Research article

Dynamical analysis of a stochastic SIRS epidemic model with saturating contact rate

  • Received: 22 June 2020 Accepted: 24 August 2020 Published: 08 September 2020
  • In this paper, a stochastic SIRS epidemic model with saturating contact rate is constructed. First, for the deterministic system, the stability of the equilibria is discussed by using eigenvalue theory. Second, for the stochastic system, the threshold conditions of disease extinction and persistence are established. Our results indicate that a large environmental noise intensity can suppress the spread of disease. Conversely, if the intensity of environmental noise is small, the system has a stationary solution which indicates the disease is persistent. Eventually, we introduce some computer simulations to validate the theoretical results.

    Citation: Yang Chen, Wencai Zhao. Dynamical analysis of a stochastic SIRS epidemic model with saturating contact rate[J]. Mathematical Biosciences and Engineering, 2020, 17(5): 5925-5943. doi: 10.3934/mbe.2020316

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  • In this paper, a stochastic SIRS epidemic model with saturating contact rate is constructed. First, for the deterministic system, the stability of the equilibria is discussed by using eigenvalue theory. Second, for the stochastic system, the threshold conditions of disease extinction and persistence are established. Our results indicate that a large environmental noise intensity can suppress the spread of disease. Conversely, if the intensity of environmental noise is small, the system has a stationary solution which indicates the disease is persistent. Eventually, we introduce some computer simulations to validate the theoretical results.


    Recently, a new type of pneumonia caused by the coronavirus, named COVID-19, is spreading around the world. The issue of infectious diseases has once again aroused people's great concern. How to prevent and control infectious diseases has been an important subject facing human beings[1,2,3,4,5,6,7,8]. The SIR model assumes that the infected person can obtain permanent immunity after recovery. However, for smallpox, cholera, malaria and other diseases, individuals recovered from treatment can return to the susceptible category after temporary immunization, which can be described by SIRS model. Moreover, for some bacterial infectious diseases, such as meningitis and sexually transmitted diseases, some individuals can not produce effective antibodies after treatment and may be infected again. Others may gain temporary immunity, but then lose immunity and become susceptible [9,10,11,12]. Literature [10] established an SIRS model with a general population-size dependent contact rate λ(N) and proportional transfer rate from the infective class to susceptible class. The authors studied the threshold conditions of disease extinction and discussed the stability of disease-free equilibrium and endemic equilibrium.

    Infection rate is an important index to measure the intensity of disease transmission. Employing an appropriate infection rate based on a specific disease for the mathematical model plays a vital role in the disease prevention and control. In the literature [13], Thieme and Castillo-Chavez proposed the incidence βϱ(N(t))S(t)I(t)N(t), where N(t) represents the total population. On that basis, Heesterbeek et al. [14] gave the following saturating contact rate

    ϱ(N(t))=bN(t)1+bN(t)+1+2bN(t).

    Obviously, ϱ(N(t)) is a non-decreasing function of N(t). ϱ(N(t))N(t) is a non-increasing function of N(t). If N(t) is sufficiently small, ϱ(N(t))bN. Conversly, if N(t) is fully large, ϱ(N(t))1. Compared with the bilinear incidence βS(t)I(t) and the standard incidence βS(t)I(t)N(t), the saturating contact rate is more closer to the transmission of many diseases. The saturated contact rate is widely used in the study of infectious disease modeling. For example, Zhang et al.[15] constructed an SEIS model with general saturated incidence rate, and proved the global asymptotic stability of the endemic equilibrium by using the autonomous convergence theorem. Lan et al.[16] considered an SIS epidemic model with saturating contact rate, by using Itô's formula, the conditions for disease extinction and the existence of stationary solutions were obtained. In reference [11], Li et al. established an SIRS epidemic model with a general incidence, which considered both the transfer from the infected to the susceptible and the transfer from the recovered to the susceptible. Motivated by the above literature, we formulate a deterministic SIRS epidemic model with saturating contact rate and transfer from infectious to susceptible:

    {dS(t)dt=ΛuS(t)βbS(t)I(t)g(N(t))+γ1I(t)+δR(t),dI(t)dt=βbS(t)I(t)g(N(t))(u+γ1+γ2+α)I(t),dR(t)dt=γ2I(t)(u+δ)R(t), (1.1)

    where g(N(t))=1+bN(t)+1+2bN(t), N(t)=S(t)+I(t)+R(t) is the total population. S(t), I(t), R(t) represent the number of susceptible individuals, infected individuals and recovered individuals, respectively. Λ is the recruitment rate of susceptible individuals. u denotes the natural mortality rate. α represents the mortality rate caused by diseases. γ1 is the transfer rate from the infected individuals to the susceptible individuals. γ2 is the transfer rate from the infected individuals to the recovered individuals, and δ denotes the immunity loss rate.

    Due to the influence of environmental noise, the prevalence and transmission of diseases is often random. For example, the change of temperature and the influence of climate will lead to the fluctuation of mortality, morbidity and so on. In recent years, mathematical models of infectious diseases described by stochastic differential equations have been widely concerned [17,18,19,20,21,22]. There are many ways to construct a stochastic differential equation model, such as adding random perturbations to the parameters of deterministic system [23,24,25,26], or introducing proportional perturbations to state variables [27,28,29,30,31]. Recently, considering the effect of two different white noises on the model parameters, reference [32] established a stochastic SIS model with two correlated Brownian motions, in which the threshold of disease extinction as well as the variance and mean of the stationary distribution were investigated. In this paper, we consider that the incidence coefficient βb is disturbed by white noise, that is βbβb+σdB(t), where σ2 is the intensity of white noise, B(t) is defined as the standard Brownian motion in the complete probability space (Ω,F,{F}t0,P). Thus, the above model (1.1) is transformed into the following SIRS stochastic epidemic model:

    {dS(t)=[ΛuS(t)βbS(t)I(t)g(N(t))+γ1I(t)+δR(t)]dtσS(t)I(t)g(N(t))dB(t),dI(t)=[βbS(t)I(t)g(N(t))(u+γ1+γ2+α)I(t)]dt+σS(t)I(t)g(N(t))dB(t),dR(t)=[γ2I(t)(u+δ)R(t)]dt. (1.2)

    As far as we know, there have been a lot of studies on the epidemic model disturbed by environmental noise, but there are few stochastic models considering saturating contact rate and transfer from infectious to susceptible, especially the existence of stationary solution. The paper is organized as follows: In section 2, we give some notations and related lemmas. The thresholds of deterministic system and stochastic system are established in sections 3 and 4, respectively. Sufficient condition for the existence of stationary solution in the stochastic system (1.2) is provided in section 5. In section 6, we verify the results of theoretical derivation by numerical simulations.

    Throughout this paper, we let R3+={xi>0,i=1,2,3}. For an integrable function h on [0,+), we define h(t)=1tt0h(π)dπ. By using the methods from Liu et al. [33], we can prove that the region

    Γ={(S(t),I(t),R(t))R3+,Λu+αN(t)Λu}

    is a positively invariant set of system (1.2).

    Lemma 2.1. For any given initial value (S(0),I(0),R(0))R3+, then the model (1.2) has a unique positive solution (S(t),I(t),R(t)) on t0, and the solution will remain in R3+ with probability 1.

    Next, we will introduce some contents of stationary Markov process. The n-dimensional stochastic differential equation can be expressed by the following formula

    dx(t)=f(x(t),t)dt+li=1gi(x(t),t)dBi(t),tt0, (2.1)

    with the initial value x(t0)=x0Rn. Integrating from 0 to t for both sides of the Eq (2.1), one can obtain that

    x(t)=x0+tt0f(x(θ),θ)dθ+li=1tt0gi(x(θ),θ)dBi(θ),tt0. (2.2)

    Assume that the vectors f(x,t), g1(x,t), ..., gl(x,t)(tt0,xRn) are continuous functions of (x,t), satisfying the following conditions for some constant D,

    (A1)|f(x,t)f(y,t)|+li=1|gi(x,t)gi(y,t)|D|xy|,(A2)|f(x,t)|+li=1|gi(x,t)|D(1+|x|). (2.3)

    According to the literature [34] Theorem 3.7, we have the following Lemma.

