Research article

Stationary distribution and extinction of a stochastic SEIQ epidemic model with a general incidence function and temporary immunity

  • Received: 25 May 2021 Accepted: 16 August 2021 Published: 27 August 2021
  • MSC : 34F05, 60H10, 92D30

  • In this paper, we propose a novel stochastic SEIQ model of a disease with the general incidence rate and temporary immunity. We first investigate the existence and uniqueness of a global positive solution for the model by constructing a suitable Lyapunov function. Then, we discuss the extinction of the SEIQ epidemic model. Furthermore, a stationary distribution for the model is obtained and the ergodic holds by using the method of Khasminskii. Finally, the theoretical results are verified by some numerical simulations. The simulation results show that the noise intensity has a strong influence on the epidemic spreading.

    Citation: Yuhuai Zhang, Xinsheng Ma, Anwarud Din. Stationary distribution and extinction of a stochastic SEIQ epidemic model with a general incidence function and temporary immunity[J]. AIMS Mathematics, 2021, 6(11): 12359-12378. doi: 10.3934/math.2021715

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  • In this paper, we propose a novel stochastic SEIQ model of a disease with the general incidence rate and temporary immunity. We first investigate the existence and uniqueness of a global positive solution for the model by constructing a suitable Lyapunov function. Then, we discuss the extinction of the SEIQ epidemic model. Furthermore, a stationary distribution for the model is obtained and the ergodic holds by using the method of Khasminskii. Finally, the theoretical results are verified by some numerical simulations. The simulation results show that the noise intensity has a strong influence on the epidemic spreading.



    Infectious diseases, such as AIDS, Ebola, Zika, influenza, Hepatitis B virus, COVID-19 and so on, are all public health concerns of the world. It has an important impact on public health, social and economic development and even human life[5,6,9,10]. By the reference of the World Health Organization (WHO) 1996: Nearly 50000 children, men and women die from infectious diseases every day[41,42]. For many diseases, there are no drugs or vaccines for treatment or cure. We are on the verge of a global epidemic crisis. No country can do without them. No country can ignore their threat any more, the Director-General of WHO says in the WHO report[41]. Thus, in order to better understand the transmission mechanism of infectious diseases, and obtain good methods to control the infectious diseases propagation, mathematicians have proposed many mathematical models to discuss the dynamic behavior of infectious disease transmission[2,16,17,22,35]. For instance, the SIS (Susceptible-Infectious-Susceptible) epidemic model[12,14,27], the SIR (Susceptible-Infected-Recovered) epidemic model[3,20,21], the SIRI (Susceptible-Infected-Recovered-Infected) epidemic model[33,37,44], the SIRS (Susceptible-Infected-Recovered-Susceptible) epidemic model[25,32], SEIR (Susceptible-Expose-Infected-Recovered) epidemic model[30,39,43] and the infectious diseases model with vaccination[4,28].

    In diseases such as influenza and COVID-19, some people can be isolated once they are found to have been infected with infectious disease in the exposed or infectious state. To portray the character of the quarantined state and combine with the characteristics of classical epidemic models, Chen et al.[8] proposed the infectious disease model with quarantined compartment as follows:

    {dS(t)dt=ΛβS(t)I(t)μS(t)+cI(t),dE(t)dt=βS(t)I(t)(μ+ε+δ1+γ1)E(t),dI(t)dt=εE(t)(μ+α+c+δ2+γ2)I(t),dQ(t)dt=δ1E(t)+δ2I(t)(μ+α+γ3)Q(t), (1.1)

    where S(t), E(t), I(t) and Q(t) represent the number of the susceptible, exposed, infected and quarantined individuals at any time t, respectively. The meanings of the parameters are shown in Table 1. In [8], many important results, such as the local and global asymptotic stability of the disease-free equilibrium and the endemic equilibrium of model (1.1), were obtained under certain conditions, and estimated the domain of attraction for the endemic equilibrium.

    Table 1.  The meaning of the parameters in model (1.1).
    ParametersMeaning
    Λ The recruitment rate of the population
    β The transmission rate that the susceptible people come into the exposed people
    μ The natural death rate
    c The rate that the infected people recover and turn into the susceptible people
    ε The rate at which some exposed individuals become infected individuals
    α The mortality rate of infected and quarantined individuals due to illness
    δ1 The quarantined rate of the exposed individuals
    δ2 The quarantined rate of the infected individuals
    γ1 The recovery rate of the exposed individuals
    γ2 The recovery rate of the infected individuals
    γ3 The recovery rate of the quarantined individuals

     | Show Table
    DownLoad: CSV

    As is known to all, the incidence rate of infectious diseases plays a key role in the investigation of mathematical epidemiology. Most classical infectious disease models employ bilinear incidence rates, which is based on the homogeneous mixing assumption[2,29,45]. However, experiments [11] have strongly suggested that the incidence is an increasing function of the parasite dose, and is usually sigmoidal in shape (see, for example, [36]). As a result, Anderson and May [1] proposed a saturated incidence αSI1+βS; Lv et al.[31] introduced a Beddington-DeAngelis incidence rate βxv1+mx+nv into the HIV model; Caraballo et al.[7] considered an incidence function (β1β2Im+I)SI to discuss the influence of media coverage on propagation dynamics. Motivated by the above discussion, we present the following SEIQ epidemic model with general incidence function:

    {dS(t)dt=ΛS(t)f(I(t))μS(t)+cI(t),dE(t)dt=S(t)f(I(t))(μ+ε+δ1+γ1)E(t),dI(t)dt=εE(t)(μ+α+c+δ2+γ2)I(t),dQ(t)dt=δ1E(t)+δ2I(t)(μ+α+γ3)Q(t), (1.2)

    where the meanings of all parameters in model (1.2) are consistent with that in model (1.1). By a simple calculation, we obtain a basic reproduction number

    R0=Λεf(0)μ(μ+ε+δ1+γ1)(μ+α+c+δ2+γ2).

    Similar to the proof method in [8], we also show that if R0<1, then system (1.2) has a unique free disease-equilibrium, which is globally asymptotically stable. The disease equilibrium is unique and also globally asymptotically stable when R0>1.

    On the other hand, due to the existence of environmental noise, the parameters involved in system (1.2) are not constants, and they always fluctuate near the average value. Therefore, numerous researchers considered the influence of random factors in the epidemic models and studied the dynamic behavior of stochastic epidemic models with general incidence rate[19,25,26]. Fan et al.[15] presented a stochastic delayed SIR epidemic model with generalized incidence rate and temporary immunity. On the basis of the strong law of large numbers, they established sufficient conditions for extinction and permanence in the mean. Fatini et al.[13] adopted parameter perturbation method to investigate the stationary distribution of a generalized SIRS epidemic model. They considered the parameter β fluctuates near the average value, and showed the extinction of the disease when Rs0<1 while the persistence in mean of the disease when Rs0>1. Liu et al.[24] considered a stochastic SIRS epidemic model with logistic growth and general nonlinear incidence rate. By constructing a suitable stochastic Lyapunov function, they obtain sufficient conditions for the existence and uniqueness of an ergodic stationary distribution of the positive solutions to the stochastic SIRS epidemic model.

    Based on the above concerns, in this paper, we try to do some work in this field, and discuss the existence of a stationary distribution of solutions of stochastic SEIQ epidemic model. Our method is similar to that of Wang et al.[40]. Now, we assume the environmental fluctuations are white noise type, which are directly proportional to S, E, I and Q, and influenced on dSdt, dEdt, dIdt and dQdt in model (1.1). Then we obtain the following stochastic SEIQ epidemic model corresponding to model (1.2):

    {dS(t)=[ΛS(t)f(I(t))μS(t)+cI(t)]dt+σ1S(t)dB1(t),dE(t)=[S(t)f(I(t))(μ+ε+δ1+γ1)E(t)]dt+σ2E(t)dB2(t),dI(t)=[εE(t)(μ+α+c+δ2+γ2)I(t)]dt+σ3I(t)dB3(t),dQ(t)=[δ1E(t)+δ2I(t)(α+μ+γ3)Q(t)]dt+σ4Q(t)dB4(t), (1.3)

    where Bi(t) are mutually independent standard one-dimensional motion of Brownian motions with Bi(0)=0, σ2i>0 mean the intensities of the white noise, i=1,2,3,4. Furthermore, we assume that the contact between a susceptible individual and a infected individual is given by an incidence function f(), which satisfies the following conditions:

    (A1) f()C1(R+,R+) such that f(I)>0 and f(0)=0 I0;

    (A2) f(I)I is monotonically non-increasing on (0,) and f(I)>If(I) for all uR+.

    From (A2), one can see that f(I)<If(0) for all I>0. These assumptions are biologically motivated, see [13] in detail. Obviously, it includes the common incidence functions such as the linear function f(I)=βI and the saturation incidence function f(I)=βI1+aI, where β, a>0.

    As is known to all, in the deterministic epidemic model, the basic reproduction number and endemic equilibrium are two very important factors. Because the basic reproduction number represents the threshold of the epidemic spreading, and the endemic equilibrium represents the prevalence of the disease. However, the influence of environmental noises is taken into account, it is difficult to determine the threshold of stochastic epidemic model, and most stochastic models have no the endemic equilibrium. Therefore, the stationary distribution of stochastic models has been widely concerned. On the other hand, from the perspective of biomathematics, the existence and ergodicity of stationary distribution illustrates that infectious diseases will exist for a long time and continue to develop. Therefore, we concentrate on two points: (i) develop a stochastic SEIQ epidemic model with generalized incidence function Sf(I), and on the basis of the properties of f(I), prove the existence and uniqueness of the global positive solution. (ii) try to give the extinction threshold of the disease and investigate the stationary distribution of stochastic epidemic model with generalized incidence function.

