness. This counter-intuitive result goes against the conventional wisdom suggesting that random networks are justifiable as they provide worst-case scenario forecasts. To further investigate this result, we provide a closed-form criterion based on a two-step branching process (i.e., the numbers of expected tertiary infections) to identify different regions in parameter space where the net effect of clustering and co-infection varies. Altogether, our results highlight once again the need to go beyond random networks in disease modeling and illustrate the type of analysis that is possible even in complex models of interacting contagions.