    Lemma 2.2. Suppose that the coefficients of (2.2) are independent of t, and the conditions (2.3) hold in UG(G>0). There exists a function V(x)C2 with the following properties in Rn

    V(x)0andsup|x|>GLV(x)=MG(G), (2.4)

    where C2 represents a class of functions that are twice continuously differentiable relative to x in Rn. Further, we assume that there is at least one xRn, such that the process Xx(t) is regular. Then there exists a solution of system (2.2) which is a stationary Markov process.

    For Lemma 2.2, we need to note the following two points.

    Remark 2.1 (ⅰ) Condition (2.3) can be replaced by the global existence of solution of system (2.2) (see [35] Remark 5);

    (ⅱ) Condition (2.4) can be replaced by the weaker condition LV(x)1 (see [34] Chapter 4).

    In this section, we concentrate on the stability of the equilibria. Firstly, using N(t) as a variable instead of the variable S(t), we convert system (1.1) into the following form

    {dN(t)dt=ΛuN(t)αI(t),dI(t)dt=βbI(t)g(N(t))(N(t)I(t)R(t))(u+γ1+γ2+α)I(t),dR(t)dt=γ2I(t)(u+δ)R(t). (3.1)

    Obviously, the system (3.1) exists a boundary equilibrium P0=(Λu,0,0). Define

    R0=Λβbu(u+γ1+γ2+α)g(Λu).

    By direct calculation, if R0>1, we get system (3.1) has a positive equilibrium P=(N,I,R) with

    I=ΛuNα,R=γ2(ΛuN)α(u+δ),

    where N is the unique positive root of the following function

    ϕ(N)=βb[NΛuNαγ2(ΛuN)α(u+δ)](u+γ1+γ2+α)g(N).

    In fact, we have

    ϕ(Λu)=(u+γ1+γ2+α)g(Λu)(R01)>0

    and

    ϕ(Λu+α)=βbγ2Λ(u+α)(u+δ)(u+γ1+γ2+α)g(Λu+α)<0.

    Let dϕ(N)dN=0, it can be got

    N={α(u+δ)(u+γ1+γ2+α)β[(α+u)(u+δ)+uγ2]α(u+δ)(u+γ1+γ2+α)}212b,

    which implies that ϕ(N) is increasing if NN, and ϕ(N) is decreasing if N<N. Therefore, function ϕ(N) has a unique positive root, then the system (3.1) exists a unique positive equilibrium P=(N,I,R).

    Theorem 3.1. For system (3.1), we have

    (i) If R0<1, then P0=(Λu,0,0) is a unique stable equilibrium, which implies the disease of system (3.1) goes extinct.

    (ii) If R0>1, then P=(N,I,R) is a stable positive equilibrium, which implies the disease of system (3.1) is permanent.

    Proof. (ⅰ) The Jacobian matrix of system (3.1) evaluated at P0=(Λu,0,0) is

    J0=[uα00Λβbug(Λu)(u+γ1+γ2+α)00γ2(u+δ)],

    which has three eigenvalues:

    λ1=u<0,λ2=(u+δ)<0,λ3=(u+γ1+γ2+α)(R01)<0.

    Therefore, according to stability theory, P0 is stable if R0<1.

    (ⅱ) The Jacobian matrix at P=(N,I,R) is

    J=[uα0a21a22a230γ2(u+δ)],

    where

    a21=βbI[g(N)(NIR)(b+b1+2bN)]g2(N)=βbI(1+1+2bNbN1+2bN)g2(N)+βbI(I+R)g2(N)(b+b1+2bN)=βbIg(N)1+2bN+βbI(I+R)g2(N)(b+b1+2bN)>0,a22=βb(NR2I)g(N)(u+γ1+γ2+α)=βbIg(N)<0,a23=βbIg(N)=a22<0.

