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. 2021 Oct 30;153:111502. doi: 10.1016/j.chaos.2021.111502

Global dynamics of a network-based SIQS epidemic model with nonmonotone incidence rate

Xinxin Cheng 1, Yi Wang 1, Gang Huang 1,
PMCID: PMC8556768  PMID: 34744326

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:

{dSk(t)dt=AβkSk(t)Θ(t)dSk(t)+γIk(t)+εQk(t),dIk(t)dt=βkSk(t)Θ(t)(d+γ)Ik(t)δIk(t),dQk(t)dt=δIk(t)(d+ε)Qk(t),k=1,2,,n, (1.1)

where Sk(t),Ik(t),Qk(t) represent the relative density of susceptible, infected and quarantined individuals with degree k at time t, respectively. β is the rate of transmission from infected to susceptible individuals. The infected nodes are quarantined with rate δ. A non-quarantined infected node recovers as a susceptible node with probability γ. ε 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 ε>γ. Based on the biological meaning, the parameters β,δ,γ and ε are all positive constants. The constant A is the birth rate, d is the natural mortality rate. Θ(t) 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 g(I)S=kIS, where g(I)=kI. 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 g(I)S=kIS1+αI, in which g(I)=kI1+αI, α>0, and as I becomes larger, g(I) 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:

g(I)S=kIS1+αI2, (1.2)

where the incidence function g(I)=kI1+αI2 is nonmonotone when I0 (see Fig. 1 ). Obviously, as I is small, g(I) gets larger, and as I increases, g(I) 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.

Fig. 1

Nonmonotone incidence function g(I) with α=1.5.

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:

{dSk(t)dt=AβkSk(t)Θ(t)1+αΘ2(t)dSk(t)+γIk(t)+εQk(t),dIk(t)dt=βkSk(t)Θ(t)1+αΘ2(t)(d+γ)Ik(t)δIk(t),dQk(t)dt=δIk(t)(d+ε)Qk(t),k=1,2,,n, (1.3)

where α is a parameter that indicates the psychological or inhibitory effect. The nonmonotone incidence rate gets bilinear and (1.3) simplifies to (1.1) when α=0. The term A 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 βkSk(t)Θ(t)1+αΘ2(t) 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, Θ(t) can be written as

Θ(t)=1kk=1nkP(k)Ik(t), (1.4)

where P(k) is the probability that a randomly chosen node has degree k (i.e., the degree distribution) and thus k=1nP(k)=1, <k>=k=1nkP(k) is the average degree of the network.

For system (1.3), we assume A=d, 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

Ik(0),Qk(0)0,Sk(0)=1Ik(0)Qk(0)>0,andΘ(0)>0. (2.1)

Therefore, it follows that Sk(t)+Ik(t)+Qk(t)1, t0 for k=1,2,,n, then it suffices to discuss the following system

{dIk(t)dt=βk[1Ik(t)Qk(t)]Θ(t)1+αΘ2(t)(d+γ+δ)Ik(t),dQk(t)dt=δIk(t)(d+ε)Qk(t),k=1,2,,n. (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

Let(S1(t),I1(t),Q1(t),,Sn(t),In(t),Qn(t))be the solution of(1.3)with initial conditions(2.1). Then for anyt>0andk=1,2,,n, one has0<Sk(t),Ik(t),Qk(t)<1and0<Θ(t)<1.

Proof

We will start by proving that Θ(t)>0 for every t>0. It follows from the second equation of (1.3) that

dΘ(t)dt=1kk=1nkP(k)dIk(t)dt=1kk=1nkP(k)[βkSk(t)Θ(t)1+αΘ2(t)(d+γ+δ)Ik(t)]=Θ(t)[βkk=1nk2P(k)Sk(t)1+αΘ2(t)(d+γ+δ)]. (2.3)

By integrating (2.3) from 0 to t yields

Θ(t)=Θ(0)exp{βkk=1nk2P(k)Sk(t)1+αΘ2(t)(d+γ+δ)}.

It’s obvious to observe that for any t>0 there is Θ(t)>0 due to Θ(0)>0.

Note that Sk(0)>0 for k=1,2,,n. It follows from the first equation of (1.3) and continuity of Sk(t) that a small enough ζ>0 exists leading to Sk(t)>0 when t(0,ζ). Then we want Sk(t)>0 holds for any t>0. Suppose that when t>0, Sk(t) may be equal to zero. There is h{1,2,,n} and the first time t1ζ>0 resulting in Sh(t1)=0 and Sh(t)>0 for t(0,t1). Together with the second equation of (1.3), it follows that when t(0,t1) yields dIh(t)dt+(d+γ+δ)Ih(t)>0. It is clear that there is Ih(t)>Ih(0)e(d+γ+δ)t0 for t(0,t1).

This gives dQh(t)dt+(d+ε)Qh(t)>0 with respect to t(0,t1) from the third equation of (1.3), which implies that with respect to t(0,t1) there is Qh(t)>Qh(0)e(d+ε)t0. Obviously, by continuity of Qh(t) we obtain Qh(t1)0. Accordingly, the first equation of (1.3) represents that dSh(t1)dt1=A+γIh(t1)+εQh(t1)>0. Then Sh(t)<Sh(t1)=0 for t(t1κ,t1)(0,t1), where κ ia an arbitrary positive constant. Clearly, it gives rise to a contradiction. As a result, Sk(t)>0 for any t>0.

Analogously, for any t>0, we get Ik(t)>0 by the second equation of (1.3). Consequently, we derive Qk(t)>0 for every t>0 from the last equation of (1.3). Notice that Sk(t)+Ik(t)+Qk(t)=1. Therefore, one can easily demonstrated that for any t>0 and all k=1,2,,n, there are 0<Sk(t),Ik(t),Qk(t)<1 and 0<Θ(t)<1. □

Lemma 2.2

For system(1.3), the following results are obtained.

(1) There always exists a disease-free equilibriumE0=(1,0,0,,1,0,0).

(2) IfR0>1, system admits a unique epidemic equilibriumE*={Sk*,Ik*,Qk*}k=1n.

