
This study aims to analyze a class of SIV systems considering the transmission rate influenced by media coverage and protective measures, in which the transmission rate is represented by a piecewise-smooth function. Firstly, for the SIV Filippov system, we take the dynamic behaviors of two subsystems into consideration, and obtain the basic reproduction number and the equilibria of the subsystems respectively. Secondly, based on the Filippov convex method, we calculate the sliding domain and the sliding mode equation, and further analyze the global dynamic behaviors of the system, through which we verify that there is no closed orbit in the system. Furthermore, we prove the global asymptotical stability of the disease-free equilibrium, two real equilibria, and the pseudo-equilibrium under certain conditions. The results demonstrate that the threshold value, the protective measures, and the media coverage could affect the number of infected individuals and the final scale of the disease. To prevent the spread of the disease, it is necessary to select an appropriate threshold and take applicable protective measures combined with media coverage. Lastly, we verify the validity of the results by numerical simulations.
Citation: Shifan Luo, Dongshu Wang, Wenxiu Li. Dynamic analysis of a SIV Filippov system with media coverage and protective measures[J]. AIMS Mathematics, 2022, 7(7): 13469-13492. doi: 10.3934/math.2022745
[1] | Qiongru Wu, Ling Yu, Xuezhi Li, Wei Li . Dynamic analysis of a Filippov blood glucose insulin model. AIMS Mathematics, 2024, 9(7): 18356-18373. doi: 10.3934/math.2024895 |
[2] | Yue Wu, Shenglong Chen, Ge Zhang, Zhiming Li . Dynamic analysis of a stochastic vector-borne model with direct transmission and media coverage. AIMS Mathematics, 2024, 9(4): 9128-9151. doi: 10.3934/math.2024444 |
[3] | Hengjie Peng, Changcheng Xiang . A Filippov tumor-immune system with antigenicity. AIMS Mathematics, 2023, 8(8): 19699-19718. doi: 10.3934/math.20231004 |
[4] | Shaymaa H. Salih, Nadia M. G. Al-Saidi . 3D-Chaotic discrete system of vector borne diseases using environment factor with deep analysis. AIMS Mathematics, 2022, 7(3): 3972-3987. doi: 10.3934/math.2022219 |
[5] | Xiangyun Shi, Xiwen Gao, Xueyong Zhou, Yongfeng Li . Analysis of an SQEIAR epidemic model with media coverage and asymptomatic infection. AIMS Mathematics, 2021, 6(11): 12298-12320. doi: 10.3934/math.2021712 |
[6] | Danni Wang, Hongli Yang, Liangui Yang . Research on nonlinear infectious disease models influenced by media factors and optimal control. AIMS Mathematics, 2024, 9(2): 3505-3520. doi: 10.3934/math.2024172 |
[7] | Zhengqi Zhang, Huaiqin Wu . Cluster synchronization in finite/fixed time for semi-Markovian switching T-S fuzzy complex dynamical networks with discontinuous dynamic nodes. AIMS Mathematics, 2022, 7(7): 11942-11971. doi: 10.3934/math.2022666 |
[8] | Xiong Zhang, Zhongyi Xiang . Piecewise immunosuppressive infection model with viral logistic growth and effector cell-guided therapy. AIMS Mathematics, 2024, 9(5): 11596-11621. doi: 10.3934/math.2024569 |
[9] | Yanhui Bi, Zhixiong Chen, Zhuo Chen, Maosong Xiang . The geometric constraints on Filippov algebroids. AIMS Mathematics, 2024, 9(5): 11007-11023. doi: 10.3934/math.2024539 |
[10] | Yi Yang, Rongfeng Li, Xiangguang Dai, Haiqing Li, Changcheng Xiang . Exploring dynamic behavior and bifurcations in a Filippov neuronal system with a double-tangency singularity. AIMS Mathematics, 2024, 9(7): 18984-19014. doi: 10.3934/math.2024924 |
This study aims to analyze a class of SIV systems considering the transmission rate influenced by media coverage and protective measures, in which the transmission rate is represented by a piecewise-smooth function. Firstly, for the SIV Filippov system, we take the dynamic behaviors of two subsystems into consideration, and obtain the basic reproduction number and the equilibria of the subsystems respectively. Secondly, based on the Filippov convex method, we calculate the sliding domain and the sliding mode equation, and further analyze the global dynamic behaviors of the system, through which we verify that there is no closed orbit in the system. Furthermore, we prove the global asymptotical stability of the disease-free equilibrium, two real equilibria, and the pseudo-equilibrium under certain conditions. The results demonstrate that the threshold value, the protective measures, and the media coverage could affect the number of infected individuals and the final scale of the disease. To prevent the spread of the disease, it is necessary to select an appropriate threshold and take applicable protective measures combined with media coverage. Lastly, we verify the validity of the results by numerical simulations.
Modeling is an important method in various kinds of scientific research which has been widely used. In mathematics particularly, it abstracts the specific problem through a reasonable mathematical model, and simplifies the research object with mathematical language. A combination of quantitative and qualitative research approaches was used to reflect the characteristics of the object in biomathematical models [1,2,3,4,5,6,7,8,9,10,11,12,13]. For example, an infectious disease model can be analyzed based on data or transmission mechanisms to predict the scale, peak, the time duration of the spread, disease control strategy, and the speed of the spread. In 1927, Kermack and McKendrick [14] first put forward the SIR model to study the epidemic law of infectious diseases, and took the plague in Bombay as an example to verify the feasibility of their model with data from December 1905 to July 1906. In this first proposed deterministic model, the population is split into three disjoint parts, where S denotes the number of the susceptible individuals, I denotes the infected individuals, and R denotes the number of individuals removed on account of death or recovery. Once S and I are determined, R is determined, so we can remove R from the model to get a simpler model. Based on the previously proposed SIR model, Kermack and McKendrick further proposed the SIS model in 1932 and obtained a threshold theory [15,16]. Since then, the literature on deterministic models has proliferated, with researchers taking into account more realistic factors to make the model more realistic. For instance, considering the effect of vaccination on the spread of disease [17], another researchers further proposed the SIV model [18], in which V represents the vaccinated individuals.
Based on previous studies, we came to a conclusion that in the prevention and treatment of infectious diseases, people need to strengthen protective measures when the epidemic is getting severe and spreading. However, when the epidemic is gradually receding, if strong measures continue to be taken while the actual effect is not obvious, it will result in a great waste of social resources, which means that a parameter in the model can be considered piecewise, commonly referred to as a threshold policy (TP) [19]. In this case, consideration of a piecewise discontinuous model is the most reasonable choice, therefore the piecewise SIV model has been put forward.
Xiao et al. [20] extended the existing non-smooth model under the condition of imperfect vaccination, and proposed a general piecewise SIV model with nonlinear incidence to explore the impact of threshold policy. The stability and bifurcation of the equilibria of the system are studied by the right-hand discontinuous differential equation theory, stability theory and bifurcation theory, and the biological significance of the imperfect vaccination is revealed. The system is as follows:
{dS(t)dt=μ−β(1−fε(t))SI−μS−ϕS+γI+θV,dI(t)dt=β(1−fε(t))SI+σβ(1−fε(t))VI−(μ+γ)I,dV(t)dt=ϕS−σβ(1−fε(t))VI−μV−θV, | (1.1) |
where
ε(t)={0,I<Ic,1,I>Ic, |
here S,I,V represent the numbers of the susceptible, infected, and vaccinated individuals at the time t, with all the parameters being positive constants respectively. μ is the natural birth and death rate, β represents the coefficient of transmission rate, ϕ denotes the vaccination rate of the susceptible population, γ is the cure rate of infected individuals, θ represents the rate at which the vaccinated people lose immunity and become susceptible. f denotes the level of protective measures taken by the crowd, when the infected population reaches a certain threshold Ic, people begin to take precautionary measures, such as wearing masks in public, washing hands frequently, not gathering in public places, and self-isolation. In addition, β decreases to β(1−fε(t)) where ε is a piecewise function whose value depends on I−Ic, ε=0 when I−Ic<0. In practical terms, the number of infected people is relatively small and no precautionary measures are taken by the general population, but individuals begin to get concerned and take measures to reduce their risk of infection if I−Ic>0, i.e., ε=1. The parameter σ(0<σ<1) is the measurement of the effectiveness of the vaccine as a multiplier to the infection rate, where σ=0 indicates that the vaccine is completely effective, while σ=1 indicates the vaccine is completely ineffective. Figure 1 shows the diagram of the system (1.1).