    Hence, the characteristic equation of J is

    λ3+a1λ2+a2λ+a3=0,

    where

    a1=u+βbIg(N)+u+δ>0,a2=α[βbIg(N)1+2bN+βbI(I+R)g2(N)(b+b1+2bN)]+(2u+δ+γ2)βbIg(N)+u(u+δ)>0

    and

    a3=α(u+δ)[βbIg(N)1+2bN+βbI(I+R)g2(N)(b+b1+2bN)]+u(u+δ+γ2)βbIg(N)>0.

    Then,

    a1a2a3=αua21[(2u+δ)(2u+δ+γ2)+uγ2]a22αa21a22+(2u+δ+γ2)a222+u(u+δ)(2u+δ)>0.

    Therefore, the equilibrium P is stable when it exists. This completes the proof of Theorem 3.1.

    In the previous section, we have obtained the threshold for ordinary differential equation (ODE) system (1.1). Similarly, the threshold of stochastic differential equation (SDE) system (1.2) is also crucial, which determines the extinction and persistence of the disease. {Define the following parameter

    Rs0=Λβbu(u+γ1+γ2+α+σ2Λ22u2g2(Λu))g(Λu),

    where g(x)=1+bx+1+2bx. In this section, we will prove that Rs0 is the threshold of system (1.2). Now, we give the following definition.

    Definition 4.1.

    (i) The disease I(t) is said to be extinct if limt+I(t)=0;

    (ii) The disease I(t) is said to be permanent in mean if there is a positive constant ϕ such that limtinfI(t)ϕ.

    Theorem 4.1. Set (S(t),I(t),R(t)) be a solution of system (1.2) with any given initial value (S(0),I(0),R(0))Γ.

    (i) If σ2>max{β2b22(u+γ1+γ2+α),βbug(Λu)Λ} holds, then

    limtsuplnI(t)tβ2b22σ2(u+γ1+γ2+α)<0a.s.,

    (ii) If Rs0<1 and σ2<βbug(Λu)Λ holds, then

    limtsuplnI(t)t(u+γ1+γ2+α+σ2Λ22u2g2(Λu))(Rs01)<0a.s.,

    which implies that the disease dies out with probability 1. In addition, we have

    limtS(t)=Λua.s.,
    limtR(t)=0a.s..

    Proof. Set V=lnI(t), by the Itô's formula, one can get

    d(lnI(t))=[βbS(t)g(N(t))(u+γ1+γ2+α)σ2S2(t)2g2(N(t))]dt+σS(t)g(N(t))dB(t)=Φ(S(t)g(N(t)))dt+σS(t)g(N(t))dB(t), (4.1)

    where Φ(x)=σ22x2+βbx(u+γ1+γ2+α).

    Case (ⅰ): If condition (ⅰ) is satisfied, then

    Φ(S(t)g(N(t)))=σ22(S(t)g(N(t))βbσ2)2+β2b22σ2(u+γ1+γ2+α)β2b22σ2(u+γ1+γ2+α). (4.2)

    Substituting (4.2) into (4.1), one can obtain that

    d(lnI(t))[β2b22σ2(u+γ1+γ2+α)]dt+σS(t)g(N(t))dB(t). (4.3)

    By using the strong law of large numbers for martingales, we obtain

    limtt0σS(ξ)g(N(ξ))dξt=0.

    Integrating from 0 to t, dividing by t, and taking superior limit on both sides of Eq (4.3) yields

    limtsuplnI(t)tβ2b22σ2(u+γ1+γ2+α)<0.a.s. (4.4)

    Case (ⅱ): If condition (ⅱ) Rs0<1 and σ2<βbug(Λu)Λ are satisfied, then

    Φ(S(t)g(N(t)))=σ22(S(t)g(N(t))βbσ2)2+β2b22σ2(u+γ1+γ2+α)σ22(Λug(Λu)βbσ2)2+β2b22σ2(u+γ1+γ2+α)=(u+γ1+γ2+α+σ2Λ22u2g2(Λu))(Rs01). (4.5)

    From Eq (4.1), one can get

    limtsuplnI(t)t(u+γ1+γ2+α+σ2Λ22u2g2(Λu))(Rs01)<0a.s.. (4.6)

    The inequalities (4.4) and (4.6) imply limtI(t)=0 and the disease goes to extinction.