Here

Sk*=(d+γ+δ)(1+α(Θ*)2)βkΘ*Ik*,Qk*=δd+εIk*,Ik*=(d+ε)βkΘ*(d+γ+δ)(d+ε)+(d+ε+δ)βkΘ*+α(d+γ+δ)(d+ε)(Θ*)2, (2.4)

withΘ*=1kk=1nkP(k)Ik*.

Proof

It is obvious that the disease-free equilibrium E0 of (1.3) always exists. To compute the endemic equilibrium E*, suppose the right sides of (1.3) is zero. In other words, the {Sk*,Ik*,Qk*}k=1n should satisfy

{βkSk*Θ*1+α(Θ*)2(d+γ+δ)Ik*=0,δIk*(d+ε)Qk*=0,Sk*+Ik*+Qk*=1,k=1,2,,n, (2.5)

where Θ*=1kk=1nkP(k)Ik*. We get from (2.5)

Ik*=(d+ε)βkΘ*(d+γ+δ)(d+ε)+(d+ε+δ)βkΘ*+α(d+γ+δ)(d+ε)(Θ*)2. (2.6)

For convenience, we replace Θ* with Θ. Substituting (2.6) into Θ*, we obtain a self-consistency equality

Θ=1kk=1n(d+ε)βk2P(k)Θ(d+γ+δ)(d+ε)+(d+ε+δ)βkΘ+α(d+γ+δ)(d+ε)Θ2=f(Θ). (2.7)

As can be easily seen, Θ=0 is a solution of (2.7), and f(1)<1. Next, the conditions for (2.7) to have nontrivial solutions in the interval 0<Θ<1 are needed to be found. That is, it satisfies the inequality

df(Θ)dΘ|Θ=0=ddΘ(1kk=1n(d+ε)βk2P(k)Θ(d+γ+δ)(d+ε)+(d+ε+δ)βkΘ+α(d+γ+δ)(d+ε)Θ2)Θ=0>1.

As a result, the basic reproduction number R0 is

R0=βk2(d+γ+δ)k,

where k2=k=1nk2P(k).

Substituting the nontrivial solution of (2.7) into (2.6), we derive Ik*. From (2.5), (2.4) is established as well as 0<Sk*,Ik*,Qk*<1 for k=1,2,,n. As a result, a unique epidemic equilibrium E* exists when R0>1. □

Remark 2.1

Epidemic thresholds determine the presence of endemic equilibrium, as shown in Lemma 2.2. In the case where α=0, system (1.3) simplies to (1.1), and R0>1 can be simplified to β>βc, where βc=(d+γ+δ)kk2, 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 Ik(t)=xk(t) and Qk(t)=xn+k(t) for k=1,2,,n. After that, we investigate (2.2) for x:=(x1,x2,,x2n)Ω, where

Ω={xR2n:xi0for1i2n,andxj+xn+j1forall1jn}. (3.1)

Firstly, the following lemma is provided.

Lemma 3.1

The setΩis positively invariant with respect to system(2.2).

Proof

It is to be shown that if x(0)Ω, there is x(t)Ω for all t>0. Define

Ω1={xΩ|xi=0},Ω2={xΩ|xn+i=0},Ω3={xΩ|xi+xn+i=1},i=1,2,,n.

Let the outer normals to the 3n hyperplanes be

ηi1=(0,,1i,,0,0,,0)(ithposition),ηi2=(0,,0,0,,1n+i,,0)((n+i)thposition),ηi3=(0,,+1i,,0,0,+1n+i,,0)(ithand(n+i)thposition).

Through the results of Nagumo [34], it suffices to demonstrate that for i=1,2,,n,

(dxdt|xΩ1·ηk1)=βi(1xn+i)Θ˜1+αΘ˜20,(dxdt|xΩ2·ηk2)=δxi0,(dxdt|xΩ3·ηk3)=(d+γ)xi(d+ε)xn+i0,whereΘ˜=1kk=1kinkP(k)xk0.

It is clear that any solutions starting from Ω1Ω2Ω3 will stay inside Ω. Accordingly, the set Ω is positively invariant. □

Next, we are ready to consider the local asymptotic stability of the disease-free equilibrium E0.

Theorem 3.1

IfR0<1, the disease-free equilibriumE0of system(1.3)is locally asymptotically stable, while it is unstable ifR0>1.

Proof

System (2.2) can be rewritten as

dz(t)dt=Bz+G(z), (3.2)

which initial condition satisfies z(0)Ω. Bz is the linear part with B being the Jacobian matrix of (2.2) evaluated at E0 is shown below

B=(B11B12B21B22)2n×2n,
B11=(l1q1(d+γ+δ)l1q2l1qnl2q1l2q2(d+γ+δ)l2qnlnq1lnq2lnqn(d+γ+δ)),

where li=βik, qj=jP(j), (1i,jn), B12=On, B21=δEn, B22=(d+ε)En. Here, On and En denote the nth-order zero and identity matrix, respectively. It follows that

dIk(t)dt=βk[1Ik(t)Qk(t)]Θ(t)1+αΘ2(t)(d+γ+δ)Ik(t)=[βkΘ(t)(d+γ+δ)Ik(t)]βkΘ(t)Ik(t)+Qk(t)+αΘ2(t)1+αΘ2(t).

As a result, the nonlinear part G(z)=(g1,g2,,gn,0,0,,0n)T, gk=βkΘIk+Qk+αΘ21+αΘ2, for k=1,2,,n.

By mathematical induction, the characteristic equation of the matrix B can be calculated as

det(λE2nB)=(λ+d+ε)n·det(λEnB11)=(λ+d+ε)n(λ+d+γ+δ)n1{λ+(d+γ+δ)k=1nlkqk}=0. (3.3)

Eq. (3.3) has a negative eigenvalue (d+ε) with multiplicity n and a negative eigenvalue (d+γ+δ) with multiplicity n1. The stability of E0 is only determined by

λ+(d+γ+δ)k=1nlkqk=λ+(d+γ+δ)βk2k=0,i.e.,λ=(d+γ+δ)(R01).