In general, there are three links in the transmission of infectious diseases: source of infection, transmission route, and susceptible population, we can also response to infectious diseases from these three links. First, for the source of infection, we can isolate and treat the infected [21] to reduce the possibility of the spread of pathogen; second, we should reduce exposure and cut off transmission routes [22]; finally, people should take protective measures in the first place to reduce their risk of infection, for example, wearing a mask [23,24,25] and not gathering in public places. Society can also increase people's awareness of self-protection through media coverage [26,27]. Besides these approaches, vaccines are also very effective [28] and people are immunized by vaccination, which provides some protection even if they are accidentally exposed to the virus.
At the early stage of an outbreak, the public and the media know little about the disease. Only when it has spread for some time and the number of infected people has reached a certain amount could the media cover it. Media coverage could raise people's awareness of the risks of infectious diseases to understand their transmission ways and means, and update essential information like the number of infections and the location of outbreaks. In this way, people could raise their awareness, avoid infected areas, and reduce their contact with infected people as well as the risk of contracting the disease. Therefore, the number of infections will decrease with the increase of media coverage, which directly affects the transmission term. But the the specific influence of media on propagation term is not the intrinsic deterministic factor, Cui et al. [29] proposed the negative exponential term function in transmission term. The coefficient of transmission rate usually expressed as β is reduced to βexp(−αI) [30,31]. If there is less media coverage and fewer people who know about it, infectious diseases could still spread extensively. Massive media coverage will greatly increase public awareness of infectious diseases, but it will consume large amounts of human and material resources. Therefore, we introduced the measure of media coverage combined with protective measures and the same threshold as the standard to consider the transmission rate in segments. In addition, the process during which the vaccinated individuals lose their immunity and become infected could be divided into two stages. First, the vaccinated individuals lose their immunity and become susceptible; afterward, they transform into infected individuals. Therefore, we do not consider the case that V directly transforms into I.
Based on the above reasons, this paper considers the extension model of the system (1.1) as follows:
{dS(t)dt=μ−β(1−εf)exp(−εαI)SI−μS−ϕS+γI+θV,dI(t)dt=β(1−εf)exp(−εαI)SI−(μ+γ)I,dV(t)dt=ϕS−μV−θV, | (1.2) |
where
ε={0,I<Ic,1,I>Ic, |
here α is the influence coefficient of media coverage. Suppose the total population is a constant, might as well we set S+I+V=1, i.e., d(S+I+V)dt=0. Figures 2 and 3 show the diagram of the system and the threshold policy.
There have been extensive studies and application of discontinuous models, especially the Filippov system, which are described by differential equations with discontinuous right-hand sides. Tang et al. [30] investigated the influence of media coverage, vaccination, and treatment on disease dynamics in a non-smooth SIR Filippov system. Wang et al. [32] have studied the model of non-smooth plant diseases with economic thresholds and cultivation strategies, and a Filippov system was proposed according to a threshold of the number of infected plants. The equilibrium, heteroclitic orbit, and global dynamic behaviors of the system were analyzed. Li et al. [33] put forward the non-smooth boundary of the discontinuous plant disease model. In this system, they combined two thresholds which are the infection threshold IT and the ratio threshold I/S and divided the plane into two regions, then the system dynamic behavior is analyzed in detail. There are many similar works and more questions for researchers to discuss. Inspired by previous studies, media coverage and protection measures are important for disease transmission dynamics, but there are few papers consider both. Then this paper aims to further investigate how the protection level f and the influence coefficient of media coverage α influence the epidemic trends. In this paper, the basic reproduction numbers of the two subsystems are different, so the global dynamic behavior analysis is more complex. In addition, the importance of the threshold Ic on the number of infected persons and the final equilibrium state of the disease was analyzed numerically. In terms of theoretical analysis, we used the methods of discontinuous differential inclusion theory, non-smooth system analysis, Filippov convex method [34] etc.
An outline of this paper is as follows. In Section 2, we expound on the knowledge of the Filippov system and explain the positivity and boundedness of the solutions with the initial value problem. The dynamic behavior analysis of the subsystems is presented in Section 3. The local stability and global stability of the equilibria of the two subsystems are analyzed respectively by calculating the basic reproduction number. In Section 4, the sliding mode dynamics are studied. In Section 5, we first exclude the existence of the closed orbit, then the global asymptotic stability of the real equilibrium point and the pseudo-equilibrium is analyzed. Finally, there are numerical simulations and the corresponding biological implications.
In this part, we first give some definitions about the to analyze the dynamic behaviors of the system. Then, the positivity and boundedness of the solutions with the initial value problem will be analyzed [8,32].
For the system (1.2), suppose V=1−S−I, then the system (1.2) can be converted to
{dS(t)dt=μ−β(1−εf)exp(−εαI)SI−μS−ϕS+γI+θ(1−S−I),dI(t)dt=β(1−εf)exp(−εαI)SI−(μ+γ)I. | (2.1) |
Let R2+={X=(S,I)T|S≥0,I≥0}, H(X)=I−Ic,
F1=[μ−βSI−μS−ϕS+γI+θ(1−S−I)βSI−(μ+γ)I], |
and
F2=[μ−β(1−f)exp(−αI)SI−μS−ϕS+γI+θ(1−S−I)β(1−f)exp(−αI)SI−(μ+γ)I]. |
So we can write the system (2.1) to the following generic planar Filippov system:
dX(t)dt={F1(X),X∈G1,F2(X),X∈G2, | (2.2) |
where G1={X∈R2+|H(X)<0}, G2={X∈R2+|H(X)>0}. Suppose HX(X) is the gradient of H(X) and directs to G2, HX(X)=(0,1)T, ⟨⋅,⋅⟩ is the standard scalar product. Then Σ={X∈R2+|H(X)=0} can be split into three regions:
(a) Σc⊂Σ is called the crossing region if the product ⟨HX(X),F1(X)⟩⟨HX(X),F2(X)⟩>0;
(b) Σs⊂Σ is called the sliding region if the product ⟨HX(X),F1(X)⟩>0, ⟨HX(X),F2(X)⟩<0;
(c)Σe⊂Σ is called the escaping region if the product ⟨HX(X),F1(X)⟩<0, ⟨HX(X),F2(X)⟩>0.
Here are some definitions about the Filippov system [31,35,36,37,38]:
Definition 2.1. (The classification of equilibrium) For the system (2.2),
(a) A real equilibrium XR is described as F1(XR)=0, XR∈G1 or F2(XR)=0, XR∈G2.
(b) A virtual equilibrium XV is described as F1(XV)=0, XV∈G2 or F2(XV)=0, XV∈G1.
(c) A pseudo-equilibrium Xp is described as λF1(Xp)+(1−λ)F2(Xp)=0, 0<λ<1, where
λ=⟨HX(Xp),F2(Xp)⟩⟨HX(Xp),F2(Xp)−F1(Xp)⟩. |
(d) A boundary equilibrium XB is described as F1(XB)=0, H(XB)=0 or F2(XB)=0, H(XB)=0.
Definition 2.2. (The tangent point) A tangent point XT of the system (2.2) is defied as:
(a) Fi(XT)≠0, i=1,2,
(b) ⟨F1(XT),HX(XT)⟩=0 or ⟨F2(XT),HX(XT)⟩=0, i.e. the trajectory of Gi(i=1,2) is tangent to the sliding region Σ.
In order to investigate the dynamic behaviors of the system (2.1), in the following, we give that the solutions of the system (2.1) with initial value are positive and bounded.
Proposition 2.1. Supposing that (S(t),I(t)) is a solution of the system (2.1) with S(0)=S0≥0, I(0)=I0≥0 on [0,T), where T∈(0,+∞], then S(t)≥0 and I(t)≥0 for all t∈[0,T).