    The paper is organized as follows. In Section 2, we introduce some basic definitions and related theories in this paper. In Section 3, we show the existence and uniqueness of the global positive solution of system (1.3) with any initial value. In Section 4, we give some sufficient conditions for extinction of the disease. In Section 5, we show the existence of a stationary distribution of solutions to model (1.3) by using the method of Khasminskii and constructing a suitable Lyapunov function. In the Section 6, some numerical simulations are presented to verify the theoretical results. The main results of this paper ends with conclusion in Section 7.

    Throughout the paper, let (Ω,F,P) be a complete probability space with filtration {Ft}t0 satisfying the usual conditions (i.e., it is right continuous and increasing while F0 contains all P-avoid set) and Bi(t) are denoted on the complete probability space. Denote R4+={xR4+:xi>0,i=1,2,3,4}, ab=max{a,b} and ab=min{a,b}, for all a,bR.

    For the four-dimensional stochastic differential equation

    dx(t)=g(x(t),t)dB(t)+f(x(t),t)dtfort0. (2.1)

    with the initial value x(0)=x0R4. Let C2,1(R4×(0,);R+) denote the family of all nonnegative functions V(x,t) which defined on R4×(0,) such that they are continuously twice differentiable in x and once in t. Define the differential operator L of (2.1) as follows[34]

    L=t+4i=1fi(x,t)xi+124i,j=1[gT(x,t)g(x,t)]2xixj.

    Acting L on VC2,1(R4×(0,);R+), we have

    LV(x,t)=Vt(x,t)+Vx(x,t)f(x,t)+12trace[Vxx(x,t)gT(x,t)g(x,t)],

    where Vt=Vt, Vx=(Vx1,Vx2,Vx3,Vx4), Vxx=(2Vxixj)4×4. Thus, by the Itô's formula, if x(t)R4, then

    dV(x(t),t)=LV(x(t),t)dt+g(x(t),t)Vx(x(t),t)dB(t).

    To obtain the stationary distribution of system (1.3), we propose some definitions and known results in the sequel. Let X(t) be homogeneous Markov process in the d-dimensional Euclidean space Rd, which satisfies the autonomous equation

    dX(t)=b(X)dt+dr=1gr(X)dBr(t). (2.2)

    It is well-known that the diffusion matrix corresponding to Eq (2.2) has the form

    A(X)=(aij(x)), where   aij(x):=dr=1gir(x)gjr(x). (2.3)

    Lemma 2.1. [23] Let URd be a bounded open domain with regular boundary Γ, which has the following properties:

    (H1) There exists a constant M>0; li,j=1aij(x)ξiξjM|ξ|2, for all xU and ξRd;

    (H2) There is a C2function V0 satisfying LV<0 for any xRdU.

    Then the Markov process X(t) admits a unique ergodic stationary distribution π(). In this situation,

    P{limT1TT0f(X(t))dt=Rdf(x)π(dx)}=1,  for  all  xRd,

    where f() is an integrable function with respect to the measure π.

    In order to investigate dynamics of an SEIQ model, the first concern is whether the solution is global and positive. In this section, we will construct a suitable Lyapunov function to verify the existence and uniqueness of global positive solutions of the model (1.3).

    Theorem 3.1. For any initial value (S(0),E(0),I(0),Q(0))R4+, a unique positive solution (S(t),E(t),I(t),Q(t)) of model (1.3) exists on t0 and the solution remains in R4+ with probability one, namely, the solution (S(t),E(t),I(t),Q(t))R4+ for all t0 almost surely.(a.s.)

    Proof. Since the coefficients of model (1.3) satisfy the local Lipschitz condition, for the initial value (S(0),E(0),I(0),Q(0))R4+, model (1.3) exists a unique local solution (S(t),E(t),I(t),Q(t)) on t[0,τe], where τe is the explosion time[34]. To prove the solution is global, we need to show τe= a.s.. Let n0 be large enough such that S(0), E(0), I(0) and Q(0) all lie within the interval [1n0,n0]. For every nn0, define the following sequence of stopping time

    τn=inf{t[0,τ):S(t)[1n,n]orE(t)[1n,n]orI(t)[1n,n]orQ(t)[1n,n]}, (3.1)

    where set inf=(in general, is as the empty set). Obviously, τn is increasing as n. Let τ=limnτn, then ττn a.s.. If we can verify τ= a.s., then τe= a.s. and (S(t),E(t),I(t),Q(t))R4+ a.s. for all t0. Namely, to complete the proof, we only need to prove τ= a.s.. If the statement is violated, then there exists a constant T>0 and ϵ(0,1) such that

    P{τnT}ϵ,nn0. (3.2)