If R0<1, one has λ<0; and if R0>1, one has λ>0. Hence, E0 is locally asymptotically stable if R0<1, whereas it is unstable if R0>1. □

We now proceed to examine the global stability of E0.

Theorem 3.2

IfR0<1, the disease-free equilibriumE0of(1.3)is globally asymptotically stable.

Proof

Rewrite (1.3) as

{dSk(t)dt=AβkSk(t)Θ(t)1+αΘ2(t)dSk(t)+γIk(t)+ε(1Sk(t)Ik(t)),dIk(t)dt=βkSk(t)Θ(t)1+αΘ2(t)(d+γ+δ)Ik(t),k=1,2,,n. (3.4)

Considering a non-negative solution {Sk(t),Ik(t)}k=1n of (3.4). Firstly, we prove that limt+Ik(t)=0. From the first equation of (3.4), we derive

dSk(t)dt(A+ε)(d+ε)Sk(t).

It can be deduced that

lim supt+Sk(t)A+εd+ε=1=:Sk0. (3.5)

Accordingly, for arbitrarily sufficiently small σ1>0, there is T1>0 resulting in Sk(t)Sk0+σ1 for t>T1. If t>T1, we get

dIk(t)dt<βk(Sk0+σ1)Θ(t)(d+γ+δ)Ik(t).

Take into account the following auxiliary system

dIk(t)dt=βk(Sk0+σ1)Θ(t)(d+γ+δ)Ik(t). (3.6)

Then it suffices to demonstrate that the positive solutions of system converge to zero as t tends to infinity. We construct the following Lyapunov function

V(t)=k=1nakIk(t),

where ak=kP(k)(d+γ+δ)k>0. Calculating the derivative of V(t) along solutions of (3.6), we have

dV(t)dt=k=1nak[βk(Sk0+σ1)Θ(t)(d+γ+δ)Ik(t)]=k=1n[βk2P(k)(d+γ+δ)k(Sk0+σ1)Θ(t)kP(k)kIk(t)]=Θ(t)(R0+βk2(d+γ+δ)kσ11).

Since R0<1, we can select an σ1>0 sufficiently small such that R0+βk2(d+γ+δ)kσ1<1. This guarantees that R0<1,dV(t)dt0 for all Ik(t)0, and that dV(t)dt=0 if and only if Ik(t)=0 for k=1,2,,n.

Next, we will prove limtSk(t)=Sk0. Since limtIk(t)=0, for arbitrary σ2>0 small enough, there exists T2>0 leading to 0Ik(t)σ2 for t>T2. From the first equation of (3.4), it follows that

dSk(t)dt(A+ε)(εγ)σ2(d+ε+Wσ2)Sk(t),

where W=βk. We have lim inft+Sk(t)A+ε(εγ)σ2d+ε+Wσ2. Taking σ20, one obtains

lim inft+Sk(t)A+εd+ε=1=:Sk0. (3.7)

Combining (3.5) and (3.7), it is obvious that limt+Sk(t)=Sk0=1.

Finally, since Qk(t)=1Sk(t)Ik(t), we obtain limt+Qk(t)=0. This shows that E0 of (1.3) is globally attractive when R0<1 and it can be deduced from Theorem 3.1 that E0 is globally asymptotically stable. □

The following result shows that (2.2) is uniformly persistent when R0>1, that is, the disease persists in the population. We will apply the following two lemmas.

Lemma 3.2 [35]

LetBbe an irreduciblen×nmatrix. Ifbij0wheneverij, then there is an eigenvectoruofBsuch thatu>0, and the corresponding eigenvalue iss(B)=maxReλi,i=1,2,,n, whereλiare the eigenvalues ofB, andRerepresents the real part of the eigenvalues.

Lemma 3.3 [16]

Consider the following system

dx(t)dt=B˜x+G˜(x),x=(x1,x2,,x2n)TFR2n, (3.8)

whereB˜is an2n×2nmatrix andG˜(x)is continuously differentiable inF. Suppose that

  • (i)

    a compact convex setDFis positively invariant for system(3.8), with0D;

  • (ii)

    there is a positive integerm2nresulting inlimx0G˜(x)/i=1mxi2=0;

  • (iii)

    there are a positive numberr˜and a real eigenvectorvcorresponding to a positive eigenvalue ofB˜Tresulting in(x,v)r˜i=1mxi2for allxD;

  • (iv)

    (G˜(x),v)0is true for allxD.

Therefore, the solutionϕ(t,x0)of(3.8)admitsliminftϕ(t,x0)ϵ0for anyx0D{0}, whereϵ0>0has no relation to the initial valuex0. Further, there is a constant solution of(3.8),x=x*withx*D{0}.

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 D=Ω. Obviously, limz0G(z)/i=1nzi2=0

i=1nzi2=0, so condition (ii) holds.

With respect to condition (iii), it is noticed that B11T=(bji)n×n is irreducible and bji>0 when ji, as a result, by Lemma 3.2 and Eq. (3.3), there exists an eigenvector v˜=(v1,v2,,vn)T of B11T such that vi>0 for all i=1,2,,n, and the corresponding eigenvalue is s(B11T)=s(B)=(d+γ+δ)(R01). If R0>1, then s(B11T)=:λ0>0. Set vn+1==v2n=0 and v=(v1,v2,,v2n)T, we get BTv=λ0v, which means that v is the eigenvector corresponding to a positive eigenvalue λ0 of BT. If one defines r˜=min1invi>0, it follows that (z,v)r˜i=1nzi2 for all zΩ, i.e., condition (iii) follows.

The condition (iv) is also confirmed since (G(z),v)=Θk=1nβkvkzk+zn+k+αΘ21+αΘ20 for all zD. As a result, all the assumptions of Lemma 3.3 are valid.

These results are summarized in the following theorem.

Theorem 3.3

IfR0>1, system(2.2)is uniformly persistent, that is, there exists a constant0<ϵ01such that

lim inft+Ik(t)ϵ0,lim inft+Qk(t)ϵ0,k=1,2,,n,

for any solution of(2.2)with(2.1).