Proof. According to the definition of the solution of the system (2.1) in Filippov sense [34] and the first equation of the system (2.1), we have
dSdt|S=0=μ+γI+θ(1−I)>0. |
Consider S(0)=S0≥0, so that S(t)≥0, t∈[0,T). Then according to the second equation of the system (2.1)
dIdt=β(1−εf)exp(−εαI)SI−(μ+γ)I=(β(1−εf)exp(−εαI)S−(μ+γ))I. | (2.3) |
Note that I(0)=I0≥0, then
I(t)=I0e∫t0β(1−εf)exp(−εαI(ξ))S(ξ)−(μ+γ))dξ≥0. |
Then, I(t)≥0 for t∈[0,T). Thus, S(t)≥0 and I(t)≥0 for all t∈[0,T).
Suppose (S(t),I(t)) is a solution of the system (2.1) with S(0)=S0≥0 and I(0)=I0≥0 on [0,T), where T∈[0,+∞). Since S+I+V=1, it is obvious that the solution (S(t),I(t)) is bounded on [0,+∞). And it is easy to obtain the invariant region is defined as Ω={(S,I)∈R2+|0<S(t)+I(t)≤1}.
In this part, we rewrite the system (2.2) to two subsystems, then the basic reproduction numbers and their equilibria are discussed respectively, so the dynamic behaviors of the two subsystems can be analyzed through above results.
If I<Ic, then system (2.2) specifies to the subsystem:
{dS(t)dt=μ−βSI−μS−ϕS+γI+θ(1−S−I),dI(t)dt=βSI−(μ+γ)I. | (3.1) |
If I>Ic, then system (2.2) is:
{dS(t)dt=μ−β(1−f)exp(−αI)SI−μS−ϕS+γI+θ(1−S−I),dI(t)dt=β(1−f)exp(−αI)SI−(μ+γ)I. | (3.2) |
By the regeneration matrix method [39], we calculate the basic reproduction number of the system (3.1) as follows
R10=β(μ+θ)(μ+γ)(μ+ϕ+θ). | (3.3) |
Meanwhile, the system (3.1) has the following two equilibria, a disease-free equilibrium E0=(μ+θμ+ϕ+θ,0) and a positive endemic equilibrium E1=(μ+γβ,1−(μ+γ)(μ+ϕ+θ)β(μ+θ)) when R10>1.
Theorem 3.1. For the subsystem (3.1), the disease-free equilibrium E0 is globally asymptotically stable (GAS) if R10<1, while the endemic equilibrium E1 is GAS if R10>1.
Proof. For the subsystem (3.1), we calculate its Jacobian matrix to be
J=[−βI−(μ+ϕ+θ)−βS+γ−θβIβS−(μ+γ)]. |
Then on the disease-free equilibrium E0, the Jacobian matrix can be written as
JE0=[−(μ+ϕ+θ)−β(μ+θ)μ+ϕ+θ+γ−θ0β(μ+θ)μ+ϕ+θ−(μ+γ)]. |
For R10=β(μ+θ)(μ+γ)(μ+ϕ+θ)<1, then β(μ+θ)μ+ϕ+θ<μ+γ, i.e., β(μ+θ)μ+ϕ+θ−(μ+γ)<0. Additionally, −(μ+ϕ+θ)<0, thus E0 is a locally asymptotically stable node(LAS). Furthermore, it is a saddle if R10>1.
Likewise, the Jacobian matrix of the system (3.1) on the endemic equilibrium is
JE1=[−β(μ+θ)−(μ+γ)(μ+ϕ+θ)(μ+θ)−(μ+ϕ+θ)−(μ+θ)β(μ+θ)−(μ+γ)(μ+ϕ+θ)(μ+θ)0]. |
Sine R10=β(μ+θ)(μ+γ)(μ+ϕ+θ)>1, then tr(JE1)=−β(μ+θ)−(μ+γ)(μ+ϕ+θ)(μ+θ)−(μ+ϕ+θ)<0, det(JE1)=β(μ+θ)−(μ+γ)(μ+ϕ+θ)>0. So JE1 has two negative characteristic roots or a pair of conjugate negative roots with negative real parts. So E1 is LAS. Meanwhile, the characteristic polynomial of the system (3.1) is λ2−tr(JE1)λ+det(JE1)=0. Thus, E1 is a stable focus if Δ<0, while it is a stable node if Δ>0, where Δ=tr2(JE1)−4det(JE1).
Next we will prove the GAS of the two equilibria, respectively. For the system (3.1), let F1=(F11,F12)T and select the Dulac function B(S,I)=1SI. Then
∂(BF11)∂S+∂(BF12)∂I=∂(μ+θSI−β−μ+ϕ+θI+γ−θS)∂S+∂(β−μ+γS)∂I=−μ+θS2I−γ−θS2. |
Since I<1, then −μ+θS2I<−μ+θS2, and all the parameters are positive constant, thus ∂(BF11)∂S+∂(BF12)∂I<−μ+θS2−γ−θS2=−μ+γS2<0. According to the Bendixson-Dulac criterion [40], the subsystem (3.1) has no close orbit. So the unique endemic equilibrium E1 of the subsystem (3.1) is GAS. Similarly, the disease-free equilibrium E0 of the subsystem (3.1) is GAS when R10<1.
We calculate the basic reproduction number of the system (3.2) as follows
R20=β(1−f)(μ+θ)(μ+γ)(μ+ϕ+θ). | (3.4) |
Meanwhile, it's easy to derive the disease-free equilibrium of the system (3.2) is E0=(μ+θμ+ϕ+θ,0). Let dS(t)dt=0 and dI(t)dt=0, we obtain that
{μ−β(1−f)exp(−αI2)S2I2−μS2−ϕS2+γI2+θ(1−S2−I2)=0,S2=μ+γβ(1−f)exp(αI2). | (3.5) |
Then we get a equation for I2
μ+θ−(μ+θ)I2−(μ+γ)(μ+ϕ+θ)β(1−f)exp(αI2)=0. |
Let g(I)=μ+θ−(μ+θ)I−(μ+γ)(μ+ϕ+θ)β(1−f)exp(αI). We derive that g(0)=μ+θ−(μ+γ)(μ+ϕ+θ)β(1−f)>0 for R20>1, and g(1)=−(μ+γ)(μ+ϕ+θ)β(1−f)exp(α)<0. Moreover, we have
d(g(I))dI=−(μ+θ)−α(μ+γ)(μ+ϕ+θ)β(1−f)exp(αI)<0 |
for all I≥0. Such that there exist unique I2 for g(I)=0 in (0,1).
Since g(I2)=0, we obtain
μ+θ−(μ+θ)I2−(μ+γ)(μ+ϕ+θ)β(1−f)exp(αI2)=0, |
simply deform the above formula, we have
α(1−I2)exp(α(1−I2))=α(μ+γ)(μ+ϕ+θ)β(1−f)(μ+θ)exp(α). |
According to the definition of Lambert W function [41], we let z=α(μ+γ)(μ+ϕ+θ)β(1−f)(μ+θ)exp(α), and W(z)=α(1−I2), then W(α(μ+γ)(μ+ϕ+θ)β(1−f)(μ+θ)exp(α))=α(1−I2), thus we derive I2=1−1αW(α(μ+γ)(μ+ϕ+θ)β(1−f)(μ+θ)exp(α)).
When R20>1, there is a unique positive equilibrium E2=(S2,I2)=(μ+γβ(1−f)exp(αI2),I2), where I2=1−1αW(α(μ+γ)(μ+ϕ+θ)β(1−f)(μ+θ)exp(α)), i.e., E2 is the endemic equilibrium of subsystem (3.2).
Theorem 3.2. For the subsystem (3.2), the disease-free equilibrium E0 is GAS if R20<1, whereas the endemic equilibrium E2 is GAS if R20>1.
Proof. The proof of LAS is similar to the Theorem 3.1, so we omit it here. Now we similarly proof the GAS of the two equilibria. Select the Dulac function B(S,I)=1SI. Then
∂(BF21)∂S+∂(BF22)∂I=∂(μ+θSI−β(1−f)exp(−αI)−μ+ϕ+θI+γ−θS)∂S+∂(β(1−f)exp(−αI)−μ+γS)∂I=−μ+θS2I−γ−θS2−αβ(1−f)exp(−αI)<0. |
According to the Bendixson-Dulac criterion, the subsystem (3.2) has no close orbit. So the disease-free equilibrium E0 of the subsystem (3.2) is GAS if R20<1, and the unique endemic equilibrium E2 of the subsystem (3.2) is GAS if R20>1.
