Estimating the reproductive number, total outbreak size, and reporting rates for Zika epidemics in South and Central America

As South and Central American countries prepare for increased birth defects from Zika virus outbreaks and plan for mitigation strategies to minimize ongoing and future outbreaks, understanding important characteristics of Zika outbreaks and how they vary across regions is a challenging and important problem. We developed a mathematical model for the 2015 Zika virus outbreak dynamics in Colombia, El Salvador, and Suriname. We fit the model to publicly available data provided by the Pan American Health Organization, using Approximate Bayesian Computation to estimate parameter distributions and provide uncertainty quantification. An important model input is the at-risk susceptible population, which can vary with a number of factors including climate, elevation, population density, and socio-economic status. We informed this initial condition using the highest historically reported dengue incidence modified by the probable dengue reporting rates in the chosen countries. The model indicated that a country-level analysis was not appropriate for Colombia. We then estimated the basic reproduction number, or the expected number of new human infections arising from a single infected human, to range between 4 and 6 for El Salvador and Suriname with a median of 4.3 and 5.3, respectively. We estimated the reporting rate to be around 16% in El Salvador and 18% in Suriname with estimated total outbreak sizes of 73,395 and 21,647 people, respectively. The uncertainty in parameter estimates highlights a need for research and data collection that will better constrain parameter ranges.Comment: 35 pages, 16 figure

Defining the Risk of Zika and Chikungunya Virus Transmission in Human Population Centers of the Eastern United States

The recent spread of mosquito-transmitted viruses and associated disease to the Americas motivates a new, data-driven evaluation of risk in temperate population centers. Temperate regions are generally expected to pose low risk for significant mosquito-borne disease; however, the spread of the Asian tiger mosquito (Aedes albopictus) across densely populated urban areas has established a new landscape of risk. We use a model informed by field data to assess the conditions likely to facilitate local transmission of chikungunya and Zika viruses from an infected traveler to Ae. albopictus and then to other humans in USA cities with variable human densities and seasonality. Mosquito-borne disease occurs when specific combinations of conditions maximize virus-to-mosquito and mosquito-to-human contact rates. We develop a mathematical model that captures the epidemiology and is informed by current data on vector ecology from urban sites. The model demonstrates that under specific but realistic conditions, fifty-percent of introductions by infectious travelers to a high human, high mosquito density city could initiate local transmission and 10% of the introductions could result in 100 or more people infected. Despite the propensity for Ae. albopictus to bite non-human vertebrates, we also demonstrate that local virus transmission and human outbreaks may occur when vectors feed from humans even just 40% of the time. Inclusion of human behavioral changes and mitigations were not incorporated into the models and would likely reduce predicted infections. This work demonstrates how a conditional series of non-average events can result in local arbovirus transmission and outbreaks of human disease, even in temperate cities

Defining the Risk of Zika and Chikungunya Virus Transmission in Human Population Centers of the Eastern United States

The recent spread of mosquito-transmitted viruses and associated disease to the Americas motivates a new, data-driven evaluation of risk in temperate population centers. Temperate regions are generally expected to pose low risk for significant mosquito-borne disease; however, the spread of the Asian tiger mosquito (Aedes albopictus) across densely populated urban areas has established a new landscape of risk. We use a model informed by field data to assess the conditions likely to facilitate local transmission of chikungunya and Zika viruses from an infected traveler to Ae. albopictus and then to other humans in USA cities with variable human densities and seasonality. Mosquito-borne disease occurs when specific combinations of conditions maximize virus-to-mosquito and mosquito-to-human contact rates. We develop a mathematical model that captures the epidemiology and is informed by current data on vector ecology from urban sites. The model demonstrates that under specific but realistic conditions, fifty-percent of introductions by infectious travelers to a high human, high mosquito density city could initiate local transmission and 10% of the introductions could result in 100 or more people infected. Despite the propensity for Ae. albopictus to bite non-human vertebrates, we also demonstrate that local virus transmission and human outbreaks may occur when vectors feed from humans even just 40% of the time. Inclusion of human behavioral changes and mitigations were not incorporated into the models and would likely reduce predicted infections. This work demonstrates how a conditional series of non-average events can result in local arbovirus transmission and outbreaks of human disease, even in temperate cities

