Abstract
The risk of propagation of infectious diseases such as avian influenza and COVID-19 is generally controlled or reduced by quarantine measures. Considering this situation, a network-based SIQS (susceptible-infected-quarantined-susceptible) infectious disease model with nonmonotone incidence rate is established and analyzed in this paper. The psychological impact of the transmission of certain diseases in heterogeneous networks at high levels of infection may be characterized by the related nonmonotone incidence rate. The expressions of the basic reproduction number and equilibria of the model are determined analytically. We demonstrate in detail the uniform persistence of system and the global asymptotic stability of the disease-free equilibrium. The global attractivity of the unique endemic equilibrium is discussed by using monotone iteration technique. We obtain that the endemic equilibrium is globally asymptotically stable under certain conditions by constructing appropriate Lyapunov function. In addition, numerical simulations are performed to indicate the theoretical results.
Keywords: Complex networks, Quarantine, Nonmonotone incidence, Global dynamics
1. Introduction
It has been known that infectious diseases not only threaten the health of human beings but can even bring great disasters to the national economy and people’s livelihood. Therefore, it is very important to investigate the transmission mechanisms and development trends of infectious diseases and then adopt appropriate measures to control their prevalence. Dynamic modeling is one of the efficient tools to research the transmission of infectious diseases in the population, not only to characterize the intrinsic transmission mechanism of infectious diseases but also to qualitatively and quantitatively study the transmission pattern, which is important in the formulation and evaluation of prevention and control measures. Traditional models, which are based on populations that are uniformly mixed, are inadequate to describe the transmission process of infectious diseases in large-scale social contact networks with distinct heterogeneity. As a matter of fact, transmission of infectious diseases at the group level occurs mainly through social contact networks, consequently, it is more realistic to use complex networks for investigating the spread of epidemics in populations.
In recent years, an increasing number of scholars have begun to focus on the dynamics of infectious diseases on complex networks [1], [2], [3], [4], [5], [6], [7], [8], [9], [10]. Pastor-Satorras and Vespignani [1], [2] first established the SIS model in scale-free networks using a mean-field approximation. The absence of prevalence threshold in these networks was the most surprising finding. The stability of the SIS model was later determined [4], [5]. These outstanding achievements have sparked several of the related projects [11], [12], [13], [14], [15], [16], [17].
How to propose effective measures of disease control is an important research theme for the complex network infectious diseases. Quarantine of symptomatic individuals is an intervention program for controlling the propagation of infectious diseases, and this method has been used to prevent diseases such as cholera and COVID-19 [18], [19], [20], [21], [22]. The most direct method of controlling the transmission of epidemic may be the quarantine of infected persons, because it disrupts the links that connect the infected persons to the susceptible persons. In particular, quarantining infected persons is probably the most efficient measure for controlling the transmission of disease until associated vaccines and valid therapy for the infectious disease are available. A novel coronavirus (COVID-19) epidemic has been reported in Wuhan, Hubei Province, China, since December 2019. On March 11, 2020, the World Health Organization (WHO) declared COVID-19 as a global pandemic. The Chinese government has controlled the spread of the epidemic by quarantining infected individuals, close contacts, and susceptible individuals as well as other measures. However, there are relatively few studies on the impacts of quarantine on transmission of epidemic on complex networks [22], [23], [24], [25]. Li et al. [23] presented an SIQRS infectious disease model on the scale-free networks, and theoretical results suggest that the prevalence threshold is actually related to the networks’ topology. In addition, the epidemic threshold goes up and the final number of infected persons decreases as quarantine rate increases. Recently, Li et al. [25] proposed the SIQS infectious disease model on complex networks:
| (1.1) |
where represent the relative density of susceptible, infected and quarantined individuals with degree at time , respectively. is the rate of transmission from infected to susceptible individuals. The infected nodes are quarantined with rate . A non-quarantined infected node recovers as a susceptible node with probability . is the recovery rate of each quarantined infected node. In reality, with improvements in the medical environment, patients who are quarantined are generally more likely to recover than those who are not, which makes . Based on the biological meaning, the parameters and are all positive constants. The constant is the birth rate, is the natural mortality rate. denotes the probability that any given edge points to an infected node on networks.