Remark 3.1. The disease-free equilibrium point E0 is always real for the subsystem (3.1), and always virtual for the subsystem (3.2). When R10>1, the endemic equilibrium E1 is real (virtual) if and only if (iff) I1−Ic<0(>0), while it is a boundary equilibrium iff I1−Ic=0. When R20>1, the endemic equilibrium E2 is virtual (real) iff I2−Ic<0(>0), while it is a boundary equilibrium iff I2−Ic=0. The pseudo-equilibrium will be described in Section 4.
In this part, we mainly solve the sliding domain and sliding mode equation of the system (2.2). According to the Section 2, the sliding domain is ⟨HX(X),F1(X)⟩>0, and ⟨HX(X),F2(X)⟩<0.
To obtain the sliding domain, we let
g1(S)=⟨HX(X),F1(X)⟩=βSI−(μ+γ)I>0. |
Thus S>μ+γβ=S1. Similarly, we have
g2(S)=⟨HX(X),F2(X)⟩=β(1−f)exp(−αI)SI−(μ+γ)I<0, |
then S<μ+γβ(1−f)exp(αI)=S2. It is obvious that S1<S2. Therefore, the sliding domain is
Σs={(S,I)∈R2+|μ+γβ<S<μ+γβ(1−f)exp(αIc),I=Ic}. |
According to the famous Filippov convex method [34], the dynamic on the sliding domain Σs of the Fiippov system (2.2) is represented as follows:
λF1+(1−λ)F2=λ[μ−βSI−μS−ϕS+γI+θ(1−S−I)βSI−(μ+γ)I]+(1−λ)[μ−β(1−f)exp(−αI)SI−μS−ϕS+γI+θ(1−S−I)β(1−f)exp(−αI)SI−(μ+γ)I]=[μ+θ−(μ+ϕ+θ)S+(γ−θ)I−λβSI−(1−λ)β(1−f)exp(−αI)SI−(μ+γ)I+λβSI+(1−λ)β(1−f)exp(−αI)SI], |
with 0≤λ≤1. Then the sliding mode equation is
f(S)=μ+θ−(μ+ϕ+θ)S−(μ+θ)Ic. |
Let f(S)=0, then
Sp=(μ+θ)(1−Ic)μ+ϕ+θ. |
At this point, f(S) has only one equilibrium Ep(Sp,Ic). Thus the pseudo-equilibrium exists iff S1<Sp<S2, which is equivalent to I2<Ic<I1.
Theorem 4.1. Ep is a stable pseudo-equilibrium on Σs when it exists.
Proof. Direct calculation yields
d(f(Sp))dS|Ep=−(μ+ϕ+θ)<0. |
Thus the solutions are attracting.
In order to better understand the dynamic behaviors of the system (2.2), we now discuss the relationship between the sliding domain Σs and the invariant region Ω. Let μ+γβ=1−I, then we get I1c=β−(μ+γ)β. Similarly, we let
μ+γβ(1−f)exp(αI)=1−I, |
by the definition of Lambert W function, we obtain
I2c=1−1αW(α(μ+γ)β(1−f)exp(α)). |
Since S1<S2, then I1c>I2c. Thus the relationship between the sliding domain Σs and the invariant region Ω can be divided into the following three cases:
(a) Σs is totally out of Ω if Ic>I1c.
(b) Σs is totally in Ω if Ic<I2c.
(c) Part of Σs is in Ω if I2c<Ic<I1c.
Remark 4.1. On the basis of the Section 4, we derive the following results:
(a) The crossing region Σc⊂Σ is ⟨HX(X),F1(X)⟩>0,⟨HX(X),F2(X)⟩>0 or ⟨HX(X),F1(X)⟩<0,⟨HX(X),F2(X)⟩<0. By simply calculation, we derive that Σc={(S,I)∈R2+∣S<S1,S>S2,I=Ic}.
(b) The escaping region is Σe=∅ (the escaping region does not exist).
(c) There are two tangent points: T1=(S1,Ic) and T2=(S2,Ic).
In this part, we prove that the system (2.2) has no closed orbit, which contains a part of the closure of the sliding domain ¯Σs or surrounds the whole sliding domain ¯Σs. And then, we analyze the global dynamics of the system using the method in [10].
Lemma 5.1. There is no closed orbit that contains a part of the closure of the sliding domain ¯Σs for the system (2.2).
Proof. First, there exists a pseudo-equilibrium Ep if I2<Ic<I1, and Ep is LAS in the sliding domain Σs, which means the nonexistence of limit cycle that containing part of the sliding domain.
Second, we shall illustrate that there is no close orbit that contains a part of the closure of the sliding domain ¯Σs if Ic>I1 or Ic<I2. Without loss of generality, we assume that Ic>I1, i.e., E1 is real (denoted by Er1) and E2 is virtual (denoted by Ev2). Then Er1 and Ev2 are in the region G1⋂Ω, and the vector field in G2⋂Ω is pointing downwards. Because f(S)<0, then the trajectory moves from right to left on T1T2. We will illustrate that the orbit C initiating at T1 will not hit the sliding domain Σs again. According to Theorem 3.1, Er1 is a stable node or focus in region G1, then the orbit C starting at T1 either tends to the stable equilibrium Er1 directly or spirally. If the latter is true, then the orbit C intersects with the horizontal isocline g11 at two points O1 and O2, where O2 is on the segment T1Er1. Obviously, the two points O1 and O2 are below the point T1. Hence, C starting at T1 cannot form a cycle, as shown in Figure 4.
Consequently, there is no closed orbit that contains a part of the closure of the sliding domain ¯Σs for the system (2.2).
Lemma 5.2. There is no closed orbit surrounding ¯Σs for the system (2.2).
Proof. Otherwise, there exists a closed orbit Γ that surrounding ¯Σs (see Figure 5). Suppose that the closed orbit Γ intersects with Σ at two points N1,N2, where N1=(P1,Ic), N2=(P2,Ic). In addition, Γ intersects with the auxiliary line Ic−ϵ1 at two points M1,M2, and Γ intersects with the auxiliary line Ic+ϵ1 at two points M3,M4, where ϵ1 is a sufficiently small number. Suppose D1 denotes the lower half region surrounded by M1,M2 and Γ1, D2 represents the upper half region surrounded by M3,M4 and Γ2. Let B(S,I)=1SI, we have
2∑i=1∬Di[∂(BFi1)∂S+∂(BFi2)∂I]dSdI=∬D1[−μ+θS2I−γ−θS2]dSdI+∬D2[−μ+θS2I−γ−θS2−αβ(1−f)exp(−αI)]dSdI<0, |
where i=1,2. Suppose that the abscissas of the points M1,M2,M3 and M4 are P1+u1(ϵ1),P2−u2(ϵ1),P2−u3(ϵ1),P1+u4(ϵ1), respectively, where ui(ϵ1) (i=1,...,4) is continuous and satisfies limϵ1→0ui(ϵ1)=0 and ui(0)=0. According to the Green's theorem, we obtain
∬D1[∂(BF11)∂S+∂(BF12)∂I]dSdI=∮Γ1⋃→M2M1BF11dI−∮Γ1⋃→M2M1BF12dS=∫Γ1B(F11F12−F12F11)dt+∫→M2M1BF11dI−∫→M2M1BF12dS=−∫→M2M1BF12dS=−β(P1−P2+u1(ϵ1)+u2(ϵ1))+(μ+γ)ln|P1+u1(ϵ1)P2−u2(ϵ1)|, |
where dS=F11dt and dI=F12dt. Similarly, for the region D2,
∬D2[∂(BF21)∂S+∂(BF22)∂I]dSdI=∮Γ2⋃→M4M3BF21dI−∮Γ2⋃→M4M3BF22dS=−∫→M4M3BF22dS=−β(1−f)exp(−αIc)(P2−P1−u3(ϵ1)−u4(ϵ1))+(μ+γ)ln|P2−u3(ϵ1)P1+u4(ϵ1)|, |
where dS=F21dt and dI=F22dt. Since P1<P2, then
limϵ1→02∑i=1∬Di[∂(BFi1)∂S+∂(BFi2)∂I]dSdI=limϵ1→0(−∫→M2M1BF12dS−∫→M4M3BF22dS)=β(P2−P1)(1−(1−f)exp(−αIc))>0, |
this is a contradiction. Therefore, there is no closed orbit surrounding ¯Σs for the system (2.2).