Decision Support for Mitigation of Livestock Disease: Rinderpest as a Case Study

A versatile, interactive model to predict geographically resolved epidemic progression after pathogen introduction into a population is presented. Deterministic simulations incorporating a compartmental disease model run rapidly, facilitating the analysis of mitigations such as vaccination and transmission reduction on epidemic spread and progression. We demonstrate the simulation model using rinderpest infection of cattle, a devastating livestock disease. Rinderpest has been extinguished in the wild, but it is still a threat due to stored virus in some laboratories. Comparison of simulations to historical outbreaks provides some validation of the model. Simulations of potential outbreaks demonstrate potential consequences of rinderpest virus release for a variety of possible disease parameters and mitigations. Our results indicate that a rinderpest outbreak could result in severe social and economic consequences

Coinfections by noninteracting pathogens are not independent and require new tests of interaction.

If pathogen species, strains, or clones do not interact, intuition suggests the proportion of coinfected hosts should be the product of the individual prevalences. Independence consequently underpins the wide range of methods for detecting pathogen interactions from cross-sectional survey data. However, the very simplest of epidemiological models challenge the underlying assumption of statistical independence. Even if pathogens do not interact, death of coinfected hosts causes net prevalences of individual pathogens to decrease simultaneously. The induced positive correlation between prevalences means the proportion of coinfected hosts is expected to be higher than multiplication would suggest. By modelling the dynamics of multiple noninteracting pathogens causing chronic infections, we develop a pair of novel tests of interaction that properly account for nonindependence between pathogens causing lifelong infection. Our tests allow us to reinterpret data from previous studies including pathogens of humans, plants, and animals. Our work demonstrates how methods to identify interactions between pathogens can be updated using simple epidemic models

Spatiotemporal incidence of Zika and associated environmental drivers for the 2015-2016 epidemic in Colombia

Despite a long history of mosquito-borne virus epidemics in the Americas, the impact of the Zika virus (ZIKV) epidemic of 2015–2016 was unexpected. The need for scientifically informed decision-making is driving research to understand the emergence and spread of ZIKV. To support that research, we assembled a data set of key covariates for modeling ZIKV transmission dynamics in Colombia, where ZIKV transmission was widespread and the government made incidence data publically available. On a weekly basis between January 1, 2014 and October 1, 2016 at three administrative levels, we collated spatiotemporal Zika incidence data, nine environmental variables, and demographic data into a single downloadable database. These new datasets and those we identified, processed, and assembled at comparable spatial and temporal resolutions will save future researchers considerable time and effort in performing these data processing steps, enabling them to focus instead on extracting epidemiological insights from this important data set. Similar approaches could prove useful for filling data gaps to enable epidemiological analyses of future disease emergence events

Agent-based hantavirus transmission model incorporating host behavior and viral shedding heterogeneities derived from field transmission experiments

Behavioural and environmental heterogeneities among host populations can play an important role in hantavirus transmission. We designed an agent-based model to determine the relative role of direct and indirect transmission on Sin Nombre hantavirus (SNV) dynamics in deer mice, incorporating host heterogeneities. We parameterized the model to reproduce aggressive encounters, movement and excretions from field-based studies and lab experiments. Our model captured known properties of SNV spread and matched the outcomes of transmission experiments. Although the model was not fit to $R_0$ values, the $R_0$ distribution from our simulations was similar to values from other hantavirus models. We also found that a small per cent of mice were responsible for a high per cent of direct transmission. Our model indicated that mouse heterogeneity and environmental contamination are both important. Model extensions can explore larger ecosystem dynamics by incorporating temporal heterogeneity, to understand how changes in host characteristics and environment influence SNV transmission