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. 2020 Dec 24;143:110601. doi: 10.1016/j.chaos.2020.110601

Stationary distribution and probability density function of a stochastic SVIS epidemic model with standard incidence and vaccination strategies

Baoquan Zhou a, Daqing Jiang a,b,, Yucong Dai a, Tasawar Hayat b,c, Ahmed Alsaedi b
PMCID: PMC7854287  PMID: 33551580

Abstract

Considering the great effect of vaccination and the unpredictability of environmental variations in nature, a stochastic Susceptible-Vaccinated-Infected-Susceptible (SVIS) epidemic model with standard incidence and vaccination strategies is the focus of the present study. By constructing a series of appropriate Lyapunov functions, the sufficient criterion R0s>1 is obtained for the existence and uniqueness of the ergodic stationary distribution of the model. In epidemiology, the existence of a stationary distribution indicates that the disease will be persistent in a long term. By taking the stochasticity into account, a quasi-endemic equilibrium related to the endemic equilibrium of the deterministic system is defined. By means of the method developed in solving the general three-dimensional Fokker-Planck equation, the exact expression of the probability density function of the stochastic model around the quasi-endemic equilibrium is derived, which is the key aim of the present paper. In statistical significance, the explicit density function can reflect all dynamical properties of an epidemic system. Next, a simple result of disease extinction is obtained. In addition, several numerical simulations and parameter analyses are performed to illustrate the theoretical results. Finally, the corresponding results and conclusions are discussed at the end of the paper.

Keywords: Stochastic SVIS epidemic model, Vaccination, Ergodic stationary distribution, Fokker-Planck equation, Probability density function, Extinction

1. Introduction

1.1. Research background

It is well established that many infectious diseases have a critical influence on global social economies and human health. More precisely, the detailed statistics reported by the World Health Organization (WHO) show that approximately one-third of all deaths worldwide are caused by various epidemics. Recently, the global outbreak of COVID-19 with high transmission has also increased awareness of the importance of preventing and controlling infectious diseases. In epidemiology, mathematical models have provided several effective approaches to describe the characteristics and spread of epidemics in the last hundred years. In 1927, by dividing the population into two clusters, which includes people susceptible to the disease and infected individuals, Kermack and McKendrick [1] initially proposed the classical susceptible-infected-susceptible (SIS) epidemic model and established the corresponding threshold theory. Since then, various realistic ordinary differential equations (ODEs) have been extended to analyze and control the transmission of diseases [2], [3], [4], [5], [6], [7], [8]. For instance, Hove-Musekwa and Nyabadza [4] developed a HIV/AIDS model with active screening of disease carriers and obtained the corresponding basic reproduction number. Considering the effect of vertical infection, Tuncer and Martcheva [6] formulated a hepatitis B model with acute infection and carriers.

With the accelerated development of science and technology, vaccination comprises a common precaution that reduces the infection rate and even immunizes against some contagious diseases, such as measles, cholera, and tuberculosis [9]. According to a 2005 WHO report, the eradication of smallpox has been considered the most spectacular success of routine vaccination. Thus, some basic epidemic models with vaccination strategies have been studied in the last several decades [9], [10], [11], [12], [13]. In [9], Liu et al. obtained the global stability of equilibria and analyzed the effect of pulse vaccination. Gao et al. [11] proposed mixed vaccination strategies in the SIRS epidemic model with seasonal variability on infection. However, the vast majority of infection processes are caused by person-to-person contact. As Ma and Wang [2] described, the classical bilinear incidence rate is reasonably assumed by the simple mass-action law. From Anderson and May [14], Hethcote [15], this law is a good approximation for some communicable diseases, such as dengue fever and avian influenza. However, studies (see, e.g., [16], [17]) have shown that the underlying assumption of homogeneous mixing and homogeneous environmental for several sexually transmitted diseases, e.g., HIV/AIDS and syphilis, may be invalid. In addition, owing to the psychological effect, susceptible individuals may tend to reduce the number of contacts with the infected per unit time as the numbers of the infected individuals increase [18], [19]. As a result, the corresponding adequate incidence rate should be modified as a nonlinear form. More importantly, Anderson and May [20], [21] pointed out that various epidemic models with standard incidence are suitable for human beings and some gregarious animals.

Given the above, a SVIS epidemic system with standard incidence and vaccination is the focus of the present study.

1.2. Deterministic SVIS model and dynamical properties

The total population N(t) is divided into three compartments, namely susceptible people S(t), infected individuals I(t), and vaccinees V(t) that are in the vaccination process at time t. Then, the corresponding deterministic SVIS epidemic model with standard incidence and vaccination strategies takes the form

{dS(t)dt=Λ(μ+ϑ)SβSIN+γV+δI,dV(t)dt=ϑS(μ+γ)V,dI(t)dt=βSIN(μ+α+δ)I, (1.1)

where Λ denotes the recruitment rate of the susceptible, β is the effective contact rate, μ depicts the natural death rate of the population, α denotes the additional death rate due to the disease, ϑ is the vaccination rate of the susceptible, γ denotes the immunity loss coefficient of the vaccinated, and δ reflects the recovery rate of the infected. In epidemiology, these biological parameters are assumed to be positive.

Following similar results described by Ma and Zhou [22], the corresponding basic reproduction number of system (1.1) takes the form

R0=β(μ+γ)(μ+γ+ϑ)(μ+α+δ). (1.2)

By defining a positive invariant set D0={(S,V,I)|S0,V0,I0,S+V+IΛμ}, two possible equilibria and their dynamical properties are then given as follows.

Assuming that R01, the disease-free, E0=(S0,V0,I0)=(Λ(μ+γ)μ(μ+γ+ϑ),Λϑμ(μ+γ+ϑ),0), are then globally asymptotically stable in D0.

If R0>1, there is a unique endemic equilibrium E+=(S+,V+,I+), where I+=Λ(R01)μ+(μ+α)(R01),S+=Λ(μ+γ)(μ+γ+ϑ)[μ+(μ+α)(R01)],V+=Λϑ(μ+γ+ϑ)[μ+(μ+α)(R01)]. Moreover, E+ is globally asymptotically stable in D0, but E0 is unstable.

1.3. Stochastic SVIS epidemic model

In fact, Truscott and Gilligan [23] pointed out that the spread of infection, travel of populations, and design of control strategies are critically perturbed by some environmental variations. Therefore, it is more reasonable to construct a corresponding stochastic model to reveal the epidemiological characteristics of infectious diseases by comparison with the deterministic model. Notably, there are various possible approaches to simulate the random effects from biological significance and mathematical perspective [24]. For instance, making use of the fatal properties and multiplex networks, Zhu et al. [25], Jia et al. [26] studied the SIR epidemic spreading process and analyzed individual decision-making behavior. In 2002, the most classical assumption that random changes always fluctuate around some average values due to continuous disturbances in nature, adopted by Mao et al. [27], became a common way of describing environmental variations. Moreover, the above random fluctuations are all assumed to be types of white noise. Therefore, many authors have formulated the relevant stochastic differential equations (SDEs) with linear noises for the transmission of various epidemics [28], [29], [30], [31], [32], [33], [34], [35], [36]. As an example, Qi and Jiang [29] studied the impact of virus carrier screening and actively seeking treatment on the dynamical behavior of a stochastic HIV/AIDS epidemic model with bilinear incidence. In [34], Shi and Zhang focused on the corresponding stochastic avian influenza system and investigated the existence of the unique ergodic stationary distribution. In addition, several dynamical analyses of the stochastic SIS models or epidemic systems with vaccination have been conducted [37], [38], [39], [40]. In [37], Zhao and Jiang creatively proposed a general theory about extinction and persistence in mean based on a stochastic SIS epidemic model with vaccination. Zhang and Jiang [39] obtained sufficient conditions for a stochastic SIS system with saturated incidence and double epidemic diseases. By taking the periodicity effect into account, they still investigated a stochastic SVIR epidemic model with vaccination strategies, and derived the criteria for the existence of non-trivial positive periodic solution [40]. Given the above, in the present study it is assumed that the environmental noises are separately proportional to the compartments S,V and I. Then, the corresponding system (1.1) with the stochastic perturbations is described by

{dS(t)=[Λ(μ+ϑ)SβSIN+γV+δI]dt+σ1SdB1(t),dV(t)=[ϑS(μ+γ)V]dt+σ2VdB2(t),dI(t)=[βSIN(μ+α+δ)I]dt+σ3IdB3(t), (1.3)

where B1(t),B2(t) and B3(t) are three independent standard Brownian motions (or Wiener processes), with σi2>0(i=1,2,3) denoting their intensities.