In this section, we will prove the global stability of the system (2.2). First, we give the following Lemma.
Lemma 5.3. (See[34])If a half trajectory T+ is bounded for the system (2.2), then its limit set Ω(T) contains either an equilibrium or a closed trajectory.
In the following, according to the relationship among the basic reproduction number of the two subsystems R10, R20 and 1, the GAS of the system (2.2) can be divided into the following three cases.
Case 1: R20<R10<1.
Theorem 5.1. The disease-free equilibrium E0 is GAS if R20<R10<1.
Proof. Since R20<R10<1, the two endemic equilibria E1 and E2 are not feasible, and there ia a real disease-free equilibrium E0 in G1⋂Ω, then Ep does not exist. Furthermore, we obtain the solution of the system (2.2) are bounded and no closed orbit of any kind exists on the basis of Proposition 2.1, Theorems 3.1 and 3.2, Lemmas 5.1 and 5.2. Thus, the only real equilibrium E0 is LAS. In this case the limit set Ω(T) of the system (2.2) is the unique real equilibrium E0 by Lemma 5.3. So that any solution of the system (2.2) eventually stabilizes at the equilibrium E0, i.e., E0 is GAS (see Figure 6).
Case 2: R20<1<R10.
It is obvious that there exist two equilibria E0 and E1, where E0 is a real saddle. However, we do not yet know whether E1 is a real or virtual and whether Ep exists. Note that the threshold Ic may be greater than or less than I1, so we discuss the following two subcases.
Theorem 5.2. The endemic equilibrium E1 is GAS if R20<1<R10 and Ic>I1.
Proof. When Ic>I1, we know E1 real (denoted by Er1) and Ep does not exists. The trajectory moves from the right to the left on the sliding domain T1T2 by Lemma 5.1. Moreover, because there are no closed orbits in the region G1, we obtain E1 is LAS. According to the relationship between the sliding domain Σs and the invariant region Ω in Section 4, we can further divide it into the following three cases.
(i) If Ic>I1c, we can easy derive S1+Ic>1, where S1 is the left endpoint of the sliding domain. Therefore, the sliding domain Σs is totaly out the invariant region Ω, as shown in Figure 7(a).
Case | α | β | μ | γ | ϕ | θ | Ic | f |
Figure 7(a) | 0.3 | 0.6 | 0.3 | 0.1 | 0.1 | 0.6 | 0.5 | 0.3 |
Figure 7(b) | 0.4 | 0.8 | 0.4 | 0.02 | 0.5 | 0.3 | 0.45 | 0.4 |
Figure 7(c) | 0.05 | 0.6 | 0.43 | 0.1 | 0.1 | 0.4 | 0.06 | 0.05 |
Figure 7(d) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.31 |
Figure 7(e) | 0.25 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.31 |
Figure 8(a) | 0.3 | 0.7 | 0.3 | 0.2 | 0.1 | 0.4 | 0.5 | 0.1 |
Figure 8(b) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.5 | 0.3 |
Figure 8(c) | 0.05 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.5 | 0.05 |
Figure 8(d) | 0.3 | 0.6 | 0.1 | 0.1 | 0.1 | 0.6 | 0.5 | 0.3 |
Figure 8(e) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.3 |
Figure 8(f) | 0.05 | 0.8 | 0.43 | 0.1 | 0.1 | 0.4 | 0.2 | 0.05 |
(ii) If max{I2c,I1}<Ic<I1c, then S1+Ic<1 and S2+Ic>1, where S1 and S2 are the left and right endpoints of the sliding domain Σs respectively. There exists a point T∗=(S∗,Ic) on T1T2, which satisfies S∗+Ic=1. Thus part of the sliding segment T1T2 (i.e., T1T∗) is in the invariant region Ω (see Figure 7(b)).
(iii) If Ic<I2c, then S2+Ic<1, where S2 is the left endpoint of the sliding domain. So Σs is totally in Ω, as shown in Figure 7(c).
Then the vector field in G2⋂Ω is pointing downwards. By Theorems 3.1 and 3.2, there is no close orbit totaly in the region G1 and G2. Furthermore, according to Lemmas 5.1 and 5.2, there is no close orbit that contains part of Σs and surrounding it. Therefore, for the subsystem (3.1), the equilibrium E1 is GAS. Additionally, according to Lemma 5.3, it's not difficult to derive that the endemic equilibrium E1 is GAS for the system (2.2).
Theorem 5.3. The pseudo-equilibrium Ep is GAS if R20<1<R10 and Ic<I1.
Proof. When R20<1<R10 and Ic<I1, we know E1 are virtual (denoted by Ev1). Therefore, the rails in G1 are oriented upward and those in G2 are oriented downward, but they can not converge to their own equilibria and intersect with the sliding domain. The trajectory moves from the right to the left on the sliding domain EpT2, and the trajectory moves from the left to the right on the sliding domain T1Ep by Theorem 3.1. Analogously, we discuss the relationship between Σs and Ω in the following two cases.
(i) If I2c<Ic<I1, we obtain part of Σs is in Ω similar to the proof of the Theorem 5.2 (ii) (see Figure 7(d)).
(ii) If Ic<min{I2c,I1}, according to the proof of the Theorem 5.2 (iii), we similarly conclude that Σs is totaly in Ω, as shown in Figure 7(e).
According to the previous proof, the system (2.2) does not have any kind of closed orbits. Accordingly, by Lemma 5.3, the pseudo-equilibrium Ep is GAS for the system (2.2).
Case 3: 1<R20<R10.
In this case, E1 and E2 are feasible, we now analyze the specific global stability of the system (2.2) in the following subcases similar to the Case 2.
Theorem 5.4. The endemic equilibrium E1 is GAS if 1<R20<R10 and Ic>I1.
Proof. When Ic>I1, we know E1 real (denoted by Er1), E2 is virtual (denoted by Ev2) and Ep does not exists. The trajectory also moves from the right to the left on the sliding domain T1T2 by Theorem 3.1. Furthermore, we obtain E1 is LAS. Analogously, there are three scenarios.
(i) If Ic>I1c, similar to the proof of the Theorem 5.2 (i), we obtain Σs is totaly out of Ω (see Figure 8(a)).
(ii) If max{I2c,I1}<Ic<I1c, similar to the proof of the Theorem 5.5 (ii), then part of Σs is in Ω (see Figure 8(b)).
(iii) If Ic<I2c, similar to the proof of the Theorem 5.2 (iii), we obtain Σs is totaly in Ω, as shown in Figure 8(c).
Then Er1 and Ev2 are in the region G1⋂Ω, and the vector field in G2⋂Ω is pointing downwards. By Theorems 3.1 and 3.2, there is no close orbit totaly in the region Gi (i=1,2). Furthermore, according to Lemma 5.1, there is no close orbit that contains part of the sliding domain Σs. Therefore, the equilibrium E1 is GAS for the subsystem (3.1). In addition, according to Lemma 5.3, we obtain E1 is GAS for the system (2.2).
Theorem 5.5. The pseudo-equilibrium Ep is GAS if 1<R20<R10 and I2<Ic<I1.
Proof. When 1<R20<R10 and I2<Ic<I1, E1 and E2 are virtual (denoted by Ev1 and Ev2 respectively), Ep does exist. Such that solutions of both subsystems can not converge to their own equilibria.
(i) If I2c<Ic<I1, according to the Theorem 5.3 (i), part of Σs is in Ω, as shown in Figure 8(d).
(ii) If Ic<min{I2c,I1}, similar to the Theorem 5.3 (ii), Σs is totaly in Ω, as shown in Figure 8(e).
Accordingly, due to the nonexistence of closed orbits in the invariant region Ω, in this case the pseudo-equilibrium Ep is GAS for the system (2.2).
Theorem 5.6. The endemic equilibrium E2 is GAS if 1<R20<R10 and Ic<I2.
Proof. When 1<R20<R10 and Ic<I2, E1 is virtual (Ev1) and E2 is real (Er2), Ep does not exist. The trajectory moves from the left to the right on the sliding domain T1T2 by Theorem 3.1. Moreover, because there are no closed orbits in G2, we obtain E2 is LAS. In addition, by Lemmas 5.1 and 5.2, we obtain E2 is GAS in the region G2. Therefore, by Lemma 5.3, the ω-limit set of the system (2.2) is the unique real equilibrium E2, which means E2 is GAS. In addition, it is not difficult to derive Σ is totaly in Ω (see Figure 8(f)).