Remark 3.1

Theorem 3.3 shows that when R0>1, the disease is permanent. In addition, according to Lemma 3.3, there is a constant solution of (2.2) when R0>1, which is the endemic equilibrium of (2.2). This is consistent with the conclusion of Lemma 2.2.

Next, the global attractivity of E* is discussed.

Theorem 3.4

Assume that(Ik(t),Qk(t))is a solution of system(2.2)satisfying(2.1). IfR0>1andδ>d+ε, thenlimt+(Ik(t),Qk(t))=(Ik*,Qk*), where(Ik*,Qk*)is the unique positive equilibrium of(2.2)satisfying(2.4)fork=1,2,,n.

Proof

Without loss of generality, fix k to be any integer of the set {1,2,,n}. In accordance with Theorem 3.3, there is a small enough constant φ0 (0<φ01) and a large enough constant T0 resulting in Ik(t)φ0 for t>T0. Accordingly,

Θ(t)=1kk=1nkP(k)Ik(t)φ0=:ψ0>0.

From the first equation of (2.2), one obtains

dIk(t)dtβk[1Ik(t)](d+γ+δ)Ik(t)=βk(βk+d+γ+δ)Ik(t).

According to the comparison principle, for any given small constant 0<ψ1(1)<d+γ+δ2(βk+d+γ+δ), there is a t1>T0 resulting in Ik(t)Xk(1)ψ1(1) for t>t1, where

Xk(1):=βkβk+d+γ+δ+2ψ1(1)<1. (3.9)

From the second equation of (2.2), it follows that

dQk(t)dt=δ[1Sk(t)Qk(t)](d+ε)Qk(t)δ(δ+d+ε)Qk(t).

Analogously, for any given small constant 0<ψ1(2)<min{12,ψ1(1),d+ε2(δ+d+ε)}, there is a t2>t1 resulting in Qk(t)Yk(1)ψ1(2) for t>t2, where

Yk(1):=δδ+d+ε+2ψ1(2)<1. (3.10)

In view of the fact that 0<ψ0Θ(t)<1. Substituting Qk(t)Yk(1) into the first equation of (2.2) yields

dIk(t)dtβk(1Yk(1))ψ01+α(βkψ01+α+d+γ+δ)Ik(t),t>t2.

As a result, for any given small constant 0<ψ1(3)<min{13,ψ1(2),βk(1Yk(1))ψ02[βkψ0+(d+γ+δ)(1+α)]}, there exists a t3>t2 such that Ik(t)xk(1)+ψ1(3) for t>t2, where

xk(1):=βk(1Yk(1))ψ0βkψ0+(d+γ+δ)(1+α)2ψ1(3)>0. (3.11)

It follows from the second equation of (2.2) that dQk(t)dtδxk(1)(d+ε)Qk(t), t>t3. In a similar way, for any given small constant 0<ψ1(4)<min{14,ψ1(3),δxk(1)2(d+ε)}, there is a t4>t3 resulting in Qk(t)yk(1)+ψ1(4) for t>t4, where

yk(1):=δxk(1)d+ε2ψ1(4)>0. (3.12)

Since φ0 is sufficiently small constant, it holds that 0<xk(1)1 and 0<yk(1)1. It can be seen from the above discussion that 0<xk(1)<Xk(1)<1 and 0<yk(1)<Yk(1)<1 for t>t4. Consequently, it can be seen that

0<u1<Θ(t)<U1<1, (3.13)

where u1=1kk=1nkP(k)xk(1) and U1=1kk=1nkP(k)Xk(1). Once again, by (2.2), we obtain

dIk(t)dtβk[1Ik(t)yk(1)]U11+αu12(d+γ+δ)Ik(t),t>t4.

Therefore, for any given constant 0<ψ2(1)<min{15,ψ1(4),(d+γ+δ)(1+αu12)+βkyk(1)U1βkU1+(d+γ+δ)(1+αu12)}, there exists a t5>t4 such that

Ik(t)Xk(2):=βk(1yk(1))U1βkU1+(d+γ+δ)(1+αu12)+2ψ2(1)<1. (3.14)

By the second equation of (2.2), one gets dQk(t)dtδXk(2)(d+ε)Qk(t), t>t5. Consequently, for any given constant 0<ψ2(2)<min{16,ψ2(1)}, there is a t6>t5 such that

Qk(t)Yk(2):=min{Yk(1)ψ1(2),δXk(2)d+ε+ψ2(2)},t>t6. (3.15)

Combining (3.9), (3.14) and (3.15), we know that Xk(2)<Xk(1) and Yk(2)<Yk(1).

Again from system (2.2), it is clear that

dIk(t)dtβk[1Ik(t)Yk(2)]u11+αU12(d+γ+δ)Ik(t),t>t6.

As a result, for any given constant 0<ψ2(3)<min{17,ψ2(2),βk(1Yk(2))u1βku1+(d+γ+δ)(1+αU12)}, there exists a t7>t6 such that Ik(t)xk(2), where

xk(2):=max{xk(1)+ψ1(2),βk(1Yk(2))u1βku1+(d+γ+δ)(1+αU12)ψ2(3)},t>t7. (3.16)

By (2.2), we arrive at dQk(t)dtδxk(2)(d+ε)Qk(t), t>t7. Therefore, for any given constant 0<ψ2(4)<min{18,ψ2(3),δxk(2)d+ε}, there is a t8>t7 such that

Qk(t)yk(2):=δxk(2)d+εψ2(4),t>t8. (3.17)

By repeating the above process, four sequences: Xk(i),Yk(i),xk(i),yk(i),i=1,2, 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 N such that for nN,

Xk(n)=βk(1yk(n1))Un1βkUn1+(d+γ+δ)(1+αun12)+ψn(1),Yk(n)=δXk(n)d+ε+ψn(2),xk(n)=βk(1Yk(n))un1βkun1+(d+γ+δ)(1+αUn12)ψn(3),yk(n)=δxk(n)d+εψn(4). (3.18)

It is evident that

0xk(n)Ik(t)Xk(n)<1,0yk(n)Qk(t)Yk(n)<1,t>Tn(4). (3.19)