    Next, adding up the three equations of system (1.2), integrating both sides from 0 to t and dividing by t, one can see that

    S(t)S(0)t+I(t)I(0)t+δu+δR(t)R(0)t=ΛuS(t)(u+α+uγ2u+δ)I(t). (4.7)

    So, from Eq (4.7) we have

    S(t)=Λu(u+αu+γ2u+δ)I(t)Θ(t), (4.8)

    where Θ(t)=1u[S(t)S(0)t+I(t)I(0)t+δu+δR(t)R(0)t]. Obviously, limtΘ(t)=0 and we have

    limtS(t)=Λua.s..

    Similarly, from the third equation of the system (1.2) yields

    R(t)=γ2u+δI(t)R(t)R(0)(u+δ)t. (4.9)

    Let t, we get that

    limtR(t)=0a.s.

    This finishes the proof.

    Theorem 4.2. If Rs0>1, the disease is persistence in mean. Moreover, we have

    limtinfI(t)I>0,limtinfΛuS(t)(u+αu+γ2u+δ)I>0,limtinfR(t)γ2u+δI>0,

    where

    I=u(u+δ)[u+γ1+γ2+α+Λ2σ22u2g2(Λu)]g(Λu)(Rs01)βb[(u+α)(u+δ)+γ2u].

    Proof. In view of Eq (4.1), we have

    d(lnI(t))[βbS(t)g(Λu)(u+γ1+γ2+α)σ2Λ22u2g2(Λu)]dt+σS(t)g(N(t))dB(t). (4.10)

    Integrating from 0 to t and dividing by t on both sides of Eq (4.10), one can get that

    lnI(t)lnI(0)tβbg(Λu)S(t)(u+γ1+γ2+α)σ2Λ22u2g2(Λu)+t0σS(ξ)g(N(ξ))dξt. (4.11)

    Substituting Eq (4.8) into Eq (4.11), we can get

    lnI(t)lnI(0)t[u+γ1+γ2+α+σ2Λ22u2g2(Λu)](Rs01)βbΘ(t)ug(Λu)+t0σS(ξ)g(N(ξ))dξtβb[(u+α)(u+δ)+γ2u]u(u+δ)g(Λu)I(t). (4.12)

    Hence,

    lnI(t)[u+γ1+γ2+α+σ2Λ22u2g2(Λu)](Rs01)t+F(t)βb[(u+α)(u+δ)+γ2u]u(u+δ)g(Λu)t0I(ξ)dξ. (4.13)

    where F(t)=lnI(0)+t0σS(ξ)g(N(ξ))dξβbtΘ(t)ug(Λu). Obviously, limtF(t)t=0a.s.. From Lemma 1 in [12], we obtain

    limtinfI(t)u(u+δ)[u+γ1+γ2+α+Λ2σ22u2g2(Λu)]g(Λu)(Rs01)βb[(u+α)(u+δ)+γ2u]=I.

    According to Eqs (4.8) and (4.9), we can see that

    limtinfΛuS(t)=(u+αu+γ2u+δ)limtinfI(t)(u+αu+γ2u+δ)I

    and

    limtinfR(t)=γ2u+δlimtinfI(t)γ2u+δI.

    The proof of Theorem 4.2 is completed.

    Remark 4.1. According to Theorem 4.1 (i), if the intensity of white noise is large enough that the condition σ2>max{β2b22(u+γ1+γ2+α),βbug(Λu)Λ} holds, then the disease goes to extinction. Therefore, a large environmental nose intensity can suppress the spread of disease. In addition, by comparing the thresholds of systems (1.2) and (1.1), it can be found that if the intensity of environmental noise σ2=0, then Rs0=R0; if σ20, then Rs0<R0. When Rs0<1<R0, the deterministic system (1.1) has a stable positive equilibrium, while the disease of the stochastic system (1.2) dies out with probability 1. This means that the presence of environmental noise is conducive to disease control.

