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Q. Liu
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Although non-Markovian processes are considerably more complicated to analyze, real-world epidemics are likely non-Markovian, because the infection time is not always exponentially distributed. Here, we present analytic expressions of the epidemic threshold in a Weibull and a Gamma SIS epidemic on any network, where the infection time is Weibull, respectively, Gamma, but the recovery time is exponential. The theory is compared with precise simulations. The mean-field non-Markovian epidemic thresholds, both for a Weibull and Gamma infection time, are physically similar and interpreted via the occurrence time of an infection during a healthy period of each node in the graph. Our theory couples the type of a viral item, specified by a shape parameter of the Weibull or Gamma distribution, to its corresponding network-wide endemic spreading power, which is specified by the mean-field non-Markovian epidemic threshold in any network.
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Although non-Markovian processes are considerably more complicated to analyze, real-world epidemics are likely non-Markovian, because the infection time is not always exponentially distributed. Here, we present analytic expressions of the epidemic threshold in a Weibull and a Gamma SIS epidemic on any network, where the infection time is Weibull, respectively, Gamma, but the recovery time is exponential. The theory is compared with precise simulations. The mean-field non-Markovian epidemic thresholds, both for a Weibull and Gamma infection time, are physically similar and interpreted via the occurrence time of an infection during a healthy period of each node in the graph. Our theory couples the type of a viral item, specified by a shape parameter of the Weibull or Gamma distribution, to its corresponding network-wide endemic spreading power, which is specified by the mean-field non-Markovian epidemic threshold in any network.
In previous modelling efforts to understand the spreading process on networks, each node can infect its neighbors and cure spontaneously, and the curing is traditionally assumed to occur uniformly over time. This traditional curing is not optimal in terms of the trade-off between the effectiveness and cost. A pulse immunization/curing strategy is more efficient and broadly applied to suppress the spreading process. We analyze the pulse curing strategy on networks with the Susceptible-Infected (SI) process. We analytically compute the mean-field epidemic threshold $\tau_c^{p}$ of the pulse SI model and show that $\tau_c^{p}=\frac{1}{\lambda_1}\ln\frac{1}{1-p}$ , where $\lambda_1$ and p are the largest eigenvalue of the adjacency matrix of the contact graph and the fraction of nodes covered by each curing, respectively. These analytical results agree with simulations. Compared to the asynchronous curing process in the extensively studied Markovian SIS process, we show that the pulse curing strategy saves about 36.8%, i.e., $p\approx 0.632$ , of the number of curing operations invariant to the network structure. Our results may help policymakers to design optimal containment strategies and minimize the controlling cost.
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In previous modelling efforts to understand the spreading process on networks, each node can infect its neighbors and cure spontaneously, and the curing is traditionally assumed to occur uniformly over time. This traditional curing is not optimal in terms of the trade-off between the effectiveness and cost. A pulse immunization/curing strategy is more efficient and broadly applied to suppress the spreading process. We analyze the pulse curing strategy on networks with the Susceptible-Infected (SI) process. We analytically compute the mean-field epidemic threshold $\tau_c^{p}$ of the pulse SI model and show that $\tau_c^{p}=\frac{1}{\lambda_1}\ln\frac{1}{1-p}$ , where $\lambda_1$ and p are the largest eigenvalue of the adjacency matrix of the contact graph and the fraction of nodes covered by each curing, respectively. These analytical results agree with simulations. Compared to the asynchronous curing process in the extensively studied Markovian SIS process, we show that the pulse curing strategy saves about 36.8%, i.e., $p\approx 0.632$ , of the number of curing operations invariant to the network structure. Our results may help policymakers to design optimal containment strategies and minimize the controlling cost.
Dynamical processes running on different networks behave differently, which makes the reconstruction of the underlying network from dynamical observations possible. However, to what level of detail the network properties can be determined from incomplete measurements of the dynamical process is still an open question. In this paper, we focus on the problem of inferring the properties of the underlying network from the dynamics of a susceptible-infected-susceptible epidemic and we assume that only a time series of the epidemic prevalence, i.e., the average fraction of infected nodes, is given. We find that some of the network metrics, namely those that are sensitive to the epidemic prevalence, can be roughly inferred if the network type is known. A simulated annealing link-rewiring algorithm, called SARA, is proposed to obtain an optimized network whose prevalence is close to the benchmark. The output of the algorithm is applied to classify the network types.
