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. 2020 Jul 2;139:110013. doi: 10.1016/j.chaos.2020.110013

Dynamical behavior of a higher order stochastically perturbed SIRI epidemic model with relapse and media coverage

Qun Liu a, Daqing Jiang b,c,d,, Tasawar Hayat d,e, Ahmed Alsaedi d, Bashir Ahmad d
PMCID: PMC7836743  PMID: 33519104

Abstract

This paper is intended to explore a higher order stochastically perturbed SIRI epidemic model with relapse and media coverage. Firstly, we derive sufficient criteria for the existence and uniqueness of an ergodic stationary distribution of positive solutions to the system by establishing a suitable stochastic Lyapunov function. Then we obtain adequate conditions for complete eradication and wiping out of the infectious disease. In a biological interpretation, the existence of a stationary distribution implies that the disease will prevail and persist in the long term. Finally, the theoretical results are illustrated by computer simulations, including two examples based on real-life disease.

Keywords: SIRI epidemic model, Relapse, Media coverage, Stationary distribution, Ergodicity, Extinction

1. Introduction

In modern society, there is no doubt that public health issue has become a great threat to the global personal and property security, we must take some self-protection measures during the epidemic period. The probe of mathematical modeling is a good way to describe the transmission dynamics of infectious disease and provide effective control strategies [1]. Recently, many scholars have constructed an idea of mathematical models to investigate the dynamics of infectious disease which is named as compartmental model. In the epidemic models the total population is classified as the susceptible compartment (S), the infected compartment (I) and the recovered compartment (R). There exist few occurrences where susceptibles become infectious, then are recovered with temporary immunity and then become infectious again which is called as SIRI model. This recurrence of disease is an important characteristic of some animal and human diseases, for example, tuberculosis including human and bovine and herpes [2], [3].

In case of the breakout of infectious disease in a particular region, the immediate endeavour of disease control authorities is to make a ultimate venture to contain the spread of disease. Educating people about the disease via numerous agencies such as mass media, etc, is one of the significant preventive measures. Mass media plays an important role in propagating the nature and the cause of assorted deadly diseases such as respiratory disease, hepatitis diseases, human immunodeficiency syndrome (HIV), Avian influenza A (H7N9), human tuberculosis (TB), acquired immunodeficiency syndrome (AIDS), severe acute respiratory syndrome (SARS), Ebola virus disease (EVD), etc. Recently, numerous mathematical models have been developed to study the influence of media coverage on the dynamics of infection disease [4], [5], [6], [7], [8], [9], [10]. Caraballo et al. [10], Sun et al. [11] and Li and Cui [12] employed deterministic models to study the impacts of media coverage on the transmission dynamics, in view of the following incidence

g(S,I)=(β1β2Im+I)SI,

where β 1 indicates the contact rate after and before media alert respectively; the term β2Im+I represents the diminished value of the transmission rate when infectious individuals are taken into account. If the infectives are adequately large then the diminished value of the transmission rate tends to its maximum β 2, and infectives reaches m, the diminished value of the transmission rate equals half of the maximum β 2. Due to the inability of the coverage report to prevent disease, spreading rampantly, we have β 1 ≥ β 2 > 0, m denotes reactive velocity of the people and media coverage to the disease. The term Im+I is a continuous bounded function that describes psychological influences or disease saturation. Then the deterministic SIR epidemic model with relapse and media coverage can be expressed as follows:

{dSdt=Λ(β1β2Im+I)SIμ1S,dIdt=(β1β2