    Define a non-negative C2function V: R4+R+

    V(S,E,I,Q)=(SaalnSa)+(E1lnE)+(I1lnI)+(Q1lnQ), (3.3)

    where a is a positive constant to be determined later. Applying Itô's formula[34], we get

    dV(S,E,I,Q)=LV(S,E,I,Q)dt+σ1(Sa)dB1(t)+σ2(E1)dB2(t)+σ3(I1)dB3(t)+σ4(Q1)dB4(t). (3.4)

    Where

    LV(S,E,I,Q)=(1aS)(ΛSf(I)μS+cI)+(11E)[Sf(I)(μ+ε+δ1+γ1)E]+(11I)[εE(μ+α+c+δ2+γ2)I]+(11Q)[δ1E+δ2I(μ+α+γ3)Q]+aσ21+σ22+σ23+σ242,=Λ+(a+3)μ+ε+δ1+γ1+2α+c+δ2+γ2+γ3μS(μ+γ1)E(μ+α+γ2)I(μ+α+γ3)Q+af(I)aΛSacISSf(I)EεEIδ1EQδ2IQ+aσ21+σ22+σ23+σ242,Λ+(a+3)μ+ε+δ1+γ1+2α+c+δ2+γ2+γ3+[af(0)(μ+α+γ2)]I+aσ21+σ22+σ23+σ242.

    Choose a=μ+α+γ2f(0) such that af(0)(μ+α+γ2)=0, then we obtain

    LV(S,E,I,Q)Λ+(μ+α+γ2f(0)+3)μ+ε+σ1+γ1+2α+c+σ2+γ2+γ3+aσ21+σ22+σ23+σ242:=K,

    where K is a suitable constant. Consequently,

    dV(S,E,I,Q)=Kdt+σ1(Sa)dB1(t)+σ2(E1)dB2(t)+σ3(I1)dB3(t)+σ4(Q1)dB4(t). (3.5)

    For any nn0, integrating the both sides of (3.5) from 0 to τnT, and taking the expectation, we have

    EV(S(τnT),E(τnT),I(τnT),Q(τnT))V(S(0),E(0),I(0),Q(0))+EτnT0KdtV(S(0),E(0),I(0),Q(0))+KT<.

    Moreover, we set Ωn={τnT} for any nn0, then (3.2) leads to P(Ωn)ϵ. For every ωΩn, at least one of S(τn,ω), E(τn,ω), I(τn,ω) or Q(τn,ω) equals to n or 1n. Thus, V(S(τn,ω),E(τn,ω),I(τn,ω),Q(τn,ω)) is no less than either

    (naalnna)(n1lnn)  or  (1na+aln(na))(1n1+lnn).

    It follows that

    V(S(ω,τn),E(ω,τn),I(ω,τn),Q(ω,τn))(naalnna)(n1lnn)(1na+aln(na))(1n1+lnn).

    Therefore,

    V(S(0),E(0),I(0),Q(0))+KTE[1Ωn(ω)V(S(τn,ω),E(τn,ω),I(τn,ω),Q(τn,ω))]ϵ[(naalnna)(n1lnn)(1na+aln(na))(1n1+lnn)],

    where 1Ωn means the indicator function of Ωn. Let n, we have

    >V(S(0),E(0),I(0),Q(0))+KT=,

    which leads to a contradiction. Therefore, the claim τ= a.s. hold. This completes the proof.

    Remark 3.1. Theorem 3.1 illustrates that for any positive initial value, model (1.3) has unique positive solution with probability one. Here, let N(t)=S(t)+E(t)+I(t)+Q(t), then

    dN(t)=[ΛμS(μ+γ1)E(μ+α+γ2)I(μ+α+γ3)Q]dt+σ1SdB1(t)+σ2EdB2(t)+σ3IdB3(t)+σ4QdB4(t),(ΛμN)dt+σ1SdB1(t)+σ2EdB2(t)+σ3IdB3(t)+σ4QdB4(t)

    Consider the following system

    {dX(t)=(ΛμX)dt+σ1SdB1(t)+σ2EdB2(t)+σ3IdB3(t)+σ4QdB4(t),X(0)=N(0).

    By Theorem 3.9 in [34], we have limtX(t)< a.s. Then according to the comparison theorem for stochastic differential equations[38], this yields lim suptN(t)< a.s.

    One of the main concerns of epidemiology is how we regulate the dynamics of the disease in order to eliminate it in a long term. In this section, we give some sufficient conditions for the extinction of the disease in model (1.3). For the convenience, we define

    x(t)t=1tt0x(s)dB(s).

    Lemma 4.1. [46] Let (S(t),E(t),I(t),Q(t)) be the solution of model (1.3) with initial value (S(0),E(0),I(0),Q(0))R4+. Then

    lim suptlnS(t)t=0,lim suptlnE(t)t=0,lim suptlnI(t)t=0,lim suptlnQ(t)t=0a.s. (4.1)

    Furthermore, if μ>σ21σ22σ23σ242, then

    limtt0S(s)dB1(s)t=0,limtt0E(s)dB2(s)t=0,limtt0I(s)dB3(s)t=0,limtt0Q(s)dB4(s)t=0a.s. (4.2)

    Define the parameter as follows:

    ˆR0=2Λεf(0)(μ+ε+δ1+γ1)μ[(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)ε2σ222].