Remark 5.1. The existence of pseudo-equilibrium Ep is one of the characteristics of a discontinuous system. Generally, the system could reach a new equilibrium state by controlling the threshold Ic, which is a new idea when infectious diseases could not be eradicated in a short time.
In this paper, the media coverage and protective measures are considered in a discontinuous SIV system, in which the transmission rate influenced by both media coverage and protective measures is represented by a discontinuous function. Assuming that the total population is a constant, we transform the three-dimensional discontinuous differential equation system into a two-dimensional discontinuous differential equation system. For the two dimensional system, the first task is to prove the solutions with initial value are positive and bounded. After that, the system (2.2) is divided into two simple subsystems. For the subsystems, we calculate the basic reproduction number and the stability of the equilibria. Next, due to the specific switching characteristics of the Filippov system, the sliding mode domain and sliding mode equation are also the objects of our analysis. According to the analysis above, we study the global dynamics of the system (2.2), and obtain that the system (2.2) has no closed orbit of any kind. Detailed conclusions are shown in Table 2.
Case | Condition | Equilibria | Global dynamics |
R20<R10<1 | Er0 | E0 is GAS (see Fig. 6) | |
R20<1<R10 | Ic>I1 | Ev0,Er1 | E1 is GAS (see Fig. 7 (a), (b), (c)) |
R20<1<R10 | Ic<I1 | Ev0,Ev1,Ep | Ep is GAS (see Fig. 7 (d), (e)) |
1<R20<R10 | Ic>I1 | Er1,Ev2 | E1 is GAS (see Fig. 8 (a), (b), (c)) |
1<R20<R10 | I2<Ic<I1 | Ev1,Ev2,Ep | Ep is GAS (see Fig. 8 (d), (e)) |
1<R20<R10 | Ic<I2 | Ev1,Er2 | E2 is GAS (see Fig. 8 (f)) |
Our ultimate goal is to reduce the scale of infection and control the spread of infectious diseases. Modeling of discontinuous systems also provides a reference for government departments to formulate prevention and control measures, such as the timing and intensity of media coverage, and the intensity of protective measures. Different regulations on prevention and control measures have been introduced in light of the actual situation, including the scale of the epidemic, to make better use of public resources.
Firstly, we discuss the impact of infection threshold Ic on disease outbreak, which can be divided into three scenarios:
(a) R20<R10<1
In this case, we hope the transmission rate β is sufficiently small, the vaccination rate of the susceptible population ϕ, and the recovery rate of infected individuals γ are sufficiently large. According to the Theorems 3.1 and 5.1, the number of infected people will extinct regardless of the number of Ic. After comparing Ic=0.1, Ic=0.3, and Ic=0.9, we could see that taking an appropriate threshold value could control the spread of disease in a relatively short time. As indicated in Figure 9(a), when the scale of the disease I>Ic decreases rapidly, the curve slope is steep. Once I is lower than the given threshold Ic and the prevention and control measures are loosened, there are still infected people, but their number will be small and slowly changing and the curve will decrease gently. At this point, if the threshold Ic is larger, i.e., more people remain infected when the prevention and control measures are lifted, the disease will die out more slowly. However, if Ic is very small, it is bound to waste large amounts of social resources and exert a long-term impact on humans' normal life. In conclusion, the selection of infection threshold Ic should suit the actual situation, being neither too large nor too small.
(b) R20<1<R10
Similar to the scenario (a), to obtain R20<1<R10, we hope the transmission rate β is not sufficiently small, the vaccination rate of the susceptible population ϕ or the cure rate of infected individuals γ are unsatisfactory, which causes the infectious disease to become endemic and pseudo-equilibrium states. According to Theorems 5.2 and 5.3, the solution of the system that satisfies any initial condition will eventually stabilize at the endemic equilibrium E1 or pseudo-equilibrium Ep. Figure 9(b) also draws the above conclusion that the smaller the Ic is, the better it is to control the spread of the disease. In addition, if Ic is sufficiently small, we could balance I to a smaller value, i.e., in a pseudo-equilibrium state, thereby controlling the endemic range to a smaller value.
(c) 1<R20<R10
As indicated in Figure 9(c), taking appropriate threshold leads to quicker control and fewer infections. There may be three equilibrium states, i.e., three possible endemic scales. The government should formulate appropriate measures and people should improve their self-protection awareness as far as possible to minimize the infection and achieve a pseudo equilibrium state.
The transmission rate is a key factor in determining the dynamics of the disease and its ultimate outcome. Through the dynamic analysis, we discover that the transmission rate is greatly influenced by the intensity of protective measures f and the influence coefficient of media coverage α. Our next step is to investigate how the infectious disease influenced by the two parameters, and to show how to achieve our goal: to control the spread of infectious diseases.
Figure 10 presents the impact of protective measures f and the influence coefficient of media coverage α on the scale of the epidemic in four cases. As indicated in Figure 10(a), when R20<R10<1, all curves eventually reach zero. As for epidemic prevention and control with the same intensity of media coverage, the stronger the protective measures, the better the effect. With the same protective measures, the more media coverage, the more effective. There is some overlap between media reports and protective measures and which method is more effective could be judged based on the following figures. According to the Theorems 5.2 and 5.3, when R20<1<R10, the solution of the system (2.2) finally stabilizes at the endemic equilibrium E1 or pseudo-equilibrium Ep, as indicated in Figure 10 (b), (c). Finally, in Figure 10(d), if 1<R20<R10, the final scale of the disease has three scenarios which are stable at endemic equilibrium E1, endemic equilibrium E2, and pseudo-equilibrium Ep respectively, where I1>I2>Ic. Similar to Figure 10(a), Figure 10(b), (c), and (d) show that media coverage and protective measures have a positive impact on the control of infectious diseases, but protective measures are more effective than media coverage. Therefore, when an epidemic occurs, government departments should formulate corresponding measures according to the actual stage of the spread of infectious diseases, select the intensity of protective measures and appropriate media reports, and prioritize protection supplemented by reporting to minimize the scale of infectious diseases as soon as possible by using the least social resources.
In conclusion, the theoretical and numerical simulation in this paper present that with reasonable control measures and appropriate threshold Ic, the spread of the disease can be taken under control in a shorter time and reduce the peak value. When an infectious disease breaks out over a period, we could make use of the characteristics of a discontinuous system to reduce its scale. If media reports were simply introduced into the original system, it would be difficult to analyze the dynamic behavior of the system. Therefore, we propose a more realistic model based on the existing work, and the results are similar. But we are focus on the biological significance of infectious diseases, we can take reasonable measures to control the disease below the threshold, rather than the outbreak of a large scale. In this paper, we only consider controlling media coverage and protection measures using the same threshold. In the future, we will separate the media coverage and protection measures, hoping to provide a more valuable reference.
The authors thank the editors and the anonymous reviewers for their resourceful and valuable comments and constructive suggestions. This work was supported by the National Natural Science Foundation of China (11871231) and the Science Foundation for Distinguished Youth Scholars of Fujian Province (2020J0625).
The authors declare no conflict of interest in this paper.