From the perspective of biomathematics, the existence and ergodicity of stationary distribution indicates that an infectious disease will prevail and persist in long-term development. More importantly, the corresponding probability density function of the stationary distribution can reflect all statistical properties of the individuals S,V and I. It can be regarded as a great intersection of epidemiological dynamics and statistics. It should be pointed out that there are relatively few studies devoted to the explicit expression of probability density function due to the difficulty of solving the corresponding Fokker-Planck equation. To the best of our ability, several general methods of solving the corresponding algebraic equations are developed herein that are equivalent to the Fokker-Planck equation, and the exact expression of density function is derived.

The rest of this paper is organized follows. In Section 2, several mathematical notations and important lemmas for the dynamical analyses of system (1.3) are presented. The sufficient conditions for the existence and uniqueness of the ergodic stationary distribution of system (1.3) are obtained in Section 3. By means of the developed approaches in solving the general three-dimensional Fokker-Planck equation, the exact expression of the probability density function for the stationary distribution is derived in Section 4. In Section 5, several simple criteria for the disease extinction of system (1.3) are given. In Section 6, several numerical simulations are performed, together with parameter analyses to validate the theoretical results. Finally, the corresponding result discussions and main conclusions are shown, compared with existing articles, at the end of the paper.

2. Preliminaries and necessary lemmas

Throughout the paper, let {Ω,F,{Ft}t0,P} be a complete probability space with a filtration {Ft}t0 with a filtration {Γt}t0 satisfying the usual conditions (i.e., it is increasing and right continuous, while Γ0 contains all P-null sets. Assuming that Am×n is a real matrix, let Aτ be the transpose matrix of A. If m=n, A1 depicts the inverse matrix of A. The reader is referred to Mao [41] for detailed descriptions. For convenience, let Rn be the n-dimensional Euclidean space, and

R+n={(x1,...,xn)|xk>0,1kn},Ξn=(1n,n)×(1n,n)×(1n,n).

Clearly, the values S,V and I that satisfy system (1.3) are required to be positive for the corresponding dynamical behavior. To this end, the existence of uniqueness of the global positive solution of system (1.3) is described by the following Lemma 2.1.

Lemma 2.1

For any initial value(S(0),V(0),I(0))R+3,there is then a unique solution(S(t),V(t),I(t))of the system(1.3)ont0,and the solution will remain inR+3with probability 1 (a.s.).

The detailed proof is almost the same as those in Zhou et al. [28], and thus it is omitted here. Next, let X(t) be a homogeneous Markov process defined on Rn that satisfies the following SDE,

dX(t)=ϕ(X(t))dt+k=1lgk(X)dBk(t),

where the diffusion matrix H(x)=(a¯ij(x)), and a¯ij(x)=k=1lgk(i)(x)gk(j)(x). Then, the corresponding ergodicity theory and the existence of stationary distribution are described by the following Lemma 2.2.

Lemma 2.2

(Has’miniskii[42]) The Markov processX(t)has a unique ergodic stationary distributionϖ(·),if there exists a bounded domainD0Rnwith a regular boundaryΓand the following are true.

(A1). In the domainD0and some neighborhood thereof, the smallest eigenvalue of the diffusion matrixH(x)is bounded away from zero.

(A2). There is a non-negativeC2-functionU(X(t))such thatLV(X(t))is negative for anyRnD0.

Then, for anyxRnand integral functionφ(·)with respect to the measureϖ(·),it follows that

P{limt1t0tφ(X(t))dt=Rnφ(x)ϖ(dx)}=1.

By Zhou et al. [28], two important lemmas of solving the special algebraic equations are given as follows.

Lemma 2.3

([28]) LetΥ1be a symmetric matrix, for the three-dimensional algebraic equationG02+A0Υ1+Υ1A0τ=0,whereG0=diag(1,0,0),

A0=(p1p2p3100010). (2.1)

Ifp1>0,p3>0andp1p2p3>0,thenΥ1is positive definite, which follows

Υ1=(p22(p1p2p3)012(p1p2p3)012(p1p2p3)012(p1p2p3)0p12p3(p1p2p3))

Lemma 2.4

([28]) Consider the three-dimensional algebraic equationG02+B0Υ2+Υ2B0τ=0,whereΥ2is a symmetric matrix,G0=diag(1,0,0),

B0=(q1q2q310001q33). (2.2)

Assuming thatq1>0andq2>0,thenΥ2is positive semi-definite, which takes the form

Υ2=(12q100012q1q20000).

Finally, combining Lemmas 2.32.4 and the Routh-Hurwitz criterion [43], two general theories are developed in solving the similar algebraic equations, i.e., Lemmas 2.5 and 2.6.

Lemma 2.5

For the three-dimensional algebraic equationG12+C0Υ3+Υ3C0τ=0,whereΥ3is a symmetric matrix,G1=diag(a0,0,0)(a00)

C0=(c11c12c130c22c230c32c33). (2.3)

Ifc11<0,thenΥ3is a positive semi-definite matrix of the form

Υ3=(a022c1100000000).

Lemma 2.6

For any real matricesA=(aij)3×3,Π=diag(α12,α22,α32),whereαi>0(i=1,2,3). Assume thatΣ0is a symmetric matrix, for the three-dimensional algebraic equation

Π+AΣ0+Σ0Aτ=0. (2.4)

By defining the characteristic polynomials ofAasψA(λ)=λ3+r1λ2+r2λ+r3,ifAhas all negative real part eigenvalues – that is,r1>0,r3>0,r1r2r3>0– thenΣ0is positive definite.

Remark 1

From Zhou et al. [28], A0 and B0 are called standard R1 and R2 matrices, respectively. Similarly, it is assumed that C0 is a standard R3 matrix. In addition, subsection (I) of Appendix A gives the detailed proof of Lemma 2.5. The corresponding proof of Lemma 2.6 and the special form of Σ0 are shown in subsection (II) of Appendix A.

3. Stationary distribution and ergodicity of system (1.3)

In this section, the focus is on the sufficient conditions for the existence and ergodicity of stationary distribution for system (1.3). Moreover, one must guarantee that the results have no difference from those in the deterministic system (1.1). Define

R0s=μβ(μ+γ+σ222)[(μ+σ122)(μ+γ+σ222)+ϑ(μ+σ222)](μ+α+δ+σ322). (3.1)

Theorem 3.1

Assuming that R0s>1, then the solution (S(t),V(t),I(t)) of system (1.3) with any initial value (S(0),V(0),I(0))R+3 is ergodic and has a unique stationary distribution ϖ(·) .

Proof

By Lemma 2.1, for any initial value (S(0),V(0),I(0))R+3, system (1.3) has a unique global positive solution (S(t),V(t),I(t))R+3. Then, the proof of Theorem 3.1 is divided into the following two steps: (i) construct a pair of a C2-Lyapunov function U(S,V,I) and bounded domain Dϵ such that LU1 for any (S,V,I)R+3Dϵ, and (ii) validate the condition (A1) of Lemma 2.2. Step 1. Consider a suitable C2-function W(S,V,I) in the form

W(S,V,I)=M0(S+V+Ia1lnSa1a2lnVa3lnI)lnSlnV+(S+V+I),

where a1,a2,a3 are all positive constant and are determined in (3.4), and M0=Λ+2μ+γ+ϑ+σ12+σ222+23Λ(R0s31)>0, which indicates

3M0Λ(R0s31)+Λ+2μ+γ+ϑ+σ12+σ222=2. (3.2)

Define, for simplicity,

W1=S+V+Ia1lnSa1a2lnVa3lnI,W2=lnSlnV,W3=S+V+I.