    Theorem 5.1. If Rs0>1, there exists a solution of system (1.2) which is a stationary Markov process.

    Proof. Let (S(t),I(t),R(t)) be a solution of system (1.2) with any given initial value (S(0),I(0),R(0))Γ. Then we construct a C2-function G as following:

    G(S(t),I(t),R(t))=M(lnI(t)c1lnS(t)c2g2(N(t))+4bc2g(Λu)u+δR(t))lnS(t)lnR(t)ln(N(t)Λu+α)ln(ΛuN(t))=MV1+V2+V3+V4+V5,

    where V1=lnI(t)c1lnS(t)c2g2(N(t))+4bc2g(Λu)u+δR(t), V2=lnS(t), V3=lnR(t), V4=ln(N(t)Λu+α), V5=ln(ΛuN(t)), c1=u+γ1+γ2+α+Λ2σ22u2g2(Λu)u and c2=u+γ1+γ2+α+Λ2σ22u2g2(Λu)2bΛg(Λu). The M is a positive constant and satisfies the following condition

    3M[u+γ1+γ2+α+Λ2σ22u2g2(Λu)](3Rs01)+βbΛug(Λu)+σ2Λ22u2g2(Λu)+4u+δ+α2. (5.1)

    Furthermore, G(S(t),I(t),R(t)) is a continuous function, which exists a minimum point (S0,I0,R0). Next, we define a nonnegative C2-function V

    V(S(t),I(t),R(t))=G(S(t),I(t),R(t))G(S0,I0,R0).

    Applying Itô's formula for V1, we can see

    LV1=1I(t)[βbS(t)I(t)g(N(t))(u+γ1+γ2+α)I(t)]+σ2S2(t)g2(N(t))c1S(t)[ΛuS(t)βbS(t)I(t)g(N(t))+γ1I(t)+δR(t)]+c1σ2I2(t)2g2(N(t))2bc2g(N(t))(1+11+2bN(t))(ΛuN(t)αI(t))+4bc2g(Λu)u+δ[γ2I(t)(u+δ)R(t)]βbS(t)g(N(t))c1ΛS(t)2bΛc2g(N(t))+(u+γ1+γ2+α)+Λ2σ22u2g2(Λu)+c1u+c1βbI(t)g(Λu+α)+c1σ2I2(t)2g2(Λu+α)+2bΛc2g(Λu)4bc2g(Λu)R(t)+2bαc2g(N(t))(1+11+2bN(t))I(t)+4bc2γ2g(Λu)u+δI(t)332Λ2βb2c1c2+3[u+γ1+γ2+α+Λ2σ22u2g2(Λu)]+c1σ2I2(t)2g2(Λu+α)+[c1βbg(Λu+α)+4bαc2g(Λu)+4bc2γ2g(Λu)u+δ]I(t)=3[u+γ1+γ2+α+Λ2σ22u2g2(Λu)](3Rs01)+c1σ2I2(t)2g2(Λu+α)+[c1βbg(Λu+α)+4bc2g(Λu)(α+γ2u+δ)]I(t). (5.2)

    Similarly, we have

    LV2=ΛS(t)+u+βbI(t)g(N(t))γ1I(t)S(t)δR(t)S(t)+σ2I2(t)2g2(N(t))ΛS(t)+u+βbΛug(Λu)+σ2Λ22u2g2(Λu), (5.3)
    LV3=γ2I(t)R(t)+u+δ, (5.4)
    LV4=ΛuN(t)αI(t)N(t)Λu+α=u+αα(S(t)+R(t))N(t)Λu+α, (5.5)
    LV5=ΛuN(t)αI(t)ΛuN(t)=uαI(t)ΛuN(t). (5.6)