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Dynamical processes running on different networks behave differently, which makes the reconstruction of the underlying network from dynamical observations possible. However, to what level of detail the network properties can be determined from incomplete measurements of the dynamical process is still an open question. In this paper, we focus on the problem of inferring the properties of the underlying network from the dynamics of a susceptible-infected-susceptible epidemic and we assume that only a time series of the epidemic prevalence, i.e., the average fraction of infected nodes, is given. We find that some of the network metrics, namely those that are sensitive to the epidemic prevalence, can be roughly inferred if the network type is known. A simulated annealing link-rewiring algorithm, called SARA, is proposed to obtain an optimized network whose prevalence is close to the benchmark. The output of the algorithm is applied to classify the network types.
Journal article
(2019)
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Yanjie Xu, Yali Si, John Takekawa, Qiang Liu, Herbert H. T. Prins, Shenglai Yin, Diann J. Prosser, Peng Gong, Willem F. de Boer
Habitat loss can trigger migration network collapse by isolating migratory bird breeding grounds from nonbreeding grounds. Theoretically, habitat loss can have vastly different impacts depending on the site's importance within the migratory corridor. However, migration‐network connectivity and the impacts of site loss are not completely understood. We used GPS tracking data on 4 bird species in the Asian flyways to construct migration networks and proposed a framework for assessing network connectivity for migratory species. We used a node‐removal process to identify stopover sites with the highest impact on connectivity. In general, migration networks with fewer stopover sites were more vulnerable to habitat loss. Node removal in order from the highest to lowest degree of habitat loss yielded an increase of network resistance similar to random removal. In contrast, resistance increased more rapidly when removing nodes in order from the highest to lowest betweenness value (quantified by the number of shortest paths passing through the specific node). We quantified the risk of migration network collapse and identified crucial sites by first selecting sites with large contributions to network connectivity and then identifying which of those sites were likely to be removed from the network (i.e., sites with habitat loss). Among these crucial sites, 42% were not designated as protected areas. Setting priorities for site protection should account for a site's position in the migration network, rather than only site‐specific characteristics. Our framework for assessing migration‐network connectivity enables site prioritization for conservation of migratory species.
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Habitat loss can trigger migration network collapse by isolating migratory bird breeding grounds from nonbreeding grounds. Theoretically, habitat loss can have vastly different impacts depending on the site's importance within the migratory corridor. However, migration‐network connectivity and the impacts of site loss are not completely understood. We used GPS tracking data on 4 bird species in the Asian flyways to construct migration networks and proposed a framework for assessing network connectivity for migratory species. We used a node‐removal process to identify stopover sites with the highest impact on connectivity. In general, migration networks with fewer stopover sites were more vulnerable to habitat loss. Node removal in order from the highest to lowest degree of habitat loss yielded an increase of network resistance similar to random removal. In contrast, resistance increased more rapidly when removing nodes in order from the highest to lowest betweenness value (quantified by the number of shortest paths passing through the specific node). We quantified the risk of migration network collapse and identified crucial sites by first selecting sites with large contributions to network connectivity and then identifying which of those sites were likely to be removed from the network (i.e., sites with habitat loss). Among these crucial sites, 42% were not designated as protected areas. Setting priorities for site protection should account for a site's position in the migration network, rather than only site‐specific characteristics. Our framework for assessing migration‐network connectivity enables site prioritization for conservation of migratory species.
To shed light on the disease localization phenomenon, we study a bursty susceptible-infected-susceptible (SIS) model and analyze the model under the mean-field approximation. In the bursty SIS model, the infected nodes infect all their neighbors periodically, and the near-threshold steady-state prevalence is non-constant and maximized by a factor equal to the largest eigenvalue λ1 of the adjacency matrix of the network. We show that the maximum near-threshold prevalence of the bursty SIS process on a localized network tends to zero even if λ1 diverges in the thermodynamic limit, which indicates that the burst of infection cannot turn a localized spreading into a delocalized spreading. Our result is evaluated both on synthetic and real networks.
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To shed light on the disease localization phenomenon, we study a bursty susceptible-infected-susceptible (SIS) model and analyze the model under the mean-field approximation. In the bursty SIS model, the infected nodes infect all their neighbors periodically, and the near-threshold steady-state prevalence is non-constant and maximized by a factor equal to the largest eigenvalue λ1 of the adjacency matrix of the network. We show that the maximum near-threshold prevalence of the bursty SIS process on a localized network tends to zero even if λ1 diverges in the thermodynamic limit, which indicates that the burst of infection cannot turn a localized spreading into a delocalized spreading. Our result is evaluated both on synthetic and real networks.
