Subscribe to the gold package and get unlimited access to Shamra Academy
Register a new userImpact of network assortativity on epidemic and vaccination behaviour
119
0
0.0
(
0
)
Ask ChatGPT about the research
No Arabic abstract
The resurgence of measles is largely attributed to the decline in vaccine adoption and the increase in mobility. Although the vaccine for measles is readily available and highly successful, its current adoption is not adequate to prevent epidemics. Vaccine adoption is directly affected by individual vaccination decisions, and has a complex interplay with the spatial spread of disease shaped by an underlying mobility (travelling) network. In this paper, we model the travelling connectivity as a scale-free network, and investigate dependencies between the networks assortativity and the resultant epidemic and vaccination dynamics. In doing so we extend an SIR-network model with game-theoretic components, capturing the imitation dynamics under a voluntary vaccination scheme. Our results show a correlation between the epidemic dynamics and the networks assortativity, highlighting that networks with high assortativity tend to suppress epidemics under certain conditions. In highly assortative networks, the suppression is sustained producing an early convergence to equilibrium. In highly disassortative networks, however, the suppression effect diminishes over time due to scattering of non-vaccinating nodes, and frequent switching between the predominantly vaccinating and non-vaccinating phases of the dynamics.
rate research
Read More
We present a series of SIR-network models, extended with a game-theoretic treatment of imitation dynamics which result from regular population mobility across residential and work areas and the ensuing interactions. Each considered SIR-network model captures a class of vaccination behaviours influenced by epidemic characteristics, interaction topology, and imitation dynamics. Our focus is the eventual vaccination coverage, produced under voluntary vaccination schemes, in response to these varying factors. Using the next generation matrix method, we analytically derive and compare expressions for the basic reproduction number $R_0$ for the proposed SIR-network models. Furthermore, we simulate the epidemic dynamics over time for the considered models, and show that if individuals are sufficiently responsive towards the changes in the disease prevalence, then the more expansive travelling patterns encourage convergence to the endemic, mixed equilibria. On the contrary, if individuals are insensitive to changes in the disease prevalence, we find that they tend to remain unvaccinated in all the studied models. Our results concur with earlier studies in showing that residents from highly connected residential areas are more likely to get vaccinated. We also show that the existence of the individuals committed to receiving vaccination reduces $R_0$ and delays the disease prevalence, and thus is essential to containing epidemics.
The contact structure of a population plays an important role in transmission of infection. Many ``structured models capture aspects of the contact structure through an underlying network or a mixing matrix. An important observation in such models, is that once a fraction $1-1/mathcal{R}_0$ has been infected, the residual susceptible population can no longer sustain an epidemic. A recent observation of some structured models is that this threshold can be crossed with a smaller fraction of infected individuals, because the disease acts like a targeted vaccine, preferentially immunizing higher-risk individuals who play a greater role in transmission. Therefore, a limited ``first wave may leave behind a residual population that cannot support a second wave once interventions are lifted. In this paper, we systematically analyse a number of mean-field models for networks and other structured populations to address issues relevant to the Covid-19 pandemic. In particular, we consider herd-immunity under several scenarios. We confirm that, in networks with high degree heterogeneity, the first wave confers herd-immunity with significantly fewer infections than equivalent models with lower degree heterogeneity. However, if modelling the intervention as a change in the contact network, then this effect might become more subtle. Indeed, modifying the structure can shield highly connected nodes from becoming infected during the first wave and make the second wave more substantial. We confirm this finding by using an age-structured compartmental model parameterised with real data and comparing lockdown periods implemented either as a global scaling of the mixing matrix or age-specific structural changes. We find that results regarding herd immunity levels are strongly dependent on the model, the duration of lockdown and how lockdown is implemented.
Mathematical disease modelling has long operated under the assumption that any one infectious disease is caused by one transmissible pathogen spreading among a population. This paradigm has been useful in simplifying the biological reality of epidemics and has allowed the modelling community to focus on the complexity of other factors such as population structure and interventions. However, there is an increasing amount of evidence that the strain diversity of pathogens, and their interplay with the host immune system, can play a large role in shaping the dynamics of epidemics. Here, we introduce a disease model with an underlying genotype network to account for two important mechanisms. One, the disease can mutate along network pathways as it spreads in a host population. Two, the genotype network allows us to define a genetic distance across strains and therefore to model the transcendence of immunity often observed in real world pathogens. We study the emergence of epidemics in this model, through its epidemic phase transitions, and highlight the role of the genotype network in driving cyclicity of diseases, large scale fluctuations, sequential epidemic transitions, as well as localization around specific strains of the associated pathogen. More generally, our model illustrates the richness of behaviours that are possible even in well-mixed host populations once we consider strain diversity and go beyond the one disease equals one pathogen paradigm.
Network-based interventions against epidemic spread are most powerful when the full network structure is known. However, in practice, resource constraints require decisions to be made based on partial network information. We investigated how the accuracy of network data available at individual and village levels affected network-based vaccination effectiveness. We simulated a Susceptible-Infected-Recovered process on empirical social networks from 75 villages. First, we used regression to predict the percentage of individuals ever infected based on village-level network. Second, we simulated vaccinating 10 percent of each of the 75 empirical village networks at baseline, selecting vaccinees through one of five network-based approaches: random individuals; random contacts of random individuals; random high-degree individuals; highest degree individuals; or most central individuals. The first three approaches require only sample data; the latter two require full network data. We also simulated imposing a limit on how many contacts an individual can nominate (Fixed Choice Design, FCD), which reduces the data collection burden but generates only partially observed networks. We found mean and standard deviation of the degree distribution to strongly predict cumulative incidence. In simulations, the Nomination method reduced cumulative incidence by one-sixth compared to Random vaccination; full network methods reduced infection by two-thirds. The High Degree approach had intermediate effectiveness. Surprisingly, FCD truncating individuals degrees at three was as effective as using complete networks. Using even partial network information to prioritize vaccines at either the village or individual level substantially improved epidemic outcomes. Such approaches may be feasible and effective in outbreak settings, and full ascertainment of network structure may not be required.
Public health services are constantly searching for new ways to reduce the spread of infectious diseases, such as public vaccination of asymptomatic individuals, quarantine (isolation) and treatment of symptomatic individuals. Epidemic models have a long history of assisting in public health planning and policy making. In this paper, we introduce epidemic models including variable population size, degree-related imperfect vaccination and quarantine on scale-free networks. More specifically, the models are formulated both on the population with and without permanent natural immunity to infection, which corresponds respectively to the susceptible-vaccinated-infected-quarantined-recovered (SVIQR) model and the susceptible-vaccinated-infected-quarantined (SVIQS) model. We develop different mathematical methods and techniques to study the dynamics of two models, including the basic reproduction number, the global stability of disease-free and endemic equilibria. For the SVIQR model, we show that the system exhibits a forward bifurcation. Meanwhile, the disease-free and unique endemic equilibria are shown to be globally asymptotically stable by constructing suitable Lyapunov functions. For the SVIQS model, conditions ensuring the occurrence of multiple endemic equilibria are derived. Under certain conditions, this system cannot undergo a backward bifurcation. The global asymptotical stability of disease-free equilibrium, and the persistence of the disease are proved. The endemic equilibrium is shown to be globally attractive by using monotone iterative technique. Finally, stochastic network simulations yield quantitative agreement with the deterministic mean-field approach.
Log in to be able to interact and post comments
comments
Fetching comments
Sign in to be able to follow your search criteria