The incidence rate is significant for the investigation of mathematical epidemiology. In the majority of classical disease transmission models, one generally uses bilinear incidence rate , where . In recent years, many researchers considered nonlinear incidence rates to describe the transmission of infectious diseases. For example, as a result of the research of the 1973 cholera pandemic in Bari, in order to avoid infinite of the contact rate, Capasso and Serio [26] proposed a saturated incidence rate , in which , , and as becomes larger, converges to saturation level. To describe the psychological effect of the spread of some diseases spread at high infective levels, Xiao and Ruan [27] presented an incidence rate:
| (1.2) |
where the incidence function is nonmonotone when (see Fig. 1 ). Obviously, as is small, gets larger, and as increases, gets smaller. It implies that during an initial stage of an outbreak, the susceptible persons are not aware of the severity of the outbreak and the transmission rate probably increases with increasing numbers of infected persons. However, in cases where there are numerous infected individuals, one usually reduces contact with others in a unit of time. Thus, the transmission rate is likely to reduce with increasing numbers of infected persons in the case of extremely large numbers of infected individuals. For example, during the outbreak of COVID-19, aggressive measures such as mask-wearing and quarantine effectively reduced transmission rate. As a matter of reality, as a result of quarantining infected persons or protective behaviors of susceptible persons, the incidence rate decreases at higher levels of infection. In [27], They analyzed the global dynamics of the SIRS model with (1.2) as well as demonstrated that as time progresses, numbers of infected persons converge toward zero or the disease is persistent. Chen and Wen [28] used (1.2) to characterize the transmission between human and poultry, which conform the effect of human intervention.
Fig. 1.
Nonmonotone incidence function with .
The incidence rate in current models of complex network infectious diseases is generally considered to be a bilinear function. Recently, to analyze effect of nonmonotone incidence rate on complex network infectious disease models, Li [29] investigated a network-based SIS infectious disease model with nonmonotone incidence rate and demonstrated that the disease will become extinct when the transmission rate is below a threshold, otherwise it will be permanent. In [30], Wei et al. proved the global stability and attractivity of the endemic equilibrium in [29]. Liu et al. [31] investigated the network-based SIRS infectious disease model with vaccination and nonmonotone incidence rate and demonstrated global stability of endemic equilibrium.
Based on the above discussions, combining (1.1) and (1.2), we establish the following SIQS epidemic model with nonmonotone incidence rate as follows:
| (1.3) |
where is a parameter that indicates the psychological or inhibitory effect. The nonmonotone incidence rate gets bilinear and (1.3) simplifies to (1.1) when . The term indicates the number of newly born nodes is the same for all different degrees per unit time, and each newly born node is susceptible. The term represents when there is a large number of infected individuals in the network, the number of effective contacts between infected individuals and susceptible individuals will decrease due to the quarantine of infected individuals or the protection measures by the susceptible individuals. Throughout this paper, we assume that complex networks are uncorrelated. Therefore, can be written as
| (1.4) |
where is the probability that a randomly chosen node has degree (i.e., the degree distribution) and thus , is the average degree of the network.
For system (1.3), we assume , which implies that births and deaths are balanced. In addition, since the network’s removing nodes and links due to births and deaths just account for a tiny portion of the total, each node’s degree is assumed to be constant. The two hypotheses mentioned above are also provided in [32], [33].
The remaining part is organized in the following: Section 2 investigates the positivity and boundedness of solutions of the SIQS model. In addition, we get equilibria and epidemic threshold. We demonstrate the global asymptotical stability of disease-free equilibrium and discuss the global dynamics of the endemic equilibrium are discussed in detail in Section 3. In Section 4, we show numerical simulations to confirm all the theoretical results. Conclusions are presented in Section 5.
2. Positivity, boundedness and equilibria
Considering the actual situation, the initial conditions of system (1.3) satisfy
| (2.1) |
Therefore, it follows that , for , then it suffices to discuss the following system
| (2.2) |
We just need to explore the dynamical properties of subsystem (2.2) to obtain the dynamical behaviors of (1.3).
The following lemma establishes the positivity of solutions.
