Modeling Coupled Disease-Behavior Dynamics of SARS-CoV-2 Using Influence Networks

SARS-CoV-2, the virus that causes COVID-19, has caused significant human morbidity and mortality since its emergence in late 2019. Not only have over three million people died, but humans have been forced to change their behavior in a variety of ways, including limiting their contacts, social distancing, and wearing masks. Early infectious disease models, like the classical SIR model by Kermack and McKendrick, do not account for differing contact structures and behavior. More recent work has demonstrated that contact structures and behavior can considerably impact disease dynamics. We construct a coupled disease-behavior dynamical model for SARS-CoV-2 by incorporating heterogeneous contact structures and decisions about masking. We use a contact network with household, work, and friend interactions to capture the variation in contact patterns. We allow decisions about masking to occur at a different time scale from disease spread which dramatically changes the masking dynamics. Drawing from the field of game theory, we construct an individual decision-making process that relies on perceived risk of infection, social influence, and individual resistance to masking. Through simulation, we find that social influence prevents masking, while perceived risk largely drives individuals to mask. Underlying contact structure also affects the number of people who mask. This model serves as a starting point for future work which could explore the relative importance of social influence and perceived risk in human decision-making

An open-access database of infectious disease transmission trees to explore superspreader epidemiology.

Historically, emerging and reemerging infectious diseases have caused large, deadly, and expensive multinational outbreaks. Often outbreak investigations aim to identify who infected whom by reconstructing the outbreak transmission tree, which visualizes transmission between individuals as a network with nodes representing individuals and branches representing transmission from person to person. We compiled a database, called OutbreakTrees, of 382 published, standardized transmission trees consisting of 16 directly transmitted diseases ranging in size from 2 to 286 cases. For each tree and disease, we calculated several key statistics, such as tree size, average number of secondary infections, the dispersion parameter, and the proportion of cases considered superspreaders, and examined how these statistics varied over the course of each outbreak and under different assumptions about the completeness of outbreak investigations. We demonstrated the potential utility of the database through 2 short analyses addressing questions about superspreader epidemiology for a variety of diseases, including Coronavirus Disease 2019 (COVID-19). First, we found that our transmission trees were consistent with theory predicting that intermediate dispersion parameters give rise to the highest proportion of cases causing superspreading events. Additionally, we investigated patterns in how superspreaders are infected. Across trees with more than 1 superspreader, we found preliminary support for the theory that superspreaders generate other superspreaders. In sum, our findings put the role of superspreading in COVID-19 transmission in perspective with that of other diseases and suggest an approach to further research regarding the generation of superspreaders. These data have been made openly available to encourage reuse and further scientific inquiry