    Theorem 4.1. Suppose (S(t),E(t),I(t),Q(t)) is the solution of model (1.3) with initial value (S(0),E(0),I(0),Q(0))R4+. If ˆR0<1 and μ>σ21σ22σ23σ242, then the solution (S(t),E(t),I(t),Q(t)) of model (1.3) has

    lim supt1tln[εE+(μ+ε+δ1+γ1)I](μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)ε2σ2222(μ+ε+δ1+γ1)2(ˆR01)<0a.s.

    and

    limtS(t)t=Λμ,limtQ(t)=0a.s.

    Proof. For model (1.3), we have

    d(S+E+I+Q)=[ΛμS(μ+γ1)E(μ+α+γ2)I(μ+α+γ3)Q]dt+σ1SdB1(t)+σ2EdB2(t)+σ3IdB3(t)+σ4QdB4(t)[Λμ(E+S+Q+I)]dt+σ1SdB1(t)+σ2EdB2(t)+σ3IdB3(t)+σ4QdB4(t) (4.3)

    Integrating the both sides of (4.3) from 0 to t and combining with Lemma 2, we obtain

    lim suptS+E+I+QtΛμa.s. (4.4)

    Let P(t)=εE(t)+(μ+ε+δ1+γ1)I(t), by the Ito's formula[34], we have

    dlnP(t)=LlnP(t)dt+εσ2EεE+(μ+ε+δ1+γ1)IdB2(t)+(μ+ε+δ1+γ1)σ3IεE+(μ+ε+δ1+γ1)IdB3(t), (4.5)

    where

    LlnP(t)=εSf(I)(μ+ε+δ1+γ1)(μ+α+c+δ2+γ2)IεE+(μ+ε+δ1+γ1)Iε2σ22E2+(μ+ε+δ1+γ1)2σ23I22[εE+(μ+ε+δ1+γ1)I]2εμ+ε+δ1+γ1Sf(I)I(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2)I2[εE+(μ+ε+δ1+γ1)I]2ε2σ22E2+(μ+ε+δ1+γ1)2σ23I22[εE+(μ+ε+δ1+γ1)I]2εμ+ε+δ1+γ1Sf(0)(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)I2+ε2σ222E2[εE+(μ+ε+δ1+γ1)I]2εμ+ε+δ1+γ1Sf(0)(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)ε2σ222[εE+(μ+ε+δ1+γ1)I]2(I2+E2)

    Obviously,

    [εE+(μ+ε+δ1+γ1)I]22[ε2E2+(μ+ε+δ1+γ1)2I2]2(μ+ε+δ1+γ1)2(I2+E2)

    Therefore, we have

    LlnP(t)εμ+ε+δ1+γ1Sf(0)(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)ε2σ2222(μ+ε+δ1+γ1)2

    Integrating the both sides of (4.5) from 0 to t, together with Lemma 2 and ˆR0<1, we obtain

    lim suptlnP(t)tΛεf(0)μ(μ+ε+δ1+γ1)(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)ε2σ2222(μ+ε+δ1+γ1)2=(μ+ε+δ1+γ1)2(μ+α+c+δ2+γ2+σ232)ε2σ2222(μ+ε+δ1+γ1)2(ˆR01)<0a.s.,

    which implies that

    limtE(t)=0,limtI(t)=0a.s. (4.6)

    Therefore, from the last equation of model (1.3), we can easily obtain limtQ(t)=0 a.s.

    On the other hand, for any small ξ>0, there exists T>0 such that Iξf(0) for tT a.s. Substituting Iξf(0) into the first equation of model (1.3), we obtain

    dS(t)(ΛμS(t)S(t)f(I(t)))dt+σ1S(t)dB1(t)(ΛμS(t)S(t)I(t)f(0))dt+σ1S(t)dB1(t)(Λ(μ+ξ)S(t))dt+σ1S(t)dB1(t)a.s. (4.7)

    Integrating the both sides of (4.6) from 0 to t and together with Lemma 2, we get

    lim inftStΛμ+ξa.s.

    The arbitrariness of ξ, one has

    lim inftStΛμa.s. (4.8)

    Thus, (4.4), (4.6) and (4.8) imply that

    limtSt=Λμa.s.

    This completes the proof.

    Remark 4.1. Theorem 4.1 illustrates that if ˆR0<1, the disease will go to extinct. Note the express of ˆR0, we notice that the larger the intensity of white noises are, the easier the extinction of the disease is. Thus, we can control the outbreak of disease by adjusting the intensity of environmental noises.