Lemma 2.1
Letbe the solution of(1.3)with initial conditions(2.1). Then for anyand, one hasand.
Proof
We will start by proving that for every . It follows from the second equation of (1.3) that
(2.3) By integrating (2.3) from 0 to yields
It’s obvious to observe that for any there is due to .
Note that for . It follows from the first equation of (1.3) and continuity of that a small enough exists leading to when . Then we want holds for any . Suppose that when , may be equal to zero. There is and the first time resulting in and for . Together with the second equation of (1.3), it follows that when yields . It is clear that there is for .
This gives with respect to from the third equation of (1.3), which implies that with respect to there is . Obviously, by continuity of we obtain . Accordingly, the first equation of (1.3) represents that . Then for , where ia an arbitrary positive constant. Clearly, it gives rise to a contradiction. As a result, for any .
Analogously, for any , we get by the second equation of (1.3). Consequently, we derive for every from the last equation of (1.3). Notice that . Therefore, one can easily demonstrated that for any and all , there are and . □
Lemma 2.2
For system(1.3), the following results are obtained.
(1) There always exists a disease-free equilibrium.
(2) If, system admits a unique epidemic equilibrium.
Here
(2.4) with.
Proof
It is obvious that the disease-free equilibrium of (1.3) always exists. To compute the endemic equilibrium , suppose the right sides of (1.3) is zero. In other words, the should satisfy
(2.5) where . We get from (2.5)
(2.6) For convenience, we replace with . Substituting (2.6) into , we obtain a self-consistency equality
(2.7) As can be easily seen, is a solution of (2.7), and . Next, the conditions for (2.7) to have nontrivial solutions in the interval are needed to be found. That is, it satisfies the inequality
As a result, the basic reproduction number is
where .
Substituting the nontrivial solution of (2.7) into (2.6), we derive . From (2.5), (2.4) is established as well as for . As a result, a unique epidemic equilibrium exists when . □
Remark 2.1
Epidemic thresholds determine the presence of endemic equilibrium, as shown in Lemma 2.2. In the case where , system (1.3) simplies to (1.1), and can be simplified to , where , which agrees with that given in [25]. That is to say, the nonmonotone incidence rate (1.2) does not affect the epidemic threshold.
3. Global dynamics analysis
In this section, a qualitative analysis of (2.2) is presented. For the purpose of studying the global dynamical behavior of (2.2), the following lemma is first given to ensure that the solutions of system are nonnegative. Set and for . After that, we investigate (2.2) for , where
| (3.1) |
Firstly, the following lemma is provided.
Lemma 3.1
The setis positively invariant with respect to system(2.2).
Proof
It is to be shown that if , there is for all . Define
Let the outer normals to the hyperplanes be
Through the results of Nagumo [34], it suffices to demonstrate that for ,
It is clear that any solutions starting from will stay inside . Accordingly, the set is positively invariant. □
Next, we are ready to consider the local asymptotic stability of the disease-free equilibrium .
Theorem 3.1
If, the disease-free equilibriumof system(1.3)is locally asymptotically stable, while it is unstable if.
Proof
System (2.2) can be rewritten as
(3.2) which initial condition satisfies . is the linear part with being the Jacobian matrix of (2.2) evaluated at is shown below
where , , , , , . Here, and denote the th-order zero and identity matrix, respectively. It follows that
As a result, the nonlinear part , , for .
By mathematical induction, the characteristic equation of the matrix can be calculated as
(3.3) Eq. (3.3) has a negative eigenvalue with multiplicity and a negative eigenvalue with multiplicity . The stability of is only determined by
If , one has ; and if , one has . Hence, is locally asymptotically stable if , whereas it is unstable if . □
We now proceed to examine the global stability of .
Theorem 3.2
If, the disease-free equilibriumof(1.3)is globally asymptotically stable.
Proof
Rewrite (1.3) as
(3.4) Considering a non-negative solution of (3.4). Firstly, we prove that . From the first equation of (3.4), we derive
It can be deduced that
(3.5) Accordingly, for arbitrarily sufficiently small , there is resulting in for . If , we get
Take into account the following auxiliary system
(3.6) Then it suffices to demonstrate that the positive solutions of system converge to zero as tends to infinity. We construct the following Lyapunov function
where . Calculating the derivative of along solutions of (3.6), we have
Since , we can select an sufficiently small such that . This guarantees that for all , and that if and only if for .
