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Dynamics of beneficial epidemics.

ABSTRACT: Pathogens can spread epidemically through populations. Beneficial contagions, such as viruses that enhance host survival or technological innovations that improve quality of life, also have the potential to spread epidemically. How do the dynamics of beneficial biological and social epidemics differ from those of detrimental epidemics? We investigate this question using a breadth-first modeling approach involving three distinct theoretical models. First, in the context of population genetics, we show that a horizontally-transmissible element that increases fitness, such as viral DNA, spreads superexponentially through a population, more quickly than a beneficial mutation. Second, in the context of behavioral epidemiology, we show that infections that cause increased connectivity lead to superexponential fixation in the population. Third, in the context of dynamic social networks, we find that preferences for increased global infection accelerate spread and produce superexponential fixation, but preferences for local assortativity halt epidemics by disconnecting the infected from the susceptible. We conclude that the dynamics of beneficial biological and social epidemics are characterized by the rapid spread of beneficial elements, which is facilitated in biological systems by horizontal transmission and in social systems by active spreading behavior of infected individuals.

SUBMITTER: Berdahl A

PROVIDER: S-EPMC6805938 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Dynamics of beneficial epidemics.

Berdahl Andrew A Brelsford Christa C Bacco Caterina De C Dumas Marion M Ferdinand Vanessa V Grochow Joshua A JA Hébert-Dufresne Laurent L Kallus Yoav Y Kempes Christopher P CP Kolchinsky Artemy A Larremore Daniel B DB Libby Eric E Power Eleanor A EA Stern Caitlin A CA Tracey Brendan D BD

Scientific reports 20191022 1

Pathogens can spread epidemically through populations. Beneficial contagions, such as viruses that enhance host survival or technological innovations that improve quality of life, also have the potential to spread epidemically. How do the dynamics of beneficial biological and social epidemics differ from those of detrimental epidemics? We investigate this question using a breadth-first modeling approach involving three distinct theoretical models. First, in the context of population genetics, we ...[more]

PMID: 31641147

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Project description:Epidemics may pose a significant dilemma for governments and individuals. The personal or public health consequences of inaction may be catastrophic; but the economic consequences of drastic response may likewise be catastrophic. In the face of these trade-offs, governments and individuals must therefore strike a balance between the economic and personal health costs of reducing social contacts and the public health costs of neglecting to do so. As risk of infection increases, potentially infectious contact between people is deliberately reduced either individually or by decree. This must be balanced against the social and economic costs of having fewer people in contact, and therefore active in the labor force or enrolled in school. Although the importance of adaptive social contact on epidemic outcomes has become increasingly recognized, the most important properties of coupled human-natural epidemic systems are still not well understood. We develop a theoretical model for adaptive, optimal control of the effective social contact rate using traditional epidemic modeling tools and a utility function with delayed information. This utility function trades off the population-wide contact rate with the expected cost and risk of increasing infections. Our analytical and computational analysis of this simple discrete-time deterministic strategic model reveals the existence of an endemic equilibrium, oscillatory dynamics around this equilibrium under some parametric conditions, and complex dynamic regimes that shift under small parameter perturbations. These results support the supposition that infectious disease dynamics under adaptive behavior change may have an indifference point, may produce oscillatory dynamics without other forcing, and constitute complex adaptive systems with associated dynamics. Implications for any epidemic in which adaptive behavior influences infectious disease dynamics include an expectation of fluctuations, for a considerable time, around a quasi-equilibrium that balances public health and economic priorities, that shows multiple peaks and surges in some scenarios, and that implies a high degree of uncertainty in mathematical projections.

Project description:Early estimates of the transmission potential of emerging and re-emerging infections are increasingly used to inform public health authorities on the level of risk posed by outbreaks. Existing methods to estimate the reproduction number generally assume exponential growth in case incidence in the first few disease generations, before susceptible depletion sets in. In reality, outbreaks can display subexponential (i.e. polynomial) growth in the first few disease generations, owing to clustering in contact patterns, spatial effects, inhomogeneous mixing, reactive behaviour changes or other mechanisms. Here, we introduce the generalized growth model to characterize the early growth profile of outbreaks and estimate the effective reproduction number, with no need for explicit assumptions about the shape of epidemic growth. We demonstrate this phenomenological approach using analytical results and simulations from mechanistic models, and provide validation against a range of empirical disease datasets. Our results suggest that subexponential growth in the early phase of an epidemic is the rule rather the exception. Mechanistic simulations show that slight modifications to the classical susceptible-infectious-removed model result in subexponential growth, and in turn a rapid decline in the reproduction number within three to five disease generations. For empirical outbreaks, the generalized-growth model consistently outperforms the exponential model for a variety of directly and indirectly transmitted diseases datasets (pandemic influenza, measles, smallpox, bubonic plague, cholera, foot-and-mouth disease, HIV/AIDS and Ebola) with model estimates supporting subexponential growth dynamics. The rapid decline in effective reproduction number predicted by analytical results and observed in real and synthetic datasets within three to five disease generations contrasts with the expectation of invariant reproduction number in epidemics obeying exponential growth. The generalized-growth concept also provides us a compelling argument for the unexpected extinction of certain emerging disease outbreaks during the early ascending phase. Overall, our approach promotes a more reliable and data-driven characterization of the early epidemic phase, which is important for accurate estimation of the reproduction number and prediction of disease impact.

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Dynamics of beneficial epidemics.

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Dynamics of beneficial epidemics.

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