A Hybrid Epidemic Model to Explore Stochasticity in COVID-19 Dynamics.

The dynamic nature of the COVID-19 pandemic has demanded a public health response that is constantly evolving due to the novelty of the virus. Many jurisdictions in the USA, Canada, and across the world have adopted social distancing and recommended the use of face masks. Considering these measures, it is prudent to understand the contributions of subpopulations-such as "silent spreaders"-to disease transmission dynamics in order to inform public health strategies in a jurisdiction-dependent manner. Additionally, we and others have shown that demographic and environmental stochasticity in transmission rates can play an important role in shaping disease dynamics. Here, we create a model for the COVID-19 pandemic by including two classes of individuals: silent spreaders, who either never experience a symptomatic phase or remain undetected throughout their disease course; and symptomatic spreaders, who experience symptoms and are detected. We fit the model to real-time COVID-19 confirmed cases and deaths to derive the transmission rates, death rates, and other relevant parameters for multiple phases of outbreaks in British Columbia (BC), Canada. We determine the extent to which SilS contributed to BC's early wave of disease transmission as well as the impact of public health interventions on reducing transmission from both SilS and SymS. To do this, we validate our model against an existing COVID-19 parameterized framework and then fit our model to clinical data to estimate key parameter values for different stages of BC's disease dynamics. We then use these parameters to construct a hybrid stochastic model that leverages the strengths of both a time-nonhomogeneous discrete process and a stochastic differential equation model. By combining these previously established approaches, we explore the impact of demographic and environmental variability on disease dynamics by simulating various scenarios in which a COVID-19 outbreak is initiated. Our results demonstrate that variability in disease transmission rate impacts the probability and severity of COVID-19 outbreaks differently in high- versus low-transmission scenarios.

A vaccination model for COVID-19 in Gauteng, South Africa.

The COVID-19 pandemic provides an opportunity to explore the impact of government mandates on movement restrictions and non-pharmaceutical interventions on a novel infection, and we investigate these strategies in early-stage outbreak dynamics. The rate of disease spread in South Africa varied over time as individuals changed behavior in response to the ongoing pandemic and to changing government policies. Using a system of ordinary differential equations, we model the outbreak in the province of Gauteng, assuming that several parameters vary over time. Analyzing data from the time period before vaccination gives the approximate dates of parameter changes, and those dates are linked to government policies. Unknown parameters are then estimated from available case data and used to assess the impact of each policy. Looking forward in time, possible scenarios give projections involving the implementation of two different vaccines at varying times. Our results quantify the impact of different government policies and demonstrate how vaccinations can alter infection spread.

Effects of environmental variability on superspreading transmission events in stochastic epidemic models.

Superspreaders (individuals with a high propensity for disease spread) have played a pivotal role in recent emerging and re-emerging diseases. In disease outbreak studies, host heterogeneity based on demographic (e.g. age, sex, vaccination status) and environmental (e.g. climate, urban/rural residence, clinics) factors are critical for the spread of infectious diseases, such as Ebola and Middle East Respiratory Syndrome (MERS). Transmission rates can vary as demographic and environmental factors are altered naturally or due to modified behaviors in response to the implementation of public health strategies. In this work, we develop stochastic models to explore the effects of demographic and environmental variability on human-to-human disease transmission rates among superspreaders in the case of Ebola and MERS. We show that the addition of environmental variability results in reduced probability of outbreak occurrence, however the severity of outbreaks that do occur increases. These observations have implications for public health strategies that aim to control environmental variables.