Next, we will prove . Since , for arbitrary small enough, there exists leading to for . From the first equation of (3.4), it follows that
where . We have . Taking , one obtains
(3.7) Combining (3.5) and (3.7), it is obvious that .
Finally, since , we obtain . This shows that of (1.3) is globally attractive when and it can be deduced from Theorem 3.1 that is globally asymptotically stable. □
The following result shows that (2.2) is uniformly persistent when , that is, the disease persists in the population. We will apply the following two lemmas.
Lemma 3.2 [35] —
Letbe an irreduciblematrix. Ifwhenever, then there is an eigenvectorofsuch that, and the corresponding eigenvalue is, whereare the eigenvalues of, andrepresents the real part of the eigenvalues.
Lemma 3.3 [16] —
Consider the following system
(3.8) whereis anmatrix andis continuously differentiable in. Suppose that
- (i)
a compact convex setis positively invariant for system(3.8), with;
- (ii)
there is a positive integerresulting in;
- (iii)
there are a positive numberand a real eigenvectorcorresponding to a positive eigenvalue ofresulting infor all;
- (iv)
is true for all.
Therefore, the solutionof(3.8)admitsfor any, wherehas no relation to the initial value. Further, there is a constant solution of(3.8),with.
In the following, system (3.2) will be verified to satisfy all assumptions of Lemma 3.3. By Lemma 3.1, condition (i) is established with respect to (3.2) by choosing . Obviously,
, so condition (ii) holds.
With respect to condition (iii), it is noticed that is irreducible and when , as a result, by Lemma 3.2 and Eq. (3.3), there exists an eigenvector of such that for all , and the corresponding eigenvalue is . If , then . Set and , we get , which means that is the eigenvector corresponding to a positive eigenvalue of . If one defines , it follows that for all , i.e., condition (iii) follows.
The condition (iv) is also confirmed since for all . As a result, all the assumptions of Lemma 3.3 are valid.
These results are summarized in the following theorem.
Theorem 3.3
If, system(2.2)is uniformly persistent, that is, there exists a constantsuch that
Remark 3.1
Theorem 3.3 shows that when , the disease is permanent. In addition, according to Lemma 3.3, there is a constant solution of (2.2) when , which is the endemic equilibrium of (2.2). This is consistent with the conclusion of Lemma 2.2.
Next, the global attractivity of is discussed.
Theorem 3.4
Assume thatis a solution of system(2.2)satisfying(2.1). Ifand, then, whereis the unique positive equilibrium of(2.2)satisfying(2.4)for.
Proof
Without loss of generality, fix to be any integer of the set . In accordance with Theorem 3.3, there is a small enough constant and a large enough constant resulting in for . Accordingly,
From the first equation of (2.2), one obtains
According to the comparison principle, for any given small constant , there is a resulting in for , where
(3.9) From the second equation of (2.2), it follows that
Analogously, for any given small constant , there is a resulting in for , where
(3.10) In view of the fact that . Substituting into the first equation of (2.2) yields
As a result, for any given small constant , there exists a such that for , where
(3.11) It follows from the second equation of (2.2) that , . In a similar way, for any given small constant , there is a resulting in for , where
(3.12) Since is sufficiently small constant, it holds that and . It can be seen from the above discussion that and for . Consequently, it can be seen that
(3.13) where and . Once again, by (2.2), we obtain
Therefore, for any given constant , there exists a such that
(3.14) By the second equation of (2.2), one gets , . Consequently, for any given constant , there is a such that
(3.15) Combining (3.9), (3.14) and (3.15), we know that and .