Applying Ito^’s formula to W1, which is shown in subsection (III) of Appendix B, obtains

LW1=ΛμNαIa1[ΛSβIN+γVS+δIS(μ+ϑ+σ122)]a1a2[ϑSV(μ+γ+σ222)]a3[βSN(μ+α+δ+σ322)]Λ(μN+a1ΛS+a3βSN)+a1(μ+ϑ+σ122)+a3(μ+α+δ+σ222)(a1γVS+a1a2ϑSV)+a1a2(μ+γ+σ222)+a1βINΛ3a1a3Λμβ32a12a2ϑγ+a1(μ+ϑ+σ122)+a3(μ+α+δ+σ222)+a1a2(μ+γ+σ222)+a1βIN. (3.3)

Choosing a1,a2 and a3 such that

a2(μ+γ+σ222)2=γϑ,a1[(μ+ϑ+σ122)γϑμ+γ+σ222]=a3(μ+α+δ+σ322)=Λ, (3.4)

which means a1=γϑ(μ+γ+σ222)2, a2=Λμ+ϑ+σ122γϑμ+γ+σ222 and a3=Λμ+α+δ+σ322, one can obtain

LW12Λ+a1[(μ+ϑ+σ122)γϑμ+γ+σ222]3a1Λ2μβμ+α+δ+σ2223+a1βIN=3Λ3ΛR0s3+a1βIN=3Λ(R0s31)+a1βIN. (3.5)

Applying Ito^’s formula to W2,W3 similarly obtains

LW2=[ΛS+(μ+ϑ+σ122)+βINγVSδIS]ϑSV+(μ+γ+σ222)ΛSϑSV+βIN+2μ+γ+ϑ+σ12+σ222, (3.6)
LW3=Λμ(S+I)(μ+α)IΛμN. (3.7)

Additionally, note that W(S,V,I) is a continuous function satisfying

lim infl+,(S,V,I)R+3ΞlW(S,V,I)=+.

Hence, W(S,V,I) has a minimum value W0. Defining a non-negative C2-function U(S,V,I):R+3R+1 by

U(S,V,I)=W(S,V,I)W0,

and combining (3.2) and (3.5)(3.7), it can be shown that

LU3M0Λ(R0s31)+a1M0βINΛSϑSV+βIN+(Λ+2μ+γ+ϑ+σ12+σ222)μN=2+(a1M0+1)βIS+V+IΛSϑSVμ(S+V+I). (3.8)

Next, the corresponding compact subset Dϵ is contructed by

Dϵ={(S,V,I)R+3|Sϵ,Vϵ2,Iϵ3,S+V+I1ϵ},

where ϵ>0 is a sufficiently small constant such that the following inequalities hold:

2+(a1M0+1)βmin(Λ,ϑ,μ)ϵ1, (3.9)
2+(a1M0+1)βϵ1. (3.10)

For convenience, consider the following four subsets of R+3Dϵ:

D1,ϵc={(S,V,I)R+3|S<ϵ},D2,ϵc={(S,V,I)R+3|V<ϵ2,Sϵ},D3,ϵc={(S,V,I)R+3|I<ϵ3,Vϵ2},D4,ϵc={(S,V,I)R+3|S+V+I>1ϵ}.

Now, it must be shown that

LU1,(S,V,I)Di,ϵ(i=1,2,3,4).

Case 1. If (S,V,I)D1,ϵ, by (3.8)(3.9), one can derive

LU2+(a1M0+1)βΛS2+(a1M0+1)βmin(Λ,ϑ,μ)ϵ1.

Case 2. For any (S,V,I)D2,ϵ, it follows from (3.8)(3.9) that

LU2+(a1M0+1)βϑSV2+(a1M0+1)βmin(Λ,ϑ,μ)ϵ1.

Case 3. Assuming that (S,V,I)D3,ϵ, by (3.8)(3.9) it can be seen that

LU2+(a1M0+1)βIV2+(a1M0+1)βϵ1.

Case 4. If (S,V,I)D1,ϵ, from (3.8) and (3.10), one has

LU2+(a1M0+1)βμ(S+V+I)2+(a1M0+1)βmin(Λ,ϑ,μ)ϵ1.

Notably, R+3Dϵ=i=14Di,ϵ. Hence, one equivalently obtains

LU1,(S,V,I)R+3Dϵ.

Therefore, the condition (A2) of Lemma 2.2 holds. The corresponding diffusion matrix is given by

H=(σ12S2000σ22V2000σ32I2).

Clearly, H is a positive-definite matrix. Then, the assumption (A1) of Lemma 2.2 also holds.

Given the above, the global positive solution (S(t),V(t),I(t)) of system (1.3) follows a unique ergodic stationary distribution ϖ(·). This completes the proof of Theorem 3.1. □

Remark 2

Under R0s>1, the existence of the ergodic stationary distribution for system (1.3) is derived. This reveals that the contagious disease will prevail and persist in a population. Furthermore, from the expressions of R0s and R0, it can be obtained that R0sR0, and the sign holds if and only if σ1=σ2=σ3=0. Consequently, not only does this reveal that random fluctuations have a critical effect on the spread of epidemic, but it also indicates that R0s is a unified threshold of the disease persistence of systems (1.1) and (1.3).

4. Probability density function analysis

By Theorem 3.1, one obtains that the global solution (S(t),V(t),I(t)) of system (1.3) follows a unique ergodic stationary distribution ϖ(·). This section is devoted to deriving the explicit expression of the density function of the distribution ϖ(·) while R0s>1. In fact, the result will present a wide range of possibilities for the further development of epidemiological dynamics. Before this, two necessary transformations of system (1.3) should be first introduced.

4.1. Two important transformations of system (1.3)

(I) (Logarithmic transformation): Let (u1,u2,u3)τ=(lnS,lnV,lnI)τ, Employing Ito^’s formula, it follows from system (1.3) that

{du1=[Λeu1(μ+ϑ+σ122)βeu3eu1+eu2+eu3+γeu2u1+δeu3u1]dt+σ1dB1(t),du2=[ϑeu1u2(μ+γ+σ222)]dt+σ2dB2(t),du3=[βeu1eu1+eu2+eu3(μ+α+δ+σ322)]dt+σ3dB3(t). (4.1)

By taking the random effect into consideration, another critical value is defined: R0c=β(μ+γ+σ222)(μ+γ+ε+σ222)(μ+α+δ+σ322). Moreover, if R0c>1, then the quasi-stable equilibrium E*=(S*,V*,I*):=(eu1*,eu2*,eu3*)R+3 is determined by the following Eq. (4.2):

{Λeu1*(μ+ϑ+σ122)βeu3*eu1*+eu2*+eu3*+γeu2*u1*+δeu3*u1*=0,ϑeu1*u2*(μ+γ+σ222)=0,βeu1*eu1*+eu2*+eu3*(μ+α+δ+σ322)=0. (4.2)

For convenience, let μi=μ+σi22 for any i=1,2,3. As a result, it can be derived by (4.2) that V*=ϑS*μ2+γ,I*=(μ2+γ+ϑ)(R0c1)S*μ2+γ,N*=S*+V*+I*=βS*μ3+α+δ, where S*=Λ(μ2+γ)μ1(μ2+γ)+ϑμ2+(μ3+α)(μ2+γ+ϑ)(R0c1).

Notably, it is easily obtained that R0s<R0c. This then indicates that E*R+3 if R0s>1. In addition, if there is no stochastic noise in system (1.3), i.e., model (1.1), then E*=E+=(S+,V+,I+).

(II) (Equilibrium offset transformation): Given the above, let X=(x1,x2,x3)τ=(u1u1*,u2u2*,u3u3*); thus, the corresponding linearized system of (4.1) takes the form

{dx1=(a11x1+a12x2+a13x3)dt+σ1dB1(t),dx2=(a21x1a21x2)dt+σ2dB2(t),dx3=[(a32+a33)x1a32x2a33x3]dt+σ3dB3(t), (4.3)

where

a11=Λ+γV*+δI*S*βS*I*(N*)2,a12=γV*S*+βV*I*(N*)2>0,a13=δI*S*β(S*+V*)I*(N*)2,
a21=μ2+γ>0,a32=βS*V*(N*)2>0,a33=βS*I*(N*)2>0.

4.2. Density function of stationary distribution ϖ(·)

Theorem 4.1

For any initial value (S(0),V(0),I(0))R+3, if R0s>1, then the stationary distribution ϖ(·) around E* follows a unique log-normal probability density function Φ(S,V,I), which is given by

Φ(S,V,I)=(2π)32|Σ|12e12(lnSS*,lnVV*,lnII*)Σ1(lnSS*,lnVV*,lnII*)τ, (4.4)

where Σ is a positive definite matrix, and the special form of Σ is given as follows.

(1) . If m10,m20 and a130, then

Σ=ϱ12(H1J1)1Θ0[(H1J1)1]τ+ϱ22(H2J3J2)1Θ0[(H2J3J2)1]τ+ϱ32(H3J4)1Θ0[(M3J3)1]τ.