As the sequential limits of (3.18) exist, let limtMk(n)=Mk, where Mk(n)=(Xk(n),Yk(n),xk(n),yk(n),Un,un) Un,un) and Mk=(Xk,Yk,xk,yk,U,u). Note that 0<ψn(i)<14n+i4(i=1,2,3,4,n>1), then ψn(i)0 as n. Consequently, assuming n, It can be deduced from (3.18) that

Xk=βk(1yk)UβkU+(d+γ+δ)(1+αu2),Yk=δXkd+ε,xk=βk(1Yk)uβku+(d+γ+δ)(1+αU2),yk=δxkd+ε, (3.20)

where u=1kk=1nkP(k)xk,U=1kk=1nkP(k)Xk,0<uU<1. In addition, by (3.20) one gets

HkXk=βkU[βku(1+αU2)(1+αu2)+d+γ+δ1+αu2βkuδ(1+αU2)(1+αu2)(d+ε)],Hkxk=βku[βkU(1+αU2)(1+αu2)+d+γ+δ1+αU2βkUδ(1+αU2)(1+αu2)(d+ε)], (3.21)

where

Hk=[βkU+(d+γ+δ)(1+αu2)][βku+(d+γ+δ)(1+αU2)](d+ε)2β2k2δ2Uu(1+αU2)(1+αu2)(d+ε)2.

For this, we declare Hk0. Noticing that Xk is the unique nonzero value decided by (3.20). If Hk=0, then βku1+αU2+(d+γ+δ)=βkuδ(1+αU2)(d+ε). According to the symmetry, we get βkU1+αu2+(d+γ+δ)=βkUδ(1+αu2)(d+ε). It is apparent that βku1+αU2βkU1+αu2=βkuδ(1+αU2)(d+ε)βkUδ(1+αu2)(d+ε), i.e., d+ε=δ. This contradicts the assumptions in the theorem. Thus, Hk0.

Combining (3.21) with the formulas of U and u, we obtain

1=1kk=1nkP(k)βkHk[βku(1+αU2)(1+αu2)+d+γ+δ1+αu2βkuδ(1+αU2)(1+αu2)(d+ε)],1=1kk=1nkP(k)βkHk[βkU(1+αU2)(1+αu2)+d+γ+δ1+αU2βkUδ(1+αU2)(1+αu2)(d+ε)]. (3.22)

By subtracting the two equations above, it yields

1kk=1nkP(k)βkHk{βk(1+αU2)(1+αu2)(Uu)(1δd+ε)+(d+γ+δ)(11+αU211+αu2)}=1kk=1nkP(k)βkHk(Uu){βk(1+αU2)(1+αu2)(1δd+ε)(d+γ+δ)(α(U+u)(1+αU2)(1+αu2))}=0. (3.23)

Since d+ε<δ, this means that U=u. Thus, we get 1kk=1nkP(k)(Xkxk)=0, which means that Xk=xk for k=1,2,,n. From (3.19) and (3.20), one arrives at limtIk(t)=Xk=xk and limtQk(t)=Yk=yk. Noticing that when R0>1, Eq. (2.7) has a unique positive solution Θ*. Therefore, substituting U=u and Xk=xk into (3.21), according to (2.4) and (3.20), we derive Xk=Ik* and Yk=Qk*. Consequently, the endemic equilibrium E* of (2.2) is globally attractive if R0>1 and δ>d+ε. □

Finally, we examine the globally asymptotic stability of the endemic equilibrium.

Theorem 3.5

IfR0>1andααc:=β2n2(R0)4512(d+γ)2orααl:=2(d+γ)nβ, the endemic equilibriumE*={Sk*,Ik*,Qk*}k=1nof system(1.3)is globally asymptotically stable.

Proof

For convenience, Sk, Ik, Qk and Θ are used to instead of Sk(t), Ik(t), Qk(t) and Θ(t) respectively. It follows from Lemma 2.1 that 0<Θ(t)<1 for all t>0. We consider a Lyapunov function candidate V(t)=VS+VQ+VΘ, the elements of which are shown below

VS=12k=1nξk(Sk(t)Sk*)2,VQ=12k=1nηk(Qk(t)Qk*)2,andVΘ=Θ(t)Θ*Θ*lnΘ(t)Θ*,

where

Qk*=1Sk*Ik*,ξk=kP(k)kSk*,k=1,2,,n,

and ηk is positive constant, which will be determined later.

In the following, we derive the derivatives of VS, VQ and VΘ, respectively. We can rewrite the first equation of (3.4) as

dSk(t)dt=(d+ε)(d+ε)Sk(t)+(γε)Ik(t)βkSk(t)Θ(t)1+αΘ2(t). (3.24)

In addition, it can be deduced from (2.3) that

dΘ(t)dt=(d+γ+δ)Θ(t)+βkk=1nk2P(k)Sk(t)Θ(t)1+αΘ2(t). (3.25)

Differentiating VS and employing the identity d+ε=(d+ε)Sk*+(εγ)Ik*+βkSk*Θ*1+α(Θ*)2, we get

VS=k=1nξk(SkSk*)dSkdt=k=1nξk(SkSk*)(d+ε(d+ε)Sk+(γε)IkβkSkΘ1+αΘ2)=k=1nξk(SkSk*){(d+ε)(SkSk*)+(γε)(IkIk*)+βk(Sk*Θ*1+α(Θ*)2SkΘ1+αΘ2)}=k=1nξk(d+ε)(SkSk*)2+k=1nξk(γε)(SkSk*)(IkIk*)Θ1+αΘ2k=1nξkβk(SkSk*)2k=1nξkβkSk*1+α(Θ*)2(SkSk*)(ΘΘ*)+k=1nξkαβkSk*(SkSk*)Θ(Θ2(Θ*)2)(1+αΘ2)(1+α(Θ*)2). (3.26)

The last term of right hand side of (3.26) can be expressed as

k=1nξkαβkSk*(SkSk*)Θ(Θ2(Θ*)2)(1+αΘ2)(1+α(Θ*)2)=k=1nξkαβkSk*(SkSk*)[(ΘΘ*)(Θ2(Θ*)2)(1+αΘ2)(1+α(Θ*)2)+Θ*(Θ2(Θ*)2)(1+αΘ2)(1+α(Θ*)2)]=k=1nξkαβkSk*Sk(ΘΘ*)(Θ2(Θ*)2)(1+αΘ2)(1+α(Θ*)2)k=1nξkαβk(Sk*)2(Θ+Θ*)(1+αΘ2)(1+α(Θ*)2)(ΘΘ*)2+k=1nξkαβkSk*Θ*(Θ+Θ*)(1+αΘ2)(1+α(Θ*)2)(SkSk*)(ΘΘ*).