Again from system (2.2), it is clear that
As a result, for any given constant , there exists a such that , where
(3.16) By (2.2), we arrive at , . Therefore, for any given constant , there is a such that
(3.17) By repeating the above process, four sequences: are derived. Through generalization, as we can see the first two sequences are monotonically decreasing and the last two are monotonically increasing. Therefore, there is a large enough positive integer such that for ,
(3.18) It is evident that
(3.19) As the sequential limits of (3.18) exist, let , where and . Note that , then as . Consequently, assuming , It can be deduced from (3.18) that
(3.20) where . In addition, by (3.20) one gets
(3.21) where
For this, we declare . Noticing that is the unique nonzero value decided by (3.20). If , then . According to the symmetry, we get . It is apparent that , i.e., . This contradicts the assumptions in the theorem. Thus, .
Combining (3.21) with the formulas of and , we obtain
(3.22) By subtracting the two equations above, it yields
(3.23) Since , this means that . Thus, we get , which means that for . From (3.19) and (3.20), one arrives at and . Noticing that when , Eq. (2.7) has a unique positive solution . Therefore, substituting and into (3.21), according to (2.4) and (3.20), we derive and . Consequently, the endemic equilibrium of (2.2) is globally attractive if and . □
Finally, we examine the globally asymptotic stability of the endemic equilibrium.
Theorem 3.5
Ifandor, the endemic equilibriumof system(1.3)is globally asymptotically stable.
Proof
For convenience, , , and are used to instead of , , and respectively. It follows from Lemma 2.1 that for all . We consider a Lyapunov function candidate , the elements of which are shown below
where
and is positive constant, which will be determined later.
In the following, we derive the derivatives of , and , respectively. We can rewrite the first equation of (3.4) as
(3.24) In addition, it can be deduced from (2.3) that
(3.25) Differentiating and employing the identity , we get
(3.26) The last term of right hand side of (3.26) can be expressed as
Substituting the above equality into (3.26), one gets
(3.27) Substituting the last equation of (1.3) and the identity into the differential process of , we derive as
(3.28) Similarly, combining (3.25) and the identity , can be constructed as follows
(3.29) Due to the fact that , we observe that the last term of (3.27) is equal to . Then combining (3.28), and selecting , is given as
(3.30) where
and
In order to ensure that , it is sufficient to show that the following inequality holds.
(3.31) It is noted that . Then when , apparently we can obtain
(3.32) which means that (3.31) holds.
Additionally, It can be deduced from the inequalities and that
(3.33) and
(3.34) From (3.34), we get
(3.35) Inserting (3.33) and (3.35) into (3.31) and utilizing the hypothesis yields
which indicates that (3.31) is confirmed. Consequently, if or then (3.31) holds, and from (3.30) we can obtain
(3.36) Moreover, if and only if and for . By LaSalle’s Invariant Principle [36], we can conclude that of system (1.3) is globally asymptotically stable. □
4. Numerical simulations
In this section, we perform some numerical simulations to verify our theoretical results obtained in the previous sections and to understand the effects of parameters on the spread of epidemics, so as to find better control strategies. The following simulations are based on a scale-free network, which satisfy a power-law degree distribution, namely, for . The parameter is chosen to make .
Example 4.1
In Figs. 2 and 3 , we show the outcome of system (1.3) when the basic reproduction number . Let and . In this case, . The time series of are performed in Fig. 2(a) and Fig. 2(b) . The initial values are given by and for any degree . From the numerical results, it can be seen that is globally asymptotically stable when , which means that the disease will eventually become extinct. In addition, when and , there is a peak in the density of infected nodes before leading to the disease-free equilibrium, however, as increases, the peak level decreases, that is, a big can efficiently reduce the epidemic peak during the initial outbreak of the disease. Fig. 3 depicts the trajectories of versus with eight different initial conditions. The parameters in Fig. 3 are the same as those in Fig. 2. Fig. 3(a) and 3(b) show that the disease-free equilibrium is indeed globally asymptotically stable.
Example 4.2
In Figs. 4 and 5 , we show the outcome of system (1.3) when the basic reproduction number . The parameters are chosen as . Subsequently, we can obtain and and . By selecting and 3500 respectively, the condition or in Theorem 3.5 holds. From Fig. 4, it can be seen that the disease will approach to a positive stationary level when . The trajectories of for eight different initial values are plotted in Fig. 5. In Figs. 4 and 5, we see that the endemic equilibrium is globally asymptotically stable when and the condition or is satisfied, in accord with Theorem 3.5. In addition, as can be seen from Fig. 4, the density of the infected nodes decreases with increasing when the disease is prevalent, indicating that a larger can weaken the epidemic level of the disease.