(2) . If m10,m20 and a13=0, then

Σ=ϱ12(H1J1)1Θ0[(H1J1)1]τ+ϱ22(H2J3J2)1Θ0[(H2J3J2)1]τ+J41Θ4(J41)τ.

(3) . If m10,m2=0 and a130, then

Σ=ϱ12(H1J1)1Θ0[(H1J1)1]τ+a322σ22(H˜2J3J2)1Θ3[(H˜2J3J2)1]τ+ϱ32(H3J4)1Θ0[(M3J3)1]τ.

(4) . If m10 and m2=a13=0, then

Σ=ϱ12(H1J1)1Θ0[(H1J1)1]τ+a322σ22(H˜2J3J2)1Θ3[(H˜2J3J2)1]τ+J41Θ4(J41)τ.

(5) . If m1=0,m20 and a130, then

Σ=a212σ12(H˜1J1)1Θ1[(H˜1J1)1]τ+ϱ22(H2J3J2)1Θ0[(H2J3J2)1]τ+ϱ32(H3J4)1Θ0[(M3J3)1]τ.

(6) . If m1=a13=0 and m20, then

Σ=a212σ12(H˜1J1)1Θ1[(H˜1J1)1]τ+ϱ22(H2J3J2)1Θ0[(H2J3J2)1]τ+J41Θ4(J41)τ.

(7) . If m1=m2=0 and a130, then

Σ=a212σ12(H˜1J1)1Θ1[(H˜1J1)1]τ+a322σ22(H˜2J3J2)1Θ3[(H˜2J3J2)1]τ+ϱ32(H3J4)1Θ0[(M3J3)1]τ.

(8) . If m1=m2=a13=0, then

Σ=a212σ12(H˜1J1)1Θ1[(H˜1J1)1]τ+a322σ22(H˜2J3J2)1Θ3[(H˜2J3J2)1]τ+J41Θ4(J41)τ,

with

J1=(1000100a32+a33a211),J2=(010001100),J3=(1000100a12a321),J4=(001100010),
Θ0=(r22(r1r2r3)012(r1r2r3)012(r1r2r3)012(r1r2r3)0r12r3(r1r2r3)),Θ1=(12w100012w1w20000),Θ3=(12w300012w3w40000),
H1=(a21m1(a21+a33)m1a3320m1a33001),H˜2=(a32a33a12a12a33a32a32+a33010001),
H2=(a32m2(a11+a33)m2(a11a12a12a33a32)2+m2(a32+a33)0m2a11+a12+a12a33a32001),Θ4=(12a3300000000),
H˜1=(a21a210010001),H3=(a13a21a21(a11+a21)a21(a12+a21)0a21a21001),

and

m1=a33(a21a32a33)a21,m2=a13+a12(a11a33)a32a122(a32+a33)a322,
ϱ1=a21m1σ1,ϱ2=a32m2σ2,ϱ3=a13a21σ3,
r1=a11+a21+a33,r2=a21(a11a12+a33)+[a11a33a13(a32+a33)],r3=a21a33(a11a12a13),
w1=a11+a21,w2=a21(a11a12a13),w3=a12+a21+a33+a12a33a32,w4=a21a32a33(a11a12a13)a32(a11a12)a12a33.

Proof

For convenience and simplicity, let B(t)=(B1(t),B2(t),B3(t))τ and

M=(σ12000σ22000σ32),A=(a11a12a13a21a210a32+a33a32a33).

Hence, system (4.3) can be rewritten as dX=AXdt+MdB(t). By the theory of Gardiner [44], the unique density function Φ(X) around the quasi-endemic equilibrium E* satisfies the following Fokker-Plauck equation:

k=13σk222Φxk2+x1[(a11x1+a12x2+a13x3)Φ]+x2[(a21x1a21x2)Φ]+x3[((a32+a33)x1a32x2a33x3)Φ]=0. (4.5)

Since the diffusion matrix M is a constant matrix, Roozen [45] pointed out that Φ(X) can be described by a quasi-Gaussian distribution, i.e., Φ(X)=c0e12XQXτ, where c0>0 is determined by the normalized condition R+3Φ(X)dX=1 and Q is a symmetric matrix.

Substituting these results into (4.5), one can obtain that Q obeys the algebraic equation QM2Q+AτQ+QA=0. If Q is a inverse matrix, by letting Σ=Q1, an equivalent equation is given by

M2+AΣ+ΣAτ=0. (4.6)

Next, it will be proved that A has all negative real-part eigenvalues. The characteristic polynomial of A is defined as ψ(λ)=λ3+p1λ2+p2λ+p3, where

r1=a11+a21+a33,r2=a21(a11a12+a33)+[a11a33a13(a32+a33)],r3=a21a33(a11a12a13).

By the expressions of S*,V*,I* and N*, it can be shown that

(i).a11=(μ1+ϑ)+βI*N*βS*I*(N*)2=(μ1+ϑ)+β(V*+I*)I*(N*)2>0,(ii).a11a12a13=[Λ+γV*+δI*S*βS*I*(N*)2][γV*S*+βV*I*(N*)2][δI*S*β(S*+V*)I*(N*)2]=ΛS*>0,(iii).a12a33a13a32=βS*(N*)2(γV*I*S*+βV*I*N*δV*I*S*)=(μ3+γ+α)βV*I*(N*)2>0,(iv).a11a12+a33>ΛS*+δI*S*βV*I*(N*)2>(μ3+α+δ)(R0c1)μ2+γ[(μ2+γ)+ϑ(R0c1)R0c]>0.

Consequently, it follows from (i)–(iv) that

(1).r1=a11+a21+a33>0,r3=a21a33(a11a12a13)>0,(2).r2=a21(a11a12+a33)+[a11a33a13(a32+a33)]>(a12+a13)a33a13(a32+a33)=a12a33a13a32>0.
(3).r1r2r3=(a11+a21+a33){a21(a11a12+a33)+[a11a33a13(a32+a33)]}a21a33(a11a12a13)=a11r2+a21[(a11+a33)a33a13a32]+a33[a11a33a13(a32+a33)]=a11r2+a21a33(a11a12+a33)+a332(a11a12a13)+(a21+a33)(a12a33a13a32)>a11r2>0.

Combining the above (1)-(3) and Lemma 2.6, that Σ of Eq. (4.6) is positive definite can be derived.

However, following the corresponding proof of Lemma 2.6, which is shown in subsection (II) of Appendix A, the exact expression of Σ is given. First, by the finite independent superposition principle, (4.6) can be equivalently transformed into the sum of solution to the following algebraic sub-equations,

Mk2+AΣk+ΣkAτ=0,

where M1=diag(σ1,0,0),M2=diag(0,σ2,0),M3=diag(0,0,σ3), and the symmetric matrices Σk(k=1,2,3) are their respective solutions. Clearly, Σ=Σ1+Σ2+Σ3. Now, the special expression of Σ are derived by the following three steps.

Step 1. For the algebraic equation

M12+AΣ1+Σ1Aτ=0, (4.7)

denote A1=J1AJ11, where the elimination matrix J1 and A1 are derived by

J1=(1000100a32+a33a211),A1=(a11a12+a13(a32+a33)a21a13a21a2100m1a33),

where m1=a33(a21a32a33)a21. By the value of w1, the relevant discussion is divided into two subcases:

(i).m10,(ii).m1=0.

Case (i). If m10, in view of the method introduced in Zhou et al. [28], it is assumed that B1=H1A1H11, where the standardized transformation matrix is

H1=(a21m1(a21+a33)m1a3320m1a33001). (4.8)

By direct calculation, one obtains

B1=(r1r2r3100010),

where r1,r2 and r3 are the same as above. Furthermore, one can equivalently transform Eq. (4.7) into

(H1J1)M12(H1J1)τ+B1[(H1J1)Σ1(H1J1)τ]+[(H1J1)Σ1(H1J1)τ]B1τ=0.

Letting Θ0=ϱ12(H1J1)Σ1(H1J1)τ, where ϱ1=a21m1σ1, we obtain

G02+B1Θ0+Θ0B1τ=0.

Noting that A has all negative real-part eigenvalues, then B1 is a standard R1 matrix. By Lemma 2.3, this means that Σ0 is positive definite, which takes the form

Θ0=(r22(r1r2r3)012(r1r2r3)012(r1r2r3)012(r1r2r3)0r12r3(r1r2r3)). (4.9)

Therefore, Σ1=ϱ12(H1J1)1Θ0[(H1J1)1]τ.