Substituting the above equality into (3.26), one gets

VS=k=1nξk(d+ε)(SkSk*)2+k=1nξk(γε)(SkSk*)(IkIk*)Θ1+αΘ2k=1nξkβk(SkSk*)2+k=1nξkαβkSk*Θ*(Θ+Θ*)(1+αΘ2)(1+α(Θ*)2)(SkSk*)(ΘΘ*)k=1nξkαβk(Sk*)2(Θ+Θ*)(1+αΘ2)(1+α(Θ*)2)(ΘΘ*)2k=1nξkβkSk*[(SkSk*)(ΘΘ*)1+α(Θ*)2αSk(ΘΘ*)(Θ2(Θ*)2)(1+αΘ2)(1+α(Θ*)2)]. (3.27)

Substituting the last equation of (1.3) and the identity δIk*(d+ε)Qk*=0 into the differential process of VQ, we derive VQ as

VQ=k=1nηk(QkQk*)dQkdt=k=1nηk(QkQk*)[δIk(d+ε)Qk]=k=1nηk(QkQk*)[δ(IkIk*)(d+ε)(QkQk*)]=k=1nηk(QkQk*)[δ(SkSk*)δ(QkQk*)(d+ε)(QkQk*)]=k=1nηk(d+ε+δ)(QkQk*)2+k=1nηkδ(SkSk*)[(SkSk*)+(IkIk*)]=k=1nηk(d+ε+δ)(QkQk*)2+k=1nηkδ(SkSk*)2+k=1nηkδ(SkSk*)(IkIk*). (3.28)

Similarly, combining (3.25) and the identity 1=β(d+γ+δ)kk=1nk2P(k)Sk*1+α(Θ*)2, VΘ can be constructed as follows

VΘ=ΘΘ*ΘdΘdt=(d+γ+δ)(ΘΘ*)(1+β(d+γ+δ)kk=1nk2P(k)Sk1+αΘ2)=(ΘΘ*)βkk=1nk2P(k)(Sk1+αΘ2Sk*1+α(Θ*)2)=βkk=1nk2P(k)[(SkSk*)(ΘΘ*)1+α(Θ*)2αSk(ΘΘ*)(Θ2(Θ*)2)(1+α(Θ*)2)(1+αΘ2)]. (3.29)

Due to the fact that ξk=kP(k)kSk*, we observe that the last term of (3.27) is equal to VΘ. Then combining (3.28), and selecting ηk=εγδξk=(εγ)kP(k)δkSk*, V is given as

V=VS+VQ+VΘ=k=1nξk(d+γ)(SkSk*)2k=1nηk(d+ε+δ)(QkQk*)2Θ1+αΘ2k=1nξkβk(SkSk*)2+k=1nξkαβkSk*Θ*(Θ+Θ*)(1+α(Θ*)2)(1+αΘ2)(SkSk*)(ΘΘ*)k=1nξkαβk(Sk*)2(Θ+Θ*)(1+α(Θ*)2)(1+αΘ2)(ΘΘ*)2=Θ1+αΘ2k=1nξkβk(SkSk*)2k=1nηk(d+ε+δ)(QkQk*)2k=1nξk(d+γ)(X˜k2bkX˜kY˜+ckY˜2)=Θ1+αΘ2k=1nξkβk(SkSk*)2k=1nηk(d+ε+δ)(QkQk*)2k=1nξk(d+γ)(X˜kbk2Y˜)2+k=1nξk(d+γ)bk24ck4Y˜2, (3.30)

where

bk=αβkSk*Θ*(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2),ck=αβk(Sk*)2(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2),

and

X˜k=SkSk*,Y˜=ΘΘ*.

In order to ensure that V0, it is sufficient to show that the following inequality holds.

bk24ck=[αβkSk*Θ*(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2)]24αβk(Sk*)2(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2)=αβk(Sk*)2(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2)[αβk(Θ*)2(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2)4]0. (3.31)

It is noted that 0<Θ,Θ*<1. Then when α2(d+γ)nβ, apparently we can obtain

αβk(Θ*)2(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2)42αβnd+γ40, (3.32)

which means that (3.31) holds.

Additionally, It can be deduced from the inequalities a2+b212(a+b)2 and a2+b22ab that

(1+αΘ2)(1+α(Θ*)2)=1+α[Θ2+(Θ*)2]+α2Θ2(Θ*)21+α[Θ2+(Θ*)2]1+α2(Θ+Θ*)22α(Θ+Θ*), (3.33)

and

Ik*(d+ε)βkΘ*(d+γ+δ)(d+ε)(1+α(Θ*)2)βk2α(d+γ+δ),k=1,2,,n. (3.34)

From (3.34), we get

Θ*=k1k=1nkP(k)Ik*β2α(d+γ+δ)kk=1nk2P(k)=R02α. (3.35)

Inserting (3.33) and (3.35) into (3.31) and utilizing the hypothesis αβ2n2(R0)4512(d+γ)2 yields

αβk(Θ*)2(Θ+Θ*)(d+γ)(1+α(Θ*)2)(1+αΘ2)4αβk2(d+γ)(R02α)24βn(R0)24α(d+γ)40,

which indicates that (3.31) is confirmed. Consequently, if ααc or ααl then (3.31) holds, and from (3.30) we can obtain

VΘ1+αΘ2k=1nξkβk(SkSk*)2k=1nηk(d+ε+δ)(QkQk*)20. (3.36)

Moreover, V=0 if and only if Sk=Sk* and Qk=Qk* for k=1,2,,n. By LaSalle’s Invariant Principle [36], we can conclude that E*={Sk*,Ik*,Qk*}k=1n 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, P(k)=Ck3 for k=1,2,,500. The parameter C is chosen to make k=1nP(k)=1.