Example 4.3
From Theorem 3.5, we know that the endemic equilibrium is globally asymptotically stable when and the condition or is satisfied, which is shown in Figs. 4 and 5. Nevertheless, in Fig. 6 , we choose and other parameters are the same as in Example 4.2, it is clear that does not satisfy the conditions of Theorem 3.5. Fig. 6 depicts the time evolution of with different , where is the relative average density of the infected nodes on the entire networks. It can be observed from Fig. 6 that the percentages of infected individuals eventually converge to a positive stationary level.
Fig. 2.
The time series of with .
Fig. 3.
The time series of with eight different initial values and .
Fig. 4.
The time series of with .
Fig. 5.
The time series of with eight different initial values and .
Fig. 6.
The time evolution of with and different .
Example 4.4. Finally, we display the effect of quarantine by numerical simulations. In Fig. 7 , the initial values are and . We fix the parameters and to graph the time evolution of with six different . From the figure, it is observed that by increasing the quarantine rate , the level of endemic disease prevalence reduces significantly, indicating that raising the quarantine rate helps in controlling the disease.
Fig. 7.
The time evolution of corresponding to different .
5. Conclusions
Quarantine strategies remain an extremely efficient method of controlling the outbreaks of epidemics when we suffer from a variety of serious infectious diseases. As a result, we have proposed and investigated a network-based SIQS infectious disease model with nonmonotone incidence rate. The psychological response of individuals during an outbreak may be characterized by the nonmonotone incidence rate, that is, in the case of a great number of infected persons, individuals consciously reduce their contact with others for fear of being infected, and thus infectivity decreases as the number of infected persons goes up. The expression for the basic reproduction number is derived, which is related to the network topology as well as some parameters.
Furthermore, we show that the basic reproduction number determines not only the existence of the endemic equilibrium but also the global dynamics of model. More specially, by utilizing the Lyapunov function, it is shown that the disease-free equilibrium is globally asymptotically stable when , namely, the disease will disappear eventually. On the other hand, the disease is uniformly persistent on the network when . At the same time, by using a novel monotone iterative scheme, we demonstrate that if and , the unique endemic equilibrium is globally attractive. Furthermore, by constructing appropriate Lyapunov function, is globally asymptotically stable if and the inhibitory effect is large or small enough.
To facilitate the understanding of theoretical results, several numerical examples are designed and simulated vividly in Section 4. Although the parameter has no effect on the epidemic threshold, it can be seen that bigger makes the disease die out faster and the level of prevalence lower, which is confirmed from the numerical consequences. Moreover, it can be seen from Fig. 6 that the average density of infected individuals eventually converges to a positive stationary level when does not satisfy the conditions in Theorem 3.5. As a result, we conjecture that the endemic equilibrium of system (1.3) is globally asymptotically stable only when . In addition, the results of Example 4.4 indicate that the level of endemic disease prevalence reduces significantly with increasing the quarantine rate , which means that quarantine strategies are efficient methods for preventing and controlling epidemic spreading.
It should be noted that, in our model, we assume that the birth rate is constant, i.e., the number of newly born nodes is the same for all different degrees per unit time. If we suppose the birth rate is distributed into group at the probability , one would expect much more complicated dynamics. Furthermore, we only consider a simple epidemic model on static networks. Nevertheless, it is known that the real contact networks are time-varying. Hence, it is also necessary to study the spreading dynamics on real contact networks. We leave these research topics for future work.
CRediT authorship contribution statement
Xinxin Cheng: Conceptualization, Methodology, Investigation, Writing – original draft, Writing – review & editing. Yi Wang: Methodology, Visualization, Writing – review & editing. Gang Huang: Methodology, Visualization, Writing – review & editing.
Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgments
This work was supported by the National Natural Science Foundation of China (11801532) and Fundamental Research Funds for the Central Universities, China University of Geosciences (Wuhan) (CUGSX01).
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