Case (ii). If m1=0, i.e., a21=a32+a33, B˜1=H˜1A1H˜11 is defined, where another standardized transformation matrix H˜1 and B˜1 are obtained by

H˜1=(a21a210010001),B˜1=(w1w2ξ101000a33), (4.10)

where w1=a11+a21,w2=a21(a11a12a13), and ξ1 is abbreviation. Obviously, B˜1 is a standard R2 matrix. Additionally, (4.7) can be equivalently transformed into

(H˜1J1)M12(H˜1J1)τ+B˜1[(H˜1J1)Σ1(H˜1J1)τ]+[(H˜1J1)Σ1(H˜1J1)τ]B˜1τ=0.

By letting Θ1=(a21σ1)2(H˜1J1)Σ1(H˜1J1)τ, it can be simplified as

G02+B˜1Θ1+Θ1B˜1τ=0.

In view of Lemma 2.4, Θ1 is described by

Θ1=(12w100012w1w20000). (4.11)

Hence, Σ1=a212σ12(H˜1J1)1Θ1[(H˜1J1)1]τ. Step 2. Consider the algebraic equation

M22+AΣ2+Σ2Aτ=0. (4.12)

For the corresponding elimination matrix J2,J3, A2=J2AJ21 is defined, where J2,J3 and A2 are obtained by

J2=(010001100),J3=(1000100a12a321),A2=(a21a12a21a32a21a32a33a12a12a33a32a32+a330m2a11+a12+a12a33a32),

where m2=a13+a12(a11a33)a32a122(a32+a33)a322. Similarly, the following two sub-conditions are considered:

(1).m20,(2).m2=0.

Case (1). If m20, let B2=H2A2H21, where the relevant standardized transformation matrix

H2=(a32m2(a11+a33)m2(a11a12a12a33a32)2+m2(a32+a33)0m2a11+a12+a12a33a32001). (4.13)

In fact, one still derives

B2=B1=(r1r2r3100010),

which means that B2 is also a standard R1 matrix. By letting Θ2=ϱ22(H2J2)Σ2(H2J2)τ, where ϱ2=a32m2σ2, (4.12) is then equivalent to the following equation:

G02+B2Θ2+Θ2B2τ=0.

By Lemma 2.3 and the result of A having all negative real-part eigenvalues again, it can be shown that

Θ2=Θ0=(r22(r1r2r3)012(r1r2r3)012(r1r2r3)012(r1r2r3)0r12r3(r1r2r3)).

In other words, Σ2=ϱ22(H2J3J2)1Θ0[(H2J3J2)1]τ.

Case (2). If m2=0, let B˜2=H˜2A2H˜21, where the corresponding standardized transformation matrix H˜2 and B˜2 are given by

H˜2=(a32a33a12a12a33a32a32+a33010001),B˜2=(w3w4ξ201000a11+a12+a12a33a32),

where w3=a12+a21+a33+a12a33a32,w4=a21a32a33(a11a12a13)a32(a11a12)a12a33, and ξ2 is also shorthand. Similarly, B˜2 is a standard R2 matrix. By defining Θ3=(a32σ2)2(H˜2J2)Σ2(H˜2J2)τ, (4.12) is then equivalent to

G02+B˜2Θ3+Θ3B˜2τ=0.

According to Lemma 2.4, Θ1 takes the form

Θ3=(12w300012w3w40000). (4.14)

Then, Σ2=a322σ22(H˜2J3J2)1Θ3[(H˜2J3J2)1]τ.

Step 3. For the following algebraic equation,

M32+AΣ3+Σ3Aτ=0, (4.15)

and for the following elimination matrix J3, let A3=J4AJ41, where J4 and A3 are given by

J4=(001100010),A3=(a33a32+a33a32a13a12a110a21a21).

Hence, (4.15) can be equivalently transformed into

J4M32J4τ+B3Θ4+Θ4B3τ=0, (4.16)

where Θ4=J4Σ3J4τ. Similarly, the proof is divided into two subcases by the value of a13. Case (I). If a130, consider the corresponding standardized transformation matrix

H3=(a13a21a21(a11+a21)a21(a12+a21)0a21a21001).

Letting B3=H3A3H31, that B3=B1 is still derived. Hence, an equivalent algebraic equation of (4.16) is described as follows:

(H3J4)M32(H3J4)τ+B3[(H3J4)Σ3(H3J4)τ]+[(H3J4)Σ3(H3J4)τ]B3τ=0.

Denoting Θ5=ϱ32(H3J4)Σ3(H3J4)τ, where ϱ3=a13a21σ3, the last equation can be also simplified as

G02+B1Θ5+Θ5B1τ=0.

Similarly, one obtains

Θ5=Θ0=(r22(r1r2r3)012(r1r2r3)012(r1r2r3)012(r1r2r3)0r12r3(r1r2r3)).

Consequently, Σ3=ϱ32(H3J4)1Θ0[(H3J4)1]τ.

Case (II). If a21=0, then A3 is a standard R3 matrix. Noting that J4M32J4τ=σ32G02=diag(σ32,0,0), by Lemma 2.5, one can obtain

Θ4=J4Σ32J4τ=(σ322a3300000000).

Based on a33>0, then Θ4 is a positive semi-definite matrix, which means that Σ3=J41Θ4(J41)τ.

In summary, the special form of Σ is divided into eight cases by the different values of m1,m2 and a13, which is shown in Theorem 4.1. Finally, in view of the relation of systems (4.1) and (4.3), the stationary distribution ϖ(·) around E* then has a unique log-normal probability density function

Φ(S,V,I)=(2π)32|Σ|12e12(lnSS*,lnVV*,lnII*)Σ1(lnSS*,lnVV*,lnII*)τ.

Therefore, this completes the proof. □

Remark 3

If R0s>1, Theorem 4.1 shows that the stationary distribution ϖ(·) around E* has the unique log-normal density function Φ(S,V,I). This reflects the stochastic permanence of system (1.3) from one side. In addition, that R0s=R0c=R0 if σi=0(i=1,2,3) is obtained.

5. Extinction of system (1.3)

As is known, all of the properties of disease persistence of system (1.3) are reflected by Theorems 3.1 and 4.1. For a comprehensive study, a simple extinction result of system (1.3) is described by the following Theorem 5.1.

Theorem 5.1

For any initial value(S(0),V(0),I(0))R+3,ifR0d=βμ+α+δ+σ322<1,then the solution(S(t),V(t),I(t))of system(1.3)follows:

lim supt+lnI(t)t(μ+α+δ+σ322)(R0d1)<0,a.s., (5.1)

which means that the epidemic of system(1.3)will go to extinction with probability 1 (a.s.).

Proof

Employing Ito^’s formula to lnI(t), one obtains

dlnI(t)=[βS(t)N(t)(μ+α+δ+σ322)]dt+σ3dB3(t). (5.2)

Integrating from 0 to t and dividing by t on both sides of (5.1), it can be seen that

lnI(t)tlnI(0)t+1t0t[βS(u)N(u)(μ+α+δ+σ322)]du+0tσ3dB3(u)tlnI(0)t+1t0t[β(μ+α+δ+σ322)]du+0tσ3dB3(u)t=lnI(0)t+(μ+α+δ+σ322)(R0d1)+0tσ3dB3(u)t. (5.3)

Next, by the strong law of large numbers [1], one derives

limt+0tσ3dB3(u)t=0,a.s. (5.4)

Taking the superior limit of t+ on both sides of (5.3), the assertion (5.1) can then be obtained by (5.4). Moreover, from the expressions of R0s and R0s, one can obtain that R0dR0s.

Consequently, the proof of Theorem 5.1 is confirmed. □

6. Simulations and parameter analyses

In this section, by means of the well-known higher-order method developed by Milstein [46], the corresponding discretization equation of system (1.3) is obtained in the form

{Sk+1=Sk+[Λ(μ+ϑ)SkβSkIkSk+Vk+Ik+γVk+δIk]Δt+σ122Sk(ξk21)Δt+σ1SkΔtξkVk+1=Vk+[ϑSk(μ+γ)Vk]Δt+σ222Vk(ηk21)Δt+σ2VkΔtηkIk+1=Ik+[βSkIkSk+Vk+Ik(μ+α+δ)Ik]Δt+σ322Ik(ζk21)Δt+σ3IkΔtζk, (6.1)

where the time increment Δt>0, and ξk,ηk,andζk are three independent Gaussian random variables that follow the distribution N(0,1) for k=1,2,...,n. Furthermore, (Sk,Vk,Ik) is the corresponding value of the kth iteration of the discretization equation. From AI-Darabsah [13], Zhao and Jiang [37], Liu et al. [38], Zhang and Jiang [39], Arino et al. [47], and the detailed data of the Central Statistical Office of Zimbabwe (CSZ), the corresponding realistic statistics of system (1.3) are shown in Table 1 . Next, several empirical examples are provided to focus on the following five aspects.