Example 4.1

In Figs. 2 and 3 , we show the outcome of system (1.3) when the basic reproduction number R0<1. Let d=0.01,β=0.01,δ=0.02,γ=0.1 and ε=0.2. In this case, R0=0.318<1. The time series of I100,I200,I300,I400,I500 are performed in Fig. 2(a) (α=0.5) and Fig. 2(b) (α=50). The initial values are given by Sk(0)=0.9,Ik(0)=0.1 and Qk(0)=0 for any degree k. From the numerical results, it can be seen that E0 is globally asymptotically stable when R0<1, which means that the disease will eventually become extinct. In addition, when α=0.5 and α=50, there is a peak in the density of infected nodes before leading to the disease-free equilibrium, however, as α increases, the peak level decreases, that is, a big α can efficiently reduce the epidemic peak during the initial outbreak of the disease. Fig. 3 depicts the trajectories of I350(t) versus t 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 R0>1. The parameters are chosen as d=0.02,β=0.05,δ=0.04,γ=0.05,ε=0.2. Subsequently, we can obtain R0=1.8793>1 and αl=0.0056 and αc=3108. By selecting α=0.005 and 3500 respectively, the condition α<αl or α>αc in Theorem 3.5 holds. From Fig. 4, it can be seen that the disease will approach to a positive stationary level when R0>1. The trajectories of I350(t) for eight different initial values are plotted in Fig. 5. In Figs. 4 and 5, we see that the endemic equilibrium E* is globally asymptotically stable when R0>1 and the condition α<αl or α>αc 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 α when the disease is prevalent, indicating that a larger α can weaken the epidemic level of the disease.

Example 4.3

From Theorem 3.5, we know that the endemic equilibrium E* is globally asymptotically stable when R0>1 and the condition α<αl or α>αc is satisfied, which is shown in Figs. 4 and 5. Nevertheless, in Fig. 6 , we choose α=500,1000,,3000 and other parameters are the same as in Example 4.2, it is clear that αl<α<αc does not satisfy the conditions of Theorem 3.5. Fig. 6 depicts the time evolution of I(t) with different α, where I(t)=k=1nP(k)Ik(t) 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.

Fig. 2

The time series of Ik(t) with R0<1.

Fig. 3.

Fig. 3

The time series of I350(t) with eight different initial values and R0<1.

Fig. 4.

Fig. 4

The time series of Ik(t) with R0>1.

Fig. 5.

Fig. 5

The time series of I350(t) with eight different initial values and R0>1.

Fig. 6.

Fig. 6

The time evolution of I(t)=k=1nP(k)Ik(t) with R0>1 and different α.

Example 4.4. Finally, we display the effect of quarantine by numerical simulations. In Fig. 7 , the initial values are Sk(0)=0.3,Ik(0)=0.7 and Qk(0)=0. We fix the parameters d=0.02,β=0.05,γ=0.05,ε=0.2 and α=100 to graph the time evolution of I(t) with six different δ. From the figure, it is observed that by increasing the quarantine rate δ, the level of endemic disease prevalence reduces significantly, indicating that raising the quarantine rate helps in controlling the disease.

Fig. 7.

Fig. 7

The time evolution of I(t) corresponding to different δ.

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 R0 is derived, which is related to the network topology as well as some parameters.

Furthermore, we show that the basic reproduction number R0 determines not only the existence of the endemic equilibrium E* but also the global dynamics of model. More specially, by utilizing the Lyapunov function, it is shown that the disease-free equilibrium E0 is globally asymptotically stable when R0<1, namely, the disease will disappear eventually. On the other hand, the disease is uniformly persistent on the network when R0>1. At the same time, by using a novel monotone iterative scheme, we demonstrate that if R0>1 and δ>d+ε, the unique endemic equilibrium E* is globally attractive. Furthermore, by constructing appropriate Lyapunov function, E* is globally asymptotically stable if R0>1 and the inhibitory effect α 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 α has no effect on the epidemic threshold, it can be seen that bigger α 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 α does not satisfy the conditions in Theorem 3.5. As a result, we conjecture that the endemic equilibrium E* of system (1.3) is globally asymptotically stable only when R0>1. In addition, the results of Example 4.4 indicate that the level of endemic disease prevalence reduces significantly with increasing the quarantine rate δ, 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 A 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 A is distributed into group k at the probability rk(0rk<1), 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).