    In studying epidemiological dynamics, we are not only concerned about when the disease will be extinct in the population, but also about when the disease will persist in the population. For model (1.3), there is no endemic equilibrium. Therefore, in this section, we use the method of Khasminskii[23] to focus on the existence of a stationary distribution, which reflects whether the disease is prevalent.

    Theorem 5.1. Suppose

    ˆR0=Λf(0)ε(μ+σ212)(μ+ε+δ1+γ1+σ222)(μ+α+c+δ2+γ2+σ232)>1, (5.1)

    then for any initial value (E(0),S(0),Q(0),I(0))R4+, model (1.3) has a ergodic stationary distribution π().

    Proof. From (2.3), we know the diffusion matrix of model (1.3) has the form

    A(X):=diag(σ21S2,σ22E2,σ23I2,σ24Q2).

    According to Lemma 1, we only need to verify the conditions (H1) and (H2). Let M:=min(S,E,I,Q)¯UnR4+{σ21S2,σ22E2,σ23I2,σ24Q2}>0, then we have

    4i,j=1aij(x)ξiξj=σ21S2ξ21+σ22E2ξ22+σ23I2ξ23+σ24Q2ξ24M|ξ|2,

    for all (S,E,I,Q)¯Un:=[1/n,n]4 provided that nZ+ is sufficiently large. Note that ξ=(ξ1,ξ2,ξ3,ξ4)R4. Hence, the condition (H1) holds.

    To verify (H2), we denote

    b:=3(μ+σ212)23{[Λεf(0)(μ+ε+δ1+γ1+σ222)(μ+α+c+δ2+γ2+σ232)]13(μ+σ212)13}.

    Since μ+σ212>0 and ˆR0>1, we have b>0. Now, define the C2-function V():R4+R+ by

    V(S,E,I,Q):=pV1+V2lnSlnElnQ,

    with

    V1:=lnSc1lnEc2lnI  and  V2:=(S+E+I+Q)ρ+1,

    where

    c1=μ+σ212μ+ε+δ1+γ1+σ222,c2=μ+σ212μ+α+c+δ2+γ2+σ232.

    p and ρ are positive constants satisfying the conditions:

    pb+B2,0<ρ<2μσ21σ22σ23σ24,m:=(μ(μ+γ1)(μ+α+γ2)(μ+α+γ3))12ρ(σ21σ22σ23σ24),

    and

    A=sup(S,E,I,Q)R4+{Λ(ρ+1)(S+E+I+Q)ρ12(ρ+1)m(S+E+I+Q)ρ+1}<,B=sup(S,E,I,Q)R4+{12(ρ+1)m(Sρ+1+Eρ+1+Iρ+1+Qρ+1)+A+3μ+ε+α+γ1+γ3+σ21+σ22+σ242}.

    Therefore, we can easily check that

    lim infk,(S,E,I,Q)R4+UkV(S,E,I,Q)=+,

    where Uk=(1k,k)×(1k,k)×(1k,k)×(1k,k). Hence, V(S,E,I,Q) is a continuous function and has a minimum point(¯E0, ¯S0, ¯Q0, ¯I0) in the interior of R4+. Then, we define the non-negative C2-function ˜V:R4+R+ as follows:

    ˜V(S,E,I,Q)=V(S,E,I,Q)V(¯S0,¯E0,¯I0,¯Q0).

    Using Itô's formula[34], we obtain

    LV1=ΛSc1Sf(I)Ec2εEI+c1(μ+ε+δ1+γ1)+c2(μ+α+c+δ2+γ2)+f(I)+μcIS+σ21+c1σ22+c2σ232(ΛS+c1Sf(I)E+c2εEI)+f(0)I+μ+σ212+c1(μ+ε+δ1+γ1+σ222)+c2(μ+α+c+δ2+γ2+σ232)3(Λεf(I)Ic1c2)13+f(0)I+3(μ+σ212)=3(μ+σ212)23{[Λεf(I)I(μ+ε+δ1+γ1+σ222)(μ+α+c+δ2+γ2+σ232)]13(μ+σ212)13}+f(0)I

    Similarly, we have

    LV2=(ρ+1)(S+E+I+Q)ρ[ΛμS(μ+γ1)E(μ+α+γ2)I(μ+α+γ3)Q]+ρ2(ρ+1)(S+E+I+Q)ρ+1(σ21S2+σ22E2+σ23I2+σ24Q2)Λ(ρ+1)(S+E+I+Q)ρ(ρ+1)[μ(μ+γ1)(μ+α+γ2)(μ+α+γ3))](S+E+I+Q)ρ+1+12ρ(ρ+1)(σ21σ22σ23σ24)(S+E+I+Q)ρ+1A12(ρ+1)m(Sρ+1+Eρ+1+Iρ+1+Qρ+1).