Table 1.

List of biological parameters of system (1.3).

Parameters Description Unit Value Source
Λ Recruitment rate of population per day 0.5 [38], [39]
β Transmission rate of susceptible individuals per day [0.390,0.432] [13]
μ Natural death rate of population per day [2.74,6.85]×105 [47],CSZ data
α Disease mortality of infected people per day 10.6×365 [13]
δ Recovery rate None [0.01,0.2] Estimated
γ Immune loss rate of vaccinated individuals None 0.2 [37]
ϑ Vaccination rate of susceptible individuals None [0.371,0.436] [13]

(i) The existence of the ergodic stationary distribution of system (1.3) while R0s>1.

(ii) The exact expression and verification of the unique log-normal density function for the stationary distribution under R0s>1.

(iii) The influence of random fluctuations on the disease persistence of system (1.3).

(iv) The effects of the main parameters of system (1.3) on the disease dynamics.

(v) The corresponding dynamical behavior of system (1.3) if R0d<1.

6.1. Dynamical behavior of system (1.3) if R0s>1

Example 6.1

By Table 1, letting the environmental noise intensities (σ1,σ2,σ3)=(0.0008,0.0004,0.0008) and main parameters (Λ,β,μ,α,δ,γ,ϑ)=(0.8,0.4,3×105,0.00457,0.05,0.2,0.4), one then obtains

R0=β(μ+γ)(μ+γ+ϑ)(μ+α+δ)=2.44>1,R0s=μβ(μ+γ+σ222)[(μ+σ122)(μ+γ+σ222)+ϑ(μ+σ222)](μ+α+δ+σ322)=2.43>1.

It follows from Theorem 3.1 that system (1.3) admits a unique ergodic stationary distribution ϖ(·). The left-hand column of Fig. 1 can be seen to validate it. By Theorem 4.1, the stationary distribution ϖ(·) around the quasi-endemic equilibrium E* has a unique log-normal density function Φ(S,V,I). Moreover, it is calculated that

m1=0.02460,m2=27.85150,a13=0.11960,

which means

Σ=ϱ12(H1J1)1Θ0[(H1J1)1]τ+ϱ22(H2J3J2)1Θ0[(H2J3J2)1]τ+ϱ32(H3J4)1Θ0[(M3J3)1]τ=104×(0.35240.34980.39470.34980.35380.38820.39470.38820.4970).

By direct calculation, one can obtain that E*=(S*,V*,I*)=(40.0428,173.2562,80.0736). Then, the corresponding marginal density functions of S(t),V(t) and I(t) are separately given as follows.

(1).P1(S)=ΦS=67.204e14188.4(lnS3.69),(ii).P2(V)=ΦV=67.07e14132.2(lnV5.15),
(iii).P3(I)=ΦI=56.59e10060.4(lnI4.38).

The curves of (i)-(iii) are shown in the right-hand column of Fig. 1. Obviously, this greatly illustrates Theorem 4.1 from the side.

Fig. 1.

Fig. 1

Left-hand column shows simulation of compartments S(t),V(t), and I(t) in deterministic system (1.1) and stochastic system (1.3) with noise intensities (σ1,σ2,σ3)=(0.0008,0.0004,0.0008) and main parameters (Λ,β,μ,α,δ,γ,ϑ)=(0.8,0.4,3×105,0.00457,0.05,0.2,0.4), respectively. Right-hand column shows frequency histogram and corresponding marginal density function curves of individuals S,V, and I.

Combining Remarks 3.14.1 and Theorem 5.1, one can derive that all random perturbations σ1,σ2, and σ3 have a critical influence on the dynamical behavior of system (1.3). Therefore, the corresponding parameter analyses of the above three white noises are shown by Example 6.2.

6.2. Impact of random noises σi(i=1,2,3) on disease extinction and the existence of stationary distribution

Example 6.2

One chooses the epidemiological parameters (Λ,β,μ,α,δ,γ,ϑ)=(0.8,0.4,3×105,0.00457,0.05,0.2, 0.4) and considers the following four subcases of stochastic perturbations:

(i).(σ1,σ2,σ3)=(0.0008,0.0004,0.0008),(ii).(σ1,σ2,σ3)=(0.008,0.0004,0.0008),
(iii).(σ1,σ2,σ3)=(0.0008,0.004,0.0008),(iv).(σ1,σ2,σ3)=(0.0008,0.0004,0.008).

First, it should be pointed out that the above four subcases (i)(iv) all guarantee the existence of a stationary distribution, which has an ergodicity property. For convenience and simplicity, only the population intensities of susceptible and infected individuals are focused on, which are presented in subfigures (2-1) and (2-2) of Fig. 2 , respectively. By only increasing the perturbation intensities of the vaccinated individuals (or infected individuals), i.e., the larger σ2 (or σ3), then the disease infection will be effectively inhibited. In contrast, by only increasing the perturbation intensity of the susceptible individuals, a great destabilizing influence on the population numbers of S and I manifests.

Fig. 2.

Fig. 2

Corresponding simulation of partial compartments S(t) and I(t) of stochastic system (1.3) under noise intensities (σ1,σ2,σ3)=(0.0008,0.0004,0.0008),(0.008,0.0004,0.0008),(0.0008,0.004,0.0008) and (0.0008,0.0004,0.008), respectively. Other fixed parameters: (Λ,β,μ,α,δ,γ,ϑ)=(0.8,0.4,3×105,0.00457,0.05,0.2,0.4).

Next, by Zhu et al. [25], Jia et al. [26], the impact of the main parameters of system (1.3) on the individual decision-making behavior is studied. From the expressions of R0s and R0d, the disease persistence and extinction of system (1.3) are critically affected by the transmission rate β and vaccination rate ϑ. Thus, the following Examples 6.3 and 6.4 will reveal the impact. In addition, the corresponding effect of the recruitment rate Λ on the dynamical behavior of system (1.3) is also shown in Example 6.5.

6.3. Impact of transmission rate β on dynamics of system (1.3)

Example 6.3

Choosing the epidemiological parameters (Λ,μ,α,δ,γ,ϑ)=(0.8,3×105,0.00457,0.128,0.2,0.4) and random noises (σ1,σ2,σ3)=(0.0008,0.0004,0.0008) and considering the subcases of transmission rate β=0.39,0.40,0.41 and 0.42, the corresponding numbers of the solution (S(t),V(t),I(t)) to system (1.3) are described in Fig. 3 . Clearly, a small transmission rate can lead to reduction of disease infection and even elimination, such as β0.39 per day.

Fig. 3.

Fig. 3

Corresponding population numbers of solution (S(t),V(t),I(t)) to system (1.3) with transmission rates of β=0.39,0.40,0.41, and 0.42, respectively. Other given parameters: (Λ,μ,α,δ,γ,ϑ)=(0.8,3×105,0.00457,0.128,0.2,0.4) and (σ1,σ2,σ3)=(0.0008,0.0004,0.0008).

6.4. Impact of vaccination rate ϑ on dynamics of system (1.3)

Example 6.4

Assuming that the parameters (Λ,β,μ,α,δ,γ)=(0.8,0.4,3×105,0.00457,0.128,0.2) and stochastic perturbations (σ1,σ2,σ3)=(0.0008,0.0004,0.0008), for the corresponding subcases of vaccination rate ϑ=0.371,0.386,0.401, and 0.416, the corresponding solutions (S(t),V(t),andI(t)) to system (1.3) are shown in Fig. 4 . Similarly, a small vaccination rate can control the disease infection more effectively than a large one.

Fig. 4.

Fig. 4

Corresponding simulation of solution (S(t),V(t),I(t)) to system (1.3) with vaccination rate ϑ=0.371,0.386,0.401, and 0.416, respectively. Other fixed parameters: (Λ,β,μ,α,δ,γ)=(0.8,0.4,3×105,0.00457,0.128,0.2) and (σ1,σ2,σ3)=(0.0008,0.0004,0.0008).