[1] |
G. Zaman, Y. H. Kang, I. H. Jung, Stability analysis and optimal vaccination of an SIR epidemic model, Biosystems, 93 (2008), 240â€"249. http://dx.doi.org/10.1016/j.biosystems.2008.05.004 doi: 10.1016/j.biosystems.2008.05.004
![]() |
[2] |
I. Cooper, A. Mondal, C. G. Antonopoulos, A SIR model assumption for the spread of COVID-19 in different communities, Chaos Soliton. Fract., 139 (2020), 110057. http://dx.doi.org/10.1016/j.chaos.2020.110057 doi: 10.1016/j.chaos.2020.110057
![]() |
[3] |
L. J. S Allen, Some discrete-time SI, SIR, and SIS epidemic models, Math. Biosci., 124 (1994), 83â€"105. http://dx.doi.org/10.1016/0025-5564(94)90025-6 doi: 10.1016/0025-5564(94)90025-6
![]() |
[4] |
Y. Enatsu, Y. Nakata, Y. Muroya, Global stability for a class of discrete SIR epidemic models, Math. Biosci. Eng., 7 (2010), 347â€"361. http://dx.doi.org/10.3934/mbe.2010.7.347 doi: 10.3934/mbe.2010.7.347
![]() |
[5] |
B. Shulgin, L. Stone, Z. Agur, Pulse vaccination strategy in the SIR epidemic model, Bull. Math. Biol., 60 (1998), 1123â€"1148. http://dx.doi.org/10.1006/s0092-8240(98)90005-2 doi: 10.1006/s0092-8240(98)90005-2
![]() |
[6] |
L. Stone, B. Shulgin, Z. Agur, Theoretical examination of the pulse vaccination policy in the SIR epidemic model, Math. Comput. Model., 31 (2000), 207â€"215. http://dx.doi.org/10.1016/S0895-7177(00)00040-6 doi: 10.1016/S0895-7177(00)00040-6
![]() |
[7] |
T. Zhao, Y. Xiao, Non-smooth plant disease models with economic thresholds, Math. Biosci., 241 (2013), 34â€"48. http://dx.doi.org/10.1016/j.mbs.2012.09.005 doi: 10.1016/j.mbs.2012.09.005
![]() |
[8] |
Z. Guo, L. Huang, X. Zou, Impact of discontinuous treatments on disease dynamics in an SIR epidemic model, Math. Biosci. Eng., 9 (2012), 97â€"110. http://dx.doi.org/10.3934/mbe.2012.9.97 doi: 10.3934/mbe.2012.9.97
![]() |
[9] |
Z. Guo, X. Zou, Impact of discontinuous harvesting on fishery dynamics in a stock-effort fishing model, Commun. Nonlinear Sci., 20 (2015), 594â€"603. http://dx.doi.org/10.1016/j.cnsns.2014.06.014 doi: 10.1016/j.cnsns.2014.06.014
![]() |
[10] |
L. Huang, H. Ma, J. Wang, C. Huang, Global dynamics of a Filippov plant disease model with an economic threshold of infected-susceptible ratio, J. Appl. Anal. Comput., 10 (2020), 2263â€"2277. http://dx.doi.org/10.11948/20190409 doi: 10.11948/20190409
![]() |
[11] |
W. Li, L. Huang, J. Wang, Global dynamics of Filippov-type plant disease models with an interaction ratio threshold, Math. Meth. Appl. Sci., 43 (2020), 6995â€"7008. http://dx.doi.org/10.1002/mma.6450 doi: 10.1002/mma.6450
![]() |
[12] |
Y. K. Xie, Z. Wang, A ratio-dependent impulsive control of an SIQS epidemic model with non-linear incidence, Appl. Math. Comput., 423 (2022), 127018. https://doi.org/10.1016/j.amc.2022.127018 doi: 10.1016/j.amc.2022.127018
![]() |
[13] |
Y. K. Xie, Z. Wang, Transmission dynamics, global stability and control strategies of a modified SIS epidemic model on complex networks with an infective medium, Math. Comput. Simul., 188 (2021), 23â€"34. https://doi.org/10.1016/j.matcom.2021.03.029 doi: 10.1016/j.matcom.2021.03.029
![]() |
[14] |
W. O. Kermack, A. G. McKendrick, A contribution to the mathematical theory of epidemics, P. Roy. Soc. A, 115 (1927), 700â€"721. http://dx.doi.org/10.1007/bf02464423 doi: 10.1007/bf02464423
![]() |
[15] |
W. O. Kermack, A. G. McKendrick, Contributions to the mathematical theory of epidemics â…¡.â€"-The problem of endemicity, P. Roy. Soc. A, 138 (1932), 55â€"83. http://dx.doi.org/10.1016/s0092-8240(05)80041-2 doi: 10.1016/s0092-8240(05)80041-2
![]() |
[16] |
W. O. Kermack, A. G. McKendrick, Contributions to the mathematical theory of epidemics â…¢.â€"-Further studies of the problem of endemicity, P. Roy. Soc. A, 141 (1933), 94â€"122. http://dx.doi.org/10.2307/96207 doi: 10.2307/96207
![]() |
[17] |
B Shulgin, L. W. Stone, Z. Agur, Pulse vaccination strategy in the SIR epidemic model, Bull. Math. Biol., 60 (1998), 1123â€"1148. http://dx.doi.org/10.1016/S0092-8240(98)90005-2 doi: 10.1016/S0092-8240(98)90005-2
![]() |
[18] |
A. B. Gumel, S. M. Moghadas, A qualitative study of a vaccination model with non-linear incidence, Appl. Math. Comput., 143 (2003), 409â€"419. http://dx.doi.org/10.1016/S0096-3003(02)00372-7 doi: 10.1016/S0096-3003(02)00372-7
![]() |
[19] |
S. Tang, J. Liang, Y. Xiao, R. A. Cheke, Sliding bifurcations of Filippov two stage pest control models with economic thresholds, SIAM J. Appl. Math., 72 (2012), 1061â€"1080. http://dx.doi.org/10.1137/110847020 doi: 10.1137/110847020
![]() |
[20] |
Y. Zhang, Y. Xiao, Global dynamics for a Filippov epidemic system with imperfect vaccination, Nonlinear Anal. Hybrid Syst., 38 (2020), 100932. http://dx.doi.org/10.1016/j.nahs.2020.100932 doi: 10.1016/j.nahs.2020.100932
![]() |
[21] |
A. P. Lemos-Paio, C. J. Silva, D. F. M. Torres, An epidemic model for cholera with optimal control treatment, J. Comput. Appl. Math., 318 (2017), 168â€"180. http://dx.doi.org/10.1016/j.cam.2016.11.002 doi: 10.1016/j.cam.2016.11.002
![]() |
[22] |
M. J. Jeger, L. V. Madden, F. V. D. Bosch, The effect of transmission route on plant virus epidemic development and disease control, J. Theor. Biol., 258 (2009), 198â€"207. http://dx.doi.org/10.1016/j.jtbi.2009.01.012 doi: 10.1016/j.jtbi.2009.01.012
![]() |
[23] |
V. C. C. Cheng, S. C. Wong, V. W. M. Chuang, S. Y. C. So, J. H. K. Chen, S. Sridhar, et al., The role of community-wide wearing of face mask for control of coronavirus disease 2019 (COVID-19) epidemic due to SARS-CoV-2, J. Infect., 81 (2020), 107â€"114. http://dx.doi.org/10.1016/j.jinf.2020.04.024 doi: 10.1016/j.jinf.2020.04.024
![]() |
[24] |
S. E. Eikenberry, M. Mancuso, E. Iboi, T. Phan, K. Eikenberry, Y. Kuang, et al., To mask or not to mask: Modeling the potential for face mask use by the general public to curtail the covid-19 pandemic, Infect. Dis. Model., 5 (2020), 293â€"308. http://dx.doi.org/10.1101/2020.04.06.20055624 doi: 10.1101/2020.04.06.20055624
![]() |
[25] |
C. R. MacIntyre, S. Cauchemez, D. E. Dwyer, H. Seale, P. Cheung, G. Browne, et al., Face mask use and control of respiratory virus transmission in households, Emerg. Infect. Dis., 15 (2009), 233. http://dx.doi.org/10.3201/eid1502.081167 doi: 10.3201/eid1502.081167
![]() |
[26] |
Z. Tai, T. Sun, Media dependencies in a changing media environment: The case of the 2003 SARS epidemic in China, New Media Soc., 9 (2007), 987â€"1009. http://dx.doi.org/10.1177/1461444807082691 doi: 10.1177/1461444807082691