    Moreover, we get

    L(lnS)=ΛS+f(I)cIS+μ+σ212ΛS+f(0)IcIS+μ+σ212,L(lnE)=Sf(I)E+μ+ε+δ1+γ1+σ222,

    and

    L(lnQ)=δ1EQδ2IQ+μ+α+γ3+σ242.

    Therefore, it follows that

    LV3p(μ+σ212)23{[Λεf(I)I(μ+ε+δ1+γ1+σ222)(μ+α+c+δ2+γ2+σ232)]13(μ+σ212)13}(p+1)f(0)IΛSSf(I)Eδ1EQδ2IQ+μ+σ212+μ+ε+δ1+γ1+σ222+μ+α+γ3+σ242+A12(ρ+1)m(Sρ+1+Eρ+1+Iρ+1+Qρ+1).

    Construct the following compact subset

    Dε1={(S,E,I,Q)R4+:ε1S1ε1,ε1I1ε1,ε31E1ε31,ε31Q1ε31},

    where ε1 is a sufficiently small constant such that

    Λε1+D1, (5.2)
    pˉb+(p+1))f(0)ε1+B1, (5.3)
    f(ε1)ε21+D1, (5.4)
    δ2ε21+D1, (5.5)
    14(ρ+1)m1ερ+11+F1, (5.6)
    14(ρ+1)m1ερ+11+G1, (5.7)
    14(ρ+1)m1ε3ρ+31+H1, (5.8)
    14(ρ+1)m1ε3ρ+31+J1, (5.9)

    here D F, G, H, J are positive constants, which satisfying

    D=sup(S,E,I,Q)R4+{12(ρ+1)m(Sρ+1+Eρ+1+Iρ+1+Qρ+1)+(p+1)f(0)I+μ+σ212+A+2μ+ε+δ1+γ1+α+γ3+σ22+σ242}, (5.10)
    F=sup(S,E,I,Q)R4+{14(ρ+1)mSρ+112(ρ+1)m(Eρ+1+Iρ+1+Qρ+1)+(p+1)f(0)I+μ+σ212+A+2μ+ε+δ1+γ1+α+γ3+σ22+σ242}, (5.11)
    G=sup(S,E,I,Q)R4+{14(ρ+1)mIρ+112(ρ+1)m(Sρ+1+Eρ+1+Qρ+1)+(p+1)f(0)I+μ+σ212+A+2μ+ε+δ1+γ1+α+γ3+σ22+σ242}, (5.12)
    H=sup(S,E,I,Q)R4+{14(ρ+1)mEρ+112(ρ+1)m(Sρ+1+Iρ+1+Qρ+1)+(p+1)f(0)I+μ+σ212+A+2μ+ε+δ1+γ1+α+γ3+σ22+σ242}, (5.13)
    J=sup(S,E,I,Q)R4+{14(ρ+1)mQρ+112(ρ+1)m(Sρ+1+Eρ+1+Iρ+1)+(p+1)f(0)I+μ+σ212+A+2μ+ε+δ1+γ1+α+γ3+σ22+σ242}, (5.14)

    and

    ˉb=3(μ+σ212)23{[Λεf(ε1)ε1(μ+ε+δ1+γ1+σ222)(μ+α+c+δ2+γ2+σ232)]13(μ+σ212)13}.

    For sufficiently small ε1, condition (5.3) holds due to pb+B2. For convenience of calculation, we divide the set R4+Dε1 into eight domains,

    D1={(S,E,I,Q)R4+:0<S<ε1},D2={(S,E,I,Q)R4+:0<I<ε1},D3={(S,E,I,Q)R4+:Sε1,Iε1,0<E<ε31},D4={(S,E,I,Q)R4+:Iε1,0<Q<ε31},D5={(S,E,I,Q)R4+:S>1ε1},D6={(S,E,I,Q)R4+:I>1ε1},D7={(S,E,I,Q)R4+:E>1ε31},D8={(S,E,I,Q)R4+:Q>1ε31}.

    then we will illustrate LV1 on the set R4+Dε1.

    Case 1. If (S,E,I,Q)D1, we obtain

    LVΛS+(p+1)f(0)I+μ+σ212+μ+ε+δ1+γ1+σ222+μ+α+γ3+σ242+A12(ρ+1)m(Sρ+1+Eρ+1+Iρ+1+Qρ+1)Λε1+D. (5.15)

    By inequality (5.2), we obtain LV1 for all (S,E,I,Q)D1.

    Making use of inequalities (5.3), (5.4) and (5.5), and being similar to the proof of Case 1, we make the conclusion that LV1 for all (S,E,I,Q)D2, (S,E,I,Q)D3 and (S,E,I,Q)D4.