6.5. Impact of recruitment rate Λ on dynamics of system (1.3)

Example 6.5

Letting the dynamical parameters be (β,μ,α,δ,γ,ϑ)=(0.4,3×105,0.00457,0.128,0.2,0.4) and stochastic fluctuations be (σ1,σ2,σ3)=(0.0008,0.0004,0.0008), and considering the sub-conditions of recruitment rate Λ=0.7,0.408,0.9, and 1.0, the corresponding intensities of the compartments S,V, and I of system (1.3) are reflected in Fig. 5 . Obviously, as the parameter Λ increases to 1 from 0.7, the spread and infection of an epidemic can be effectively controlled by the small recruitment rate.

Fig. 5.

Fig. 5

Corresponding population intensities of individuals S,V, and I of system (1.3) with recruitment rate Λ=0.7,0.8,0.9, and 1.0, respectively. Other given parameters: (β,μ,α,δ,γ,ϑ)=(0.4,3×105,0.00457,0.128,0.2,0.4) and (σ1,σ2,σ3)=(0.0008,0.0004,0.0008).

6.6. Dynamical behaviors of system (1.3) under R0d<1

Example 6.6

Considering the stochastic noises (σ1,σ2,σ3)=(0.01,0.01,0.78) and main parameters (Λ,β,μ,α,δ,γ,ϑ)=(0.8,0.4,3×105,0.00457,0.13,0.2,0.38), one can then obtain

R0=β(μ+γ)(μ+γ+ϑ)(μ+α+δ)=1.0249>1,R0d=βμ+α+δ+σ322=0.9116<1,R0s=0.1179<1.

By Theorem 3.1, one cannot derive the existence of the ergodic stationary distribution of system (1.3). In contrast, it follows from Theorem 5.1 that the disease of stochastic system (1.3) will be extinct in a long term. In addition, the deterministic model (1.1) has a globally asymptotically stable endemic equilibrium E+. On the one hand, these results validate the fact that large white noises lead to disease elimination from the side. On the other hand, the large random fluctuation σ3(i.e.,σ3σ1=σ3σ2=78>>1) indicates that it is necessary to isolate and control the infected individuals during the outbreak of an epidemic. These results are verified by Fig. 6 .

Fig. 6.

Fig. 6

Corresponding population numbers of solution (S(t),V(t),I(t)) to system (1.3) with random perturbations (σ1,σ2,σ3)=(0.01,0.01,0.78) and main parameters (Λ,β,μ,α,δ,γ,ϑ)=(0.8,0.4,3×105,0.00457,0.13,0.2,0.38).

For epidemiological study, combining the above numerical simulations and parameter analyses, several reasonable and effective measures to reduce the threat of infectious diseases to human life, and even eliminate the epidemic, are provided. The special approaches are the following.

(i) Several reasonable policies of joint prevention and control are implemented to reduce the population mobility in differential risk epidemic areas. Then, the small recruitment rate Λ may lead to the elimination of disease (see Fig. 5).

(ii) Controlling the activities of the susceptible individuals in highly pathogenic areas to decrease the contact rate of population. Hence, β0+ can be guaranteed, which means R0s<1 and R0d<1 (see Fig. 3).

(iii) Developing several effective vaccines and carrying out other prophylactic measures to improve the immune rate of disease (see Fig. 4).

7. Conclusions and result discussions

7.1. Conclusions

The corresponding theoretical results of this paper are the following.

(i) By Theorem 3.1, system (1.3) admits a unique ergodic stationary distribution ϖ(·) under

R0s=μβ(μ+γ+σ222)[(μ+σ122)(μ+γ+σ222)+ϑ(μ+σ222)](μ+α+δ+σ322).

(ii) By taking the effect of random perturbations into account, a quasi-endemic equilibrium E* related to E+ is defined while R0c=β(μ+γ+σ222)(μ+γ+ε+σ222)(μ+α+δ+σ322)>1. In view of the expressions of R0c and R0s, it is further proved that the stationary distribution ϖ(·) around E* has a log-normal density function in the following form:

Φ(S,V,I)=(2π)32|Σ|12e12(lnSS*,lnVV*,lnII*)Σ1(lnSS*,lnVV*,lnII*)τ,

where the special form of Σ is shown in Theorem 4.1. (iii) The disease of system (1.3) will go to extinction with probability 1 if R0d=βμ+α+δ+σ322<1. The above results (i) and (ii) reflect the stochastic persistence and ergodicity of the epidemic. Moreover, the corresponding disease extinction of system (1.3) is described by result (iii).

7.2. Result discussions

In this paper, combining the great effect of vaccination and the unpredictability of environmental fluctuations in the real world, a stochastic SVIS infectious disease model with vaccination and standard incidence is the object of concern. Adopting the descriptions in [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], linear perturbation, which is the most intuitive assumption of a random effect, is similarly taken into consideration in this paper. Subsequently, several dynamical properties of stochastic system (1.3) are analyzed, such as the existence and uniqueness of a global positive solution, existence and ergodicity of a stationary distribution, and disease elimination. By comparison with the existing results ([28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40]), several highlights developed in the present study are detailed in the following two points.

As is known, the endemic equilibrium and basic reproduction number, two important results of a deterministic epidemic, reflect disease permanence and elimination. Similarly, for the corresponding stochastic model, the existence of stationary distribution indicates the stochastic positive equilibrium state. In this paper, it is first proved that stochastic system (1.3) admits a unique ergodic stationary distribution under the critical value R0s>1. It should be pointed out that R0s>1 is a unified threshold for the disease persistence of systems (1.1) and (1.3). Moreover, the sufficient condition R0d<1 is obtained for the disease extinction of system (1.3). Both R0s>1 and R0d<1 reveal that the dynamical behavior of system (1.3) is critically affected by the random fluctuations, i.e., σ1,σ2, and σ3. In view of the method of controlling variables and numerical simulations, this means that a large white noise leads to the disease eradication, while a small one guarantees stochastic permanence. In addition, by the main parameter analyses, several effective measures to stop the spread of an epidemic are provided.

It is generally accepted that the existence of an ergodic stationary distribution incurs difficulty in studying more exact statistical properties. Hence, this paper is devoted to obtaining the corresponding probability density function for further dynamical investigation. The results of Zhou et al. [28] are further perfected and general solving theories of algebraic equations with respect to the three-dimensional Fokker-Planck equation are developed, which are described in Lemmas 2.5 and 2.6. By taking the effect of stochasticity into account again, the quasi-endemic equilibrium E* corresponding to the endemic equilibrium E+ is defined. For practical application, the exact expression of the log-normal three-dimensional density function Φ(S,V,I) of system (1.3) is given. Furthermore, it is worth mentioning that the methods and theories developed herein are still suitable for the case of the diffusion matrix M being positive semi-definite, such as delay stochastic differential equations [32], [48].

Several remaining issues are now proposed and analyzed. First, by virtue of the limitation of the present mathematical approaches for epidemiological dynamics, a value gap exists between R0s and R0d, and it is unfortunate that difficulty is encountered in obtaining the most precise threshold for disease extinction and persistence. Second, the impact of telegraph noises and periodicity on the dynamics of system (1.3) should also be studied; the reader is referred to [30], [34], [45], [49], [50]. These problems are expected to be studied and solved as planned future work.

CRediT authorship contribution statement

Baoquan Zhou: Validation, Software, Formal analysis, Writing - original draft, Writing - review & editing. Daqing Jiang: Conceptualization, Investigation, Methodology, Writing - review & editing. Yucong Dai: Methodology, Formal analysis, Writing - original draft, Writing - review & editing. Tasawar Hayat: Conceptualization, Writing - review & editing. Ahmed Alsaedi: Investigation, Writing - original draft, Writing - review & editing.

Declaration of Competing Interest

We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted.

Acknowledgements

This work was supported by the National Natural Science Foundation of China (Grant No. 11871473) and Shandong Provincial Natural Science Foundation (Grant Nos. ZR2019MA010 and ZR2019MA006).

Appendix A.  

(I) (Proof of Lemma 2.5): Consider the algebraic equation G12+C0Υ3+Υ3C0τ=0, where Υ3 is a symmetric matrix. Letting Υ3:=(κij)3×3, by direct calculation one has

Υ3=(κ1100000000), (A.1)

where κ11=a022c11. If c11<0, then it means that Υ3 is a positive semi-definite matrix. The proof is then completed.