![]() |
[27] |
S. Collinson, J. M. Heffernan, Modelling the effects of media during an influenza epidemic, BMC Public Health, 14 (2014), 1â€"10. http://dx.doi.org/10.1186/1471-2458-14-376 doi: 10.1186/1471-2458-14-376
![]() |
[28] | R. M. Anderson, R. M. May, Infectious diseases of humans: Dynamics and control, Oxford: Oxford Science Publications, 1992. http://dx.doi.org/10.1126/science.254.5031.591 |
[29] |
J. Cui, Y. Sun, H. Zhu, The impact of media on the spreading and control of infectious disease, J. Dyn. Differ. Equ., 20 (2008), 31â€"53. http://dx.doi.org/10.1007/s10884-007-9075-0 doi: 10.1007/s10884-007-9075-0
![]() |
[30] |
J. Deng, S. Tang, H. Shu, Joint impacts of media, vaccination and treatment on an epidemic Filippov model with application to COVID-19, J. Theor. Biol., 523 (2021), 110698. http://dx.doi.org/10.1016/j.jtbi.2021.110698 doi: 10.1016/j.jtbi.2021.110698
![]() |
[31] |
A. Wang, Y. Xiao, A Filippov system describing media effects on the spread of infectious diseases, Nonlinear Anal. Hybrid Syst., 11 (2014), 84â€"97. http://dx.doi.org/10.1016/j.nahs.2013.06.005 doi: 10.1016/j.nahs.2013.06.005
![]() |
[32] |
J. Wang, F. Zhang, L. Wang, Equilibrium, pseudoequilibrium and sliding-mode heteroclinic orbit in a Filippov-type plant disease model, Nonlinear Anal.-Real, 31 (2016), 308â€"324. http://dx.doi.org/10.1016/j.nonrwa.2016.01.017 doi: 10.1016/j.nonrwa.2016.01.017
![]() |
[33] |
W. Li, L. Huang, J. Wang, Dynamic analysis of discontinuous plant disease models with a non-smooth separation line, Nonlinear Dyn., 99 (2020), 1675â€"1697. http://dx.doi.org/10.1007/s11071-019-05384-w doi: 10.1007/s11071-019-05384-w
![]() |
[34] | A. F. Filippov, Differential equations with discontinuous right-hand side, Dordrecht: Kluwer Academic, 1988. http://dx.doi.org/10.1016/0022-247X(91)90044-Z |
[35] |
X. Chen, L. Huang, A Filippov system describing the effect of prey refuge use on a ratio-dependent predator-prey model, J. Math. Anal. Appl., 428 (2015), 817â€"837. http://dx.doi.org/10.1016/j.jmaa.2015.03.045 doi: 10.1016/j.jmaa.2015.03.045
![]() |
[36] |
A. Wang, Y. Xiao, Sliding bifurcation and global dynamics of a Filippov epidemic model with vaccination, Int. J. Bifurcat. Chaos, 23 (2013), 1350144. http://dx.doi.org/10.1142/S0218127413501447 doi: 10.1142/S0218127413501447
![]() |
[37] |
M. di Bernardo, C. J. Budd, A. R. Champneys, P. Kowalczyk, A. B. Nordmark, Bifurcation in nonsmooth dynamical systems, SIAM Rev., 50 (2008), 629â€"701. http://dx.doi.org/10.1137/050625060 doi: 10.1137/050625060
![]() |
[38] |
Y. A. Kuznetsov, S. Rinaldi, A. Gragnani, One parameter bifurcations in planar Filippov systems, Int. J. Bifurcat. Chaos, 13 (2003), 2157â€"2188. http://dx.doi.org/10.1142/S0218127403007874 doi: 10.1142/S0218127403007874
![]() |
[39] |
P. V. D. Driessche, J. Watmough, Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission, Math. Biosci., 180 (2002), 29â€"48. http://dx.doi.org/10.1016/S0025-5564(02)00108-6 doi: 10.1016/S0025-5564(02)00108-6
![]() |
[40] | Z. Ma, Y. Zhou, C. Li, Qualitative and stability methods for ordinary differential equations, Beijing: Science Press, 2015. |
[41] |
R. M. Corless, G. H. Gonnet, D. E. G. Hare, D. J. Jeffrey, D. E. Kunth, On the Lambert W function, Adv. Comput. Math., 5 (1996), 329â€"359. http://dx.doi.org/10.1007/BF02124750 doi: 10.1007/BF02124750
![]() |
1. | Dongshu Wang, Shifan Luo, Wenxiu Li, Global Dynamic Analysis of a Discontinuous Infectious Disease System with Two Thresholds, 2022, 32, 0218-1274, 10.1142/S0218127422502157 | |
2. | Hany A. Hosham, Thoraya N. Alharthi, Bifurcation and chaos in simple discontinuous systems separated by a hypersurface, 2024, 9, 2473-6988, 17025, 10.3934/math.2024826 | |
3. | Dongshu Wang, Shifan Luo, Wenxiu Li, Global dynamics of a non-smooth SIV system with uncertain effective vaccine protection rate, 2024, 112, 0924-090X, 8739, 10.1007/s11071-024-09499-7 |
Case | α | β | μ | γ | ϕ | θ | Ic | f |
Figure 7(a) | 0.3 | 0.6 | 0.3 | 0.1 | 0.1 | 0.6 | 0.5 | 0.3 |
Figure 7(b) | 0.4 | 0.8 | 0.4 | 0.02 | 0.5 | 0.3 | 0.45 | 0.4 |
Figure 7(c) | 0.05 | 0.6 | 0.43 | 0.1 | 0.1 | 0.4 | 0.06 | 0.05 |
Figure 7(d) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.31 |
Figure 7(e) | 0.25 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.31 |
Figure 8(a) | 0.3 | 0.7 | 0.3 | 0.2 | 0.1 | 0.4 | 0.5 | 0.1 |
Figure 8(b) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.5 | 0.3 |
Figure 8(c) | 0.05 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.5 | 0.05 |
Figure 8(d) | 0.3 | 0.6 | 0.1 | 0.1 | 0.1 | 0.6 | 0.5 | 0.3 |
Figure 8(e) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.3 |
Figure 8(f) | 0.05 | 0.8 | 0.43 | 0.1 | 0.1 | 0.4 | 0.2 | 0.05 |
Case | Condition | Equilibria | Global dynamics |
R20<R10<1 | Er0 | E0 is GAS (see Fig. 6) | |
R20<1<R10 | Ic>I1 | Ev0,Er1 | E1 is GAS (see Fig. 7 (a), (b), (c)) |
R20<1<R10 | Ic<I1 | Ev0,Ev1,Ep | Ep is GAS (see Fig. 7 (d), (e)) |
1<R20<R10 | Ic>I1 | Er1,Ev2 | E1 is GAS (see Fig. 8 (a), (b), (c)) |
1<R20<R10 | I2<Ic<I1 | Ev1,Ev2,Ep | Ep is GAS (see Fig. 8 (d), (e)) |
1<R20<R10 | Ic<I2 | Ev1,Er2 | E2 is GAS (see Fig. 8 (f)) |
Case | α | β | μ | γ | ϕ | θ | Ic | f |
Figure 7(a) | 0.3 | 0.6 | 0.3 | 0.1 | 0.1 | 0.6 | 0.5 | 0.3 |
Figure 7(b) | 0.4 | 0.8 | 0.4 | 0.02 | 0.5 | 0.3 | 0.45 | 0.4 |
Figure 7(c) | 0.05 | 0.6 | 0.43 | 0.1 | 0.1 | 0.4 | 0.06 | 0.05 |
Figure 7(d) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.31 |
Figure 7(e) | 0.25 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.31 |
Figure 8(a) | 0.3 | 0.7 | 0.3 | 0.2 | 0.1 | 0.4 | 0.5 | 0.1 |
Figure 8(b) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.5 | 0.3 |
Figure 8(c) | 0.05 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.5 | 0.05 |
Figure 8(d) | 0.3 | 0.6 | 0.1 | 0.1 | 0.1 | 0.6 | 0.5 | 0.3 |
Figure 8(e) | 0.3 | 0.9 | 0.3 | 0.1 | 0.4 | 0.4 | 0.3 | 0.3 |
Figure 8(f) | 0.05 | 0.8 | 0.43 | 0.1 | 0.1 | 0.4 | 0.2 | 0.05 |
Case | Condition | Equilibria | Global dynamics |
R20<R10<1 | Er0 | E0 is GAS (see Fig. 6) | |
R20<1<R10 | Ic>I1 | Ev0,Er1 | E1 is GAS (see Fig. 7 (a), (b), (c)) |
R20<1<R10 | Ic<I1 | Ev0,Ev1,Ep | Ep is GAS (see Fig. 7 (d), (e)) |
1<R20<R10 | Ic>I1 | Er1,Ev2 | E1 is GAS (see Fig. 8 (a), (b), (c)) |
1<R20<R10 | I2<Ic<I1 | Ev1,Ev2,Ep | Ep is GAS (see Fig. 8 (d), (e)) |
1<R20<R10 | Ic<I2 | Ev1,Er2 | E2 is GAS (see Fig. 8 (f)) |