In this paper, we focus on the autocorrelation of the susceptible-infected-susceptible (SIS) process on networks. The N-intertwined mean-field approximation (NIMFA) is applied to calculate the autocorrelation properties of the exact SIS process. We derive the autocorrelation of the infection state of each node and the fraction of infected nodes both in the steady and transient states as functions of the infection probabilities of nodes. Moreover, we show that the autocorrelation can be used to estimate the infection and curing rates of the SIS process. The theoretical results are compared with the simulation of the exact SIS process. Our work fully utilizes the potential of the mean-field method and shows that NIMFA can indeed capture the autocorrelation properties of the exact SIS process.
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In this paper, we focus on the autocorrelation of the susceptible-infected-susceptible (SIS) process on networks. The N-intertwined mean-field approximation (NIMFA) is applied to calculate the autocorrelation properties of the exact SIS process. We derive the autocorrelation of the infection state of each node and the fraction of infected nodes both in the steady and transient states as functions of the infection probabilities of nodes. Moreover, we show that the autocorrelation can be used to estimate the infection and curing rates of the SIS process. The theoretical results are compared with the simulation of the exact SIS process. Our work fully utilizes the potential of the mean-field method and shows that NIMFA can indeed capture the autocorrelation properties of the exact SIS process.
Since a real epidemic process is not necessarily Markovian, the epidemic threshold obtained under the Markovian assumption may be not realistic. To understand general non-Markovian epidemic processes on networks, we study the Weibullian susceptible-infected-susceptible (SIS) process in which the infection process is a renewal process with a Weibull time distribution. We find that, if the infection rate exceeds 1/ln(λ1+1), where λ1 is the largest eigenvalue of the network's adjacency matrix, then the infection will persist on the network under the mean-field approximation. Thus, 1/ln(λ1+1) is possibly the largest epidemic threshold for a general non-Markovian SIS process with a Poisson curing process under the mean-field approximation. Furthermore, non-Markovian SIS processes may result in a multimodal prevalence. As a byproduct, we show that a limiting Weibullian SIS process has the potential to model bursts of a synchronized infection.
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Since a real epidemic process is not necessarily Markovian, the epidemic threshold obtained under the Markovian assumption may be not realistic. To understand general non-Markovian epidemic processes on networks, we study the Weibullian susceptible-infected-susceptible (SIS) process in which the infection process is a renewal process with a Weibull time distribution. We find that, if the infection rate exceeds 1/ln(λ1+1), where λ1 is the largest eigenvalue of the network's adjacency matrix, then the infection will persist on the network under the mean-field approximation. Thus, 1/ln(λ1+1) is possibly the largest epidemic threshold for a general non-Markovian SIS process with a Poisson curing process under the mean-field approximation. Furthermore, non-Markovian SIS processes may result in a multimodal prevalence. As a byproduct, we show that a limiting Weibullian SIS process has the potential to model bursts of a synchronized infection.
An accurate approximate formula of the die-out probability in a SIS epidemic process on a network is proposed. The formula contains only three essential parameters: the largest eigenvalue of the adjacency matrix of the network, the effective infection rate of the virus, and the initial number of infected nodes in the network. The die-out probability formula is compared with the exact die-out probability in complete graphs, Erdȍs-Rényi graphs, and a power-law graph. Furthermore, as an example, the formula is applied to the N-Intertwined Mean-Field Approximation, to explicitly incorporate the die-out.
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An accurate approximate formula of the die-out probability in a SIS epidemic process on a network is proposed. The formula contains only three essential parameters: the largest eigenvalue of the adjacency matrix of the network, the effective infection rate of the virus, and the initial number of infected nodes in the network. The die-out probability formula is compared with the exact die-out probability in complete graphs, Erdȍs-Rényi graphs, and a power-law graph. Furthermore, as an example, the formula is applied to the N-Intertwined Mean-Field Approximation, to explicitly incorporate the die-out.
One of the most important quantities of the exact Markovian SIS epidemic process is the time-dependent prevalence, which is the average fraction of infected nodes. Unfortunately, the Markovian SIS epidemic model features an exponentially increasing computational complexity with growing network size N. In this paper, we evaluate a recently proposed analytic approximate prevalence function introduced in Van Mieghem (2016). We compare the approximate function with the N-Intertwined Mean-Field Approximation (NIMFA) and with simulation of the Markovian SIS epidemic process. The results show that the new analytic prevalence function is comparable with other approximate methods.
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One of the most important quantities of the exact Markovian SIS epidemic process is the time-dependent prevalence, which is the average fraction of infected nodes. Unfortunately, the Markovian SIS epidemic model features an exponentially increasing computational complexity with growing network size N. In this paper, we evaluate a recently proposed analytic approximate prevalence function introduced in Van Mieghem (2016). We compare the approximate function with the N-Intertwined Mean-Field Approximation (NIMFA) and with simulation of the Markovian SIS epidemic process. The results show that the new analytic prevalence function is comparable with other approximate methods.