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Register a new userThe impact of network properties and mixing on control measures and disease-induced herd immunity in epidemic models: a mean-field model perspective
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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.
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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.
We model and calculate the fraction of infected population necessary to reach herd immunity, taking into account the heterogeneity in infectiousness and susceptibility, as well as the correlation between those two parameters. We show that these cause the effective reproduction number to decrease more rapidly, and consequently have a drastic effect on the estimate of the necessary percentage of the population that has to contract the disease for herd immunity to be reached. We quantify the difference between the size of the infected population when the effective reproduction number decreases below 1 vs. the ultimate fraction of population that had contracted the disease. This sheds light on an important distinction between herd immunity and the end of the disease and highlights the importance of limiting the spread of the disease even if we plan to naturally reach herd immunity. We analyze the effect of various lock-down scenarios on the resulting final fraction of infected population. We discuss implications to COVID-19 and other pandemics and compare our theoretical results to population-based simulations. We consider the dependence of the disease spread on the architecture of the infectiousness graph and analyze different graph architectures and the limitations of the graph models.
Epidemics generally spread through a succession of waves that reflect factors on multiple timescales. On short timescales, super-spreading events lead to burstiness and overdispersion, while long-term persistent heterogeneity in susceptibility is expected to lead to a reduction in the infection peak and the herd immunity threshold (HIT). Here, we develop a general approach to encompass both timescales, including time variations in individual social activity, and demonstrate how to incorporate them phenomenologically into a wide class of epidemiological models through parameterization. We derive a non-linear dependence of the effective reproduction number Re on the susceptible population fraction S. We show that a state of transient collective immunity (TCI) emerges well below the HIT during early, high-paced stages of the epidemic. However, this is a fragile state that wanes over time due to changing levels of social activity, and so the infection peak is not an indication of herd immunity: subsequent waves can and will emerge due to behavioral changes in the population, driven (e.g.) by seasonal factors. Transient and long-term levels of heterogeneity are estimated by using empirical data from the COVID-19 epidemic as well as from real-life face-to-face contact networks. These results suggest that the hardest-hit areas, such as NYC, have achieved TCI following the first wave of the epidemic, but likely remain below the long-term HIT. Thus, in contrast to some previous claims, these regions can still experience subsequent waves.
In this paper, we deal with the study of the impact of nationwide measures COVID-19 anti-pandemic. We drive two processes to analyze COVID-19 data considering measures. We associate level of nationwide measure with value of parameters related to the contact rate of the model. Then a parametric solve, with respect to those parameters of measures, shows different possibilities of the evolution of the pandemic. Two machine learning tools are used to forecast the evolution of the pandemic. Finally, we show comparison between deterministic and two machine learning tools.
Until a vaccine or therapy is found against the SARS-CoV-2 coronavirus, reaching herd immunity appears to be the only mid-term option. However, if the number of infected individuals decreases and eventually fades only beyond this threshold, a significant proportion of susceptible may still be infected until the epidemic is over. A containment strategy is likely the best policy in the worst case where no vaccine or therapy is found. In order to keep the number of newly infected persons to a minimum, a possible strategy is to apply strict containment measures, so that the number of susceptible individuals remains close to herd immunity. Such an action is unrealistic since containment can only last for a finite amount of time and is never total. In this article, using a classical SIR model, we determine the (partial or total) containment strategy on a given finite time interval that maximizes the number of susceptible individuals over an infinite horizon, or equivalently that minimizes the total infection burden during the curse of the epidemic. The existence and uniqueness of the optimal strategy is proved and the latter is fully characterized. If applicable in practice, such a strategy would lead theoretically to an increase by 30% of the proportion of susceptible on an infinite horizon, for a containment level corresponding to the sanitary measures put in place in France from March to May 2020. We also analyze the minimum intervention time to reach a fixed distance from herd immunity, and show the relationship with the previous problem. Simulations are provided that illustrate and validate the theoretical results.
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