    Case 2. If (S,E,I,Q)D5, we have that

    LV14(ρ+1)mSρ+1+(p+1)f(0)I+μ+σ212+μ+ε+δ1+γ1+σ222+μ+α+γ3+σ242+A14(ρ+1)mSρ+112(ρ+1)m(Eρ+1+Iρ+1+Qρ+1)14(ρ+1)m1ερ+1+F. (5.16)

    According to inequality (5.6), we achieve that LV1 for all (S,E,I,Q)D5. Furthermore, being similar to the proof of Case 2 and combining with (5.7), (5.8) and (5.9), the conclusion LV1 can be obtained for all (S,E,I,Q)D6, (S,E,I,Q)D7 and (S,E,I,Q)D8.

    On the basis of the above discussion, it follows that

    LV1,(S,E,I,Q)R4+Dε1. (5.17)

    which illustrates the condition (H2) of Lemma 1 is satisfied, and model (1.3) has a unique stationary distribution and the ergodicity holds. The proof is completed.

    Remark 5.1. Theorem 5.1 reveals that if ˆR0>1, model (1.3) has a unique stationary distribution, that is to say, the disease will persist. Note the express of ˆR0, we can see that the smaller the intensity of white noises are, the easier the persistence of the disease is. Especially, when σi=0,i=1,2,3,4, ˆR0 will degenerate into the basic reproduction number R0 of the deterministic model (1.2).

    In this section, we use two concrete examples to illustrate the obtained the theoretical results. For this purpose, we choose f(I)=βI1+nI with n=0.15 and use the Milstein method mentioned in [18] with time Δt=0.01, the following discretization system is obtained

    {Sk+1=Sk+(ΛβSkIk1+nIkμSk+cIk)Δt+σ1SkΔtτ1,k+σ212SkΔt(τ21,k1),Ek+1=Ek+[βSkIk1+nIk(μ+ε+δ1+γ1)Ek]Δt+σ2EkΔtτ2,k+σ222EkΔt(τ22,k1),Ik+1=Ik+[εEk(μ+α+c+δ2+γ2)Ik]Δt+σ3IkΔtτ3,k+σ232IkΔt(τ23,k1),Qk+1=Qk+[δ1Ek+δ2Ik(μ+α+γ3)Qk]Δt+σ4QkΔtτ4,k+σ242QkΔt(τ24,k1), (6.1)

    where τi,k(i=1,2,3,4) are four independent the Gaussian random variables with N(0,1).

    Example 6.1. Let Λ=0.4, β=0.07, μ=0.35, c=0.25, ε=0.5, δ1=0.05, γ1=0.05, α=0.1, δ2=0.2, γ2=0.1, γ3=0.03 and the initial values (S(0),E(0),I(0),Q(0))=(57,0,37,0). By a simple calculation, we obtain ˆR0=0.95<1 and μ=0.35>σ21σ22σ23σ242=0.32, so the condition of Theorem 4.1 holds. In other word, the disease will go to extinction exponentially, which is shown in Figure 1.

    Figure 1.  Trajectories of the solutions of model (1.3) with σ1=0.1, σ2=0.8, σ3=0.3, σ4=0.5 and parameters are given in Example 1.

    Example 6.2. Taking Λ=2, β=0.5, μ=0.25, c=0.25, ε=0.5, δ1=0.125, γ1=0.125, α=0.5, δ2=0.25, γ2=0.25, γ3=0.5 and the initial values (S(0),E(0),I(0),Q(0))=(6,0,2,0). By the condition of Theorem 5.1, we have ˆR0=1.3221>1. Thus, model (1.3) has a unique ergodic stationary distribution as shown in Figure 2 and Figure 3, which means that the disease is persistent.

    Figure 2.  Trajectories of the solutions of model (1.3) with σ1=0.009,σ2=σ3=σ4=0.1 and parameters are given in Example 2.
    Figure 3.  The histogram of the probability density function of the solutions of model (1.3) using the parameter values in Example 2.

    In this paper, we have investigated the dynamic behavior of a novel stochastic SEIQ disease model with general incidence rate and temporary immunity, which include the bilinear incidence rate (f(I)=βI) and the saturation incidence rate (f(I)=βI1+aI). We set up sufficient conditions for extinction of the disease. By using the method of Khasminskii and constructing a suitable Lyapunov function, we prove the existence of a stationary distribution to the model (1.3). From the numerical examples, we observe the stationary distribution of model (1.3) is governed by ^R0, which leads to the persistence of infectious diseases. In addition, the persistence of infectious diseases is also affected by the intensity of environmental noises.

    Some interesting and open topics deserve further consideration. For one thing, if the system is affected by other factors, such as time delay or pulse interference, how will the dynamic properties of the system change. For another, we can propose some realistic but complex models, such as considering the influence of Markov switching or lévy jump. We leave these problems as our future work.

    We will say thanks to reviewers for the valuable ideas and comments on improving the article. The said article is supported by Funding for Outstanding Doctoral Dissertation in NUAA (No. BCXJ18-09), Postgraduate Research & Practice Innovation Program of Jiangsu Province (No. KYCX18_0234), and the Fundamental Research Funds for the central Universities (No. 2021qntd21).

    The authors declare that there are no conflicts of interest.



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