    Therefore, in view of Eqs (5.2)–(5.6), we get that

    LV3M[u+γ1+γ2+α+Λ2σ22u2g2(Λu)](3Rs01)+Mc1σ2I2(t)2g2(Λu+α)ΛS(t)+M[c1βbg(Λu+α)+4bc2g(Λu)(α+γ2u+δ)]I(t)+u+βbΛug(Λu)+σ2Λ22u2g2(Λu)γ2I(t)R(t)+u+δ+u+αα(S(t)+R(t))N(t)Λu+α+uαI(t)ΛuN(t)2+M[c1βbg(Λu+α)+4bc2g(Λu)(α+γ2u+δ)]I(t)+Mc1σ2I2(t)2g2(Λu+α)ΛS(t)γ2I(t)R(t)α(S(t)+R(t))N(t)Λu+ααI(t)ΛuN(t):=2+MλI(t)+Mc1σ2I2(t)2g2(Λu+α)ΛS(t)γ2I(t)R(t)α(S(t)+R(t))N(t)Λu+ααI(t)ΛuN(t),

    where λ=c1βbg(Λu+α)+4bc2g(Λu)(α+γ2u+δ).

    Define the following bounded closed set

    Dε={(S(t),I(t),R(t))Γ:εS(t)Λu,εI(t)Λu,ε2R(t)Λu,
    Λu+α+ε3N(t)Λuε3},

    where ε is a sufficiently small constant satisfying the following inequalities (5.7)–(5.11)

    2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)Λε1, (5.7)
    2+Mλε+Mc1σ2ε22g2(Λu+α)1, (5.8)
    2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)γ2ε1, (5.9)
    2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)α(1+ε)ε21, (5.10)
    2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)αε21. (5.11)

    For convenience, we divide ΓDε into five domains

    D1={(S(t),I(t),R(t))Γ,0<S(t)<ε},D2={(S(t),I(t),R(t))Γ,0<I(t)<ε},D3={(S(t),I(t),R(t))Γ,I(t)ε,0<R(t)<ε2},D4={(S(t),I(t),R(t))Γ,S(t)ε,I(t)ε,R(t)ε2,Λu+α<N(t)<Λu+α+ε2},D5={(S(t),I(t),R(t))Γ,S(t)ε,I(t)ε,R(t)ε2,Λuε2<N(t)<Λu}.

    So, we only need to prove LV1 on the above five domains.

    Case ⅰ: If (S(t),I(t),R(t))D1, from Eq (5.7), one can obtain that

    LV2+MλI(t)+Mc1σ2I2(t)2g2(Λu+α)ΛS(t)2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)Λε1. (5.12)

    Case ⅱ: If (S(t),I(t),R(t))D2, in view of Eq (5.8), we have

    LV2+MλI(t)+Mc1σ2I2(t)2g2(Λu+α)2+Mλε+Mc1σ2ε22g2(Λu+α)1. (5.13)

    Case ⅲ: If (S(t),I(t),R(t))D3, according to Eq (5.9), we obtain

    LV2+MλI(t)+Mc1σ2I2(t)2g2(Λu+α)γ2I(t)R(t)2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)γ2ε1. (5.14)

    Case ⅳ: If (S(t),I(t),R(t))D4, by Eq (5.10), one can see that

    LV2+MλI(t)+Mc1σ2I2(t)2g2(Λu+α)α(S(t)+R(t))N(t)Λu+α2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)α(1+ε)ε21. (5.15)

    Case ⅴ: If (S(t),I(t),R(t))D5, in view Eq (5.11), we derive

    LV2+MλI(t)+Mc1σ2I2(t)2g2(Λu+α)αI(t)ΛuN(t)2+MλΛu+Mc1σ2Λ22u2g2(Λu+α)αε21. (5.16)

    Consequently, for a sufficiently small ε, we have

    LV(S(t),I(t),R(t))1,for(S(t),I(t),R(t))ΓDε.

    In view of Lemma 2.2, there exists a solution of system (1.2) which is a stationary Markov process. This completes the proof.

    Remark 5.1. Theorem 5.1 shows that if the intensity of white noise is small enough to make Rs0>1, then the system (1.2) has a stationary solution. That is to say, disease will exist for a long time and form endemic disease.