References

  • 1.Pastor-Satorras R., Vespignani A. Epidemic spreading in scale-free networks. Phys Rev Lett. 2001;86:3200–3203. doi: 10.1103/PhysRevLett.86.3200. [DOI] [PubMed] [Google Scholar]
  • 2.Pastor-Satorras R., Vespignani A. Epidemic dynamics in finite size scale-free networks. Phys Rev E. 2002;65:035108. doi: 10.1103/PhysRevE.65.035108. [DOI] [PubMed] [Google Scholar]
  • 3.Newman M.E.J. Spread of epidemic disease on networks. Phys Rev E. 2002;66:016128. doi: 10.1103/PhysRevE.66.016128. [DOI] [PubMed] [Google Scholar]
  • 4.d’Onofrio A. A note on the global behaviour of the network-based SIS epidemic model. Nonlinear Anal RWA. 2008;9:1567–1572. [Google Scholar]
  • 5.Wang L., Dai G. Global stability of virus spreading in complex heterogeneous networks. SIAM J Appl Math. 2008;68:1495–1502. [Google Scholar]
  • 6.Moreno Y., Pastor-Satorras R., Vespignani A. Epidemic outbreaks in complex heterogeneous networks. Eur Phys J B. 2002;26:521–529. [Google Scholar]
  • 7.Wang Y., Jin Z., Yang Z., Zhang Z., Zhou T., Sun G. Global analysis of an SIS model with an infective vector on complex networks. Nonlinear Anal RWA. 2012;13:543–557. [Google Scholar]
  • 8.Huang S., Chen F., Zhang Y. Global analysis of epidemic spreading with a general feedback mechanism on complex networks. Adv Differ Equ. 2019;2019:154. [Google Scholar]
  • 9.Wang Y., Cao J., Li M., Li L. Global behavior of a two-stage contact process on complex networks. J Franklin Inst B. 2019;356:3571–3589. [Google Scholar]
  • 10.Wang Y., Wei Z., Cao J. Epidemic dynamics of influenza-like diseases spreading in complex networks. Nonlinear Dyn. 2020;101:1801–1820. [Google Scholar]
  • 11.Fu X., Small M., Walker D.M., Zhang H. Epidemic dynamics on scale-free networks with piecewise linear infectivity and immunization. Phys Rev E. 2008;77:036113. doi: 10.1103/PhysRevE.77.036113. [DOI] [PubMed] [Google Scholar]
  • 12.Zhang J., Jin Z. The analysis of an epidemic model on networks. Appl Math Comput. 2011;217:7053–7064. [Google Scholar]
  • 13.Zhu G., Fu X., Chen G. Global attractivity of a network-based epidemic SIS model with nonlinear infectivity. Commun Nonlinear Sci Numer Simul. 2012;17:2588–2594. [Google Scholar]
  • 14.Zhu G., Fu X., Chen G. Spreading dynamics and global stability of a generalized epidemic model on complex heterogeneous networks. Appl Math Model. 2012;36:5808–5817. [Google Scholar]
  • 15.Li C.H., Tsai C.C., Yang S.Y. Analysis of epidemic spreading of an SIRS model in complex heterogeneous networks. Commun Nonlinear Sci Numer Simul. 2014;19:1042–1054. [Google Scholar]
  • 16.Zhu G., Chen G., Fu X. Effects of active links on epidemic transmission over social networks. Physica A. 2017;468:614–621. [Google Scholar]
  • 17.Cheng X., Wang Y., Huang G. Dynamics of a competing two-strain SIS epidemic model with general infection force on complex networks. Nonlinear Anal RWA. 2021;59:103247. [Google Scholar]
  • 18.Hethcote H., Ma Z., Liao S. Effects of quarantine in six endemic models for infectious diseases. Math Biosci. 2002;180:141–160. doi: 10.1016/s0025-5564(02)00111-6. [DOI] [PubMed] [Google Scholar]
  • 19.Esquivel-Gómez J.D.J., Barajas-Ramírez J.G. Efficiency of quarantine and self-protection processes in epidemic spreading control on scale-free networks. Chaos. 2018;28:013119. doi: 10.1063/1.5001176. [DOI] [PubMed] [Google Scholar]
  • 20.Upadhyay R.K., Chatterjee S., Saha S., Azad R.K. Age-group-targeted testing for COVID-19 as a new prevention strategy. Nonlinear Dyn. 2020;101:1921–1932. doi: 10.1007/s11071-020-05879-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Zhang X., Zhang X. The threshold of a deterministic and a stochastic SIQS epidemic model with varying total population size. Appl Math Model. 2021;91:749–767. doi: 10.1016/j.apm.2020.09.050. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Yang J., Tang S., Cheke R.A. Impacts of varying strengths of intervention measures on secondary outbreaks of COVID-19 in two different regions. Nonlinear Dyn. 2021;104:863–882. doi: 10.1007/s11071-021-06294-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.Li T., Wang Y., Guan Z. Spreading dynamics of a SIQRS epidemic model on scale-free networks. Commun Nonlinear Sci Numer Simul. 2014;19:686–692. [Google Scholar]
  • 24.Huang S., Chen F., Chen L. Global dynamics of a network-based SIQRS epidemic model with demographics and vaccination. Commun Nonlinear Sci Numer Simul. 2017;43:296–310. [Google Scholar]
  • 25.Li K., Zhu G., Ma Z., Chen L. Dynamic stability of an SIQS epidemic network and its optimal control. Commun Nonlinear Sci Numer Simul. 2019;66:84–95. [Google Scholar]
  • 26.Capasso V., Serio G. A generalization of the Kermack-McKendrick deterministic epidemic model. Math Biosci. 1978;42:43–61. [Google Scholar]
  • 27.Xiao D., Ruan S. Global analysis of an epidemic model with nonmonotone incidence rate. Math Biosci. 2007;208:419–429. doi: 10.1016/j.mbs.2006.09.025. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Chen Y., Wen Y. Modelling and analyzing the epidemic of human infections with the avian influenza A(H7N9) virus in 2017 in China. Math Method Appl Sci. 2019;42:4456–4471. [Google Scholar]
  • 29.Li C.H. Dynamics of a network-based SIS epidemic model with nonmonotone incidence rate. Physica A. 2015;427:234–243. [Google Scholar]
  • 30.Wei X., Liu L., Zhou W. Global stability and attractivity of a network-based SIS epidemic model with nonmonotone incidence rate. Physica A. 2017;469:789–798. [Google Scholar]
  • 31.Liu L., Wei X., Zhang N. Global stability of a network-based SIRS epidemic model with nonmonotone incidence rate. Physica A. 2019;515:587–599. [Google Scholar]
  • 32.Sanz J., Floria L.M., Moreno Y. Spreading of persistent infections in heterogeneous populations. Phys Rev E. 2010;81:056108. doi: 10.1103/PhysRevE.81.056108. [DOI] [PubMed] [Google Scholar]
  • 33.Fu X., Small M., Chen G. Methods and Stability Analysis. Higher Education Press; Beijing: 2014. Propagation dynamics on complex networks: models. [Google Scholar]
  • 34.Yorke J.A. Invariance for ordinary differential equations. Math Syst Theory. 1967;1:353–372. [Google Scholar]
  • 35.Lajmanovich A., Yorke J.A. A deterministic model for gonorrhea in a nonhomogeneous population. Math Biosci. 1976;28:221–236. [Google Scholar]
  • 36.La Salle J.P. SIAM, Philadelphia. 1976. The stability of dynamical systems, regional conference series in applied mathematics. [Google Scholar]

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