(II) (Proof of Lemma 2.6): Denote

Π1=(100000000),Π2=(000010000),Π3=(000000001).

Let Σi(i=1,2,3) be the solutions of the following algebraic equations, respectively:

Πi+AΣi+ΣiAτ=0.

Obviously, one can obtain

Σ0=α12Σ1+α22Σ2+α32Σ3.

Before proving the positive definiteness of Σ0, the following two theories of matrix algebra should be described first.

(T1). The positive definiteness of the matrix is not affected by the inverse congruence transformation.

(T2). The similarity transformation does not change the eigenvalues of the matrix.

For convenience and simplicity, an important notation is introduced as follows. For the same dimensional square matrix A and B, define

AB:ABisatleastapositivesemi-definitematrix.

Given the above, it is easily derived that A is also positive definite if B is a positive definite matrix.

First, consider the following algebraic equation,

Π1+AΣ1+Σ1Aτ=0, (A.2)

after which the relevant proof can be divided into the following two conditions:

(B1).a21=a31=0,(B2).a210ora310.

Next, one must demonstrate that the elements a21 and a31 have the equivalent status in A. Let A˜=F1AF11:=(a˜ij)3×3, where A˜ and the invertible matrix F1 are given by

F1=(100001010),A˜=(a11a13a12a31a33a32a21a23a22),

respectively. Hence, (A.2) can be equivalently transformed as

F1Π1F1τ+A˜(F1Σ1F1τ)+(F1Σ1F1τ)A˜τ=0. (A.3)

By defining Π˜1=F1Π1F1τ,Σ˜1=F1Σ1F1τ, it can be noticed that

(i).Π˜1=Π1,(ii).Σ˜1andΣ1havethesamepositivedefiniteness.

In addition, a˜21=a31,a˜31=a21. Therefore, the validation is completed. Namely, one must only discuss the following two cases, which are equivalent to conditions (B1) and (B2), respectively:

(C1).a21=a31=0,(C2).a210.

Case (C1). If a21=a31=0, by directly solving Eq. (A.2), one obtains

Σ1=(12a1100000000):=Δ11.

Since A has all negative real part eigenvalues, by the similarity invariance of ψA(λ), it indicates that

λ3+r1λ2+r2λ+r3=ψA(λ)=(λa11)[λ2(a22+a33)λ+(a22a33a23a32)].

Consequently, φA(λ) has an eigenvalue λ1=a11, which has a negative real part. By a11R, then a11<0. In other words, Δ11 is positive semi-definite. Moreover,

Σ1Δ11. (A.4)

Case (C2). If a210, let ω0=a32+a31(a33a22)a21a23a312a212.

If ω0=0, which means a21(a21a32a22a31)a31(a31a23a21a33)=0, let A^=(F3F2)A(F3F2)1, where

F2=(1000100a31a211),F3=(a21a22+a23a31a21a23010001).

Thus, (A.2) can be equivalently rewritten as

(F3F2)Λ1(F3F2)τ+A^[(F3F2)Σ1(F3F2)τ]+[(F3F2)Σ1(F3F2)τ]A^τ=0. (A.5)

Denoting Π^1=(F3F2)Π1(F3F2)τ and Σ^1=(F3F2)Σ1(F3F2)τ, one computes

Π^1=(a21200000000),A^=(ξ1ξ2ξ310000a33a23a31a21),Σ^1=(a2122ξ1000a2122ξ1ξ20000),

where the parameters ξk(k=1,2,3) can be obtained by (A.5). Because their sign is the only object of concern, they are omitted here. Furthermore, the characteristic polynomial ψA(λ) follows from A^ that

ψA(λ)=(λa33+a23a31a21)(λ2+ξ1λ+ξ2).

By the condition that A has all negative real part eigenvalues, it thus means that the equation λ2+ξ1λ+ξ2=0 has two negative real part roots. By the Routh-Hurwitz stability criterion [43], it can be shown that

ξ1>0,ξ2>0. (A.6)

In view of

Σ^1=(a2122ξ1000a2122ξ1ξ20000)=(a2122ξ100000000)+(0000a2122ξ1ξ20000):=L1+L2,

one hence obtains

Σ1=(F3F2)1Σ^1[(F3F2)1]τ=(F3F2)1(L1+L2)[(F3F2)1]τ=(F3F2)1L1[(F3F2)1]τ+(F3F2)1L2[(F3F2)1]τ=(12ξ100000000)+(F3F2)1L2[(F3F2)1]τ:=Δ12+(F3F2)1L2[(F3F2)1]τ. (A.7)

By means of ξ1>0 and ξ2>0, it is derived that Δ12,L2 and (F3F2)1L2[(F3F2)1]τ are all positive semi-definite. It is then implied that

Σ1Δ12. (A.8)

If ω00, let A¯=(F4F2)A(F4F2)1, where the invertible matrix F4 is given by

F4=(a21ω0(a22+a33)ω0(a33a23a31a21)2+a23ω00ω0a33a23a31a21001).

Denoting Π¯1=(F4F2)Λ1(F4F2)τ,Σ¯1=(F4F2)Σ1(F4F2)τ, (A.2) can then be equivalently transformed into the following equation:

Π¯1+A¯Σ¯1+Σ¯1A¯τ=0. (A.9)

Similarly, by direct calculation, one obtains that Π^1=diag((a21ω0)2,0,0), and

A^=(r1r2r3100010),Σ^1=(a21ω0)2(r22(r1r2r3)012(r1r2r3)012(r1r2r3)012(r1r2r3)0r12r3(r1r2r3)),

where r1,r2,r3 are the same as those in Lemma 2.6. Considering

Σ¯1=(a21ω0)2(12r100000000)+(a21ω0)2(r12r3(r1r2r3)012(r1r2r3)012(r1r2r3)012(r1r2r3)0r12r3(r1r2r3)):=L3+L4,

one can therefore derive, by a similar method as that described in (A.7),

Σ1=(F4F2)1Σ¯1[(F4F2)1]τ=(F4F2)1(L3+L4)[(F4F2)1]τ=(F4F2)1L3[(F4F2)1]τ+(F4F2)1L4[(F4F2)1]τ=(12r100000000)+(F4F2)1L4[(F4F2)1]τ:=Δ13+(F4F2)1L4[(F4F2)1]τ.

Noting that Δ13,L4 and (F4F2)1L4[(F4F2)1]τ are all positive semi-definite, one then has

Σ1Δ13. (A.10)

Consequently, by (A.4), (A.8) and (A.10), a constant η1>0 always exists such that

Σ1(η100000000). (A.11)

In addition, for the following two algebraic equations,

(i).Π2+AΣ2+Σ2Aτ=0,(ii).Π3+AΣ3+Σ3Aτ=0,

and letting Π˜2=F5Π2F5τ,Π˜3=F6Π3F6τ,Σ˜2=F5Σ2F5τ,Σ˜3=F6Σ3F6τ,andA2=F5AF51,A3=F6AF61, where

F5=(010001100),F6=(001100010).

Noting that Π˜2=Π˜3=Π1, by a method similar to that shown in (A.2), one can see that

Σ˜2(η200000000),Σ˜3(η300000000),

where the constants η2>0andη3>0; that is to say,

Σ2=F51Σ˜2F51(0000η20000),Σ3=F61Σ˜3F61(00000000η3). (A.12)

In summary, it can be derived that

Σ0=α12Σ1+α22Σ2+α32Σ3(α12η1000α22η2000α32η3).

Given the above definitions and discussions, Σ0 is a positive-definite matrix. This completes the proof.

(III). (SED Preliminaries): For the above complete probability space {Ω,F,{Ft}t0,P}, it is assumed that B(t) is an n-dimensional standard Brownian motion defined on it. Consider the following n-dimensional SDE,

dX(t)=f(X(t),t)dt+g(X(t),t)dB(t),fortt0

, with the initial value X(t0)=X0Rn. A common differential operator L is given by

L=t+k=1nfk(X,t)Xk+12i,j=1n[gτ(X,t)g(X,t)]ij2XiXj.

Letting the operator L act on a function VC2,1(Rn×[t0,+];R+1), one has

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

where Vt=Vt, Vx=(Vx1,...,Vxn) and Vxx=(2Vxixj)n×n. If X(t)Rn, one has

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

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