    In this paper, we study the dynamics of a stochastic SIRS epidemic model with saturating contact rate. Firstly, the threshold of disease extinction for deterministic system (1.1) is obtained by using the Jacobian matrix. If R0<1, system (1.1) has a unique stable equilibrium and the disease goes to extinct. If R0>1, system (1.1) forms endemic disease after a sufficiently long time. Secondly, the threshold parameter Rs0 of stochastic system (1.2) is established. If the intensity of the white noise is small enough to satisfy the condition Rs0>1, the disease is persistent. Otherwise, the disease will die out. Finally, we prove that there exists a stationary solution under condition Rs0>1 in system (1.2).

    In order to demonstrate the above theoretical derivation, we use MATLAB software to carry out some numerical simulations. Next, we choose the relevant parameters of system (1.1) as follows:

    Λ=1, u=0.1, b=0.6, δ=0.13, γ1=0.1, γ2=0.08, α=0.12.

    Firstly, we simulate the deterministic system and set β=0.66. By an ordinary computation, R0=0.9335<1. From the first condition of the Theorem 3.1, one can obtain that the system (1.1) has a unique stable equilibrium point E0=(10,0,0) (Figure 1). Furthermore, if we increase β to 0.8, in this case, we have R0=1.1315>1. The condition (ⅱ) in Theorem 3.1 is established, then by Theorem 3.1, the disease of system (1.1) is persistent (Figure 2).

    Figure 1.  Numerical simulation of the deterministic system (1.1), where Λ=1, u=0.1, b=0.6, δ=0.13, γ1=0.1, γ2=0.08, α=0.12,β=0.66,R0=0.9335<1.
    Figure 2.  Computer simulation of the deterministic system (1.1), where Λ=1, u=0.1, b=0.6, δ=0.13, γ1=0.1, γ2=0.08, α=0.12,β=0.8,R0=1.1315>1.

    Next, we perform numerical simulations on stochastic system. We keep the parameters of deterministic system (1.1) unchanged, and only select different intensities of white noise σ in system (1.2).

    Case ⅰ: In order to verify the conclusion (ⅰ) of the Theorem 4.1, we let σ=0.8. By computing, we can obtain σ2=0.64, g(Λu)=10.6056 and max{β2b22(u+γ1+γ2+α),βbug(Λu)Λ}=0.5091, which implies the parameters satisfy the condition (ⅰ) σ2>max{β2b22(u+γ1+γ2+α),βbug(Λu)Λ}. This shows that the disease in system (1.2) dies out with probability 1 (Figure 3).

    Figure 3.  Time series diagram of (S(t),I(t),R(t)), where Λ=1, u=0.1, b=0.6, δ=0.13, γ1=0.1, γ2=0.08, α=0.12,β=0.8,σ=0.8,R0=1.1315>1.

    Case ⅱ: In Figure 4, we assume that σ=0.45. It is not difficult to obtain that σ satisfies the second condition of Theorem 4.1. {Then, we have Rs0=0.9236<1 and 0.2025=σ2<βbug(Λu)Λ=0.5091.} As can be seen from Figure 4, the disease is going extinct.

    Figure 4.  Time series diagram of (S(t),I(t),R(t)), where Λ=1, u=0.1, b=0.6, δ=0.13, γ1=0.1, γ2=0.08, α=0.12,β=0.8,σ=0.45,R0=1.1315>1,Rs0=0.9236.

    Case ⅲ: If σ=0.1, by calculation, we get Rs0=1.1190>1. According to Theorem 4.2, the disease in system (1.2) is permanent in the time mean (Figure 5). Furthermore, by Theorem 5.1, the system (1.2) has a stationary solution (Figure 6).

    Figure 5.  Time series diagram of (S(t),I(t),R(t)), where Λ=1, u=0.1, b=0.6, δ=0.13, γ1=0.1, γ2=0.08, α=0.12,β=0.8,σ=0.1,R0=1.1315>1,Rs0=1.1190.
    Figure 6.  The density function distribution of (S(t),I(t),R(t)) with σ=0.1,Rs0=1.1190.

    This work is supported by Shandong Provincial Natural Science Foundation of China (No. ZR2019MA003).

    The authors declare that there is no conflict of interests regarding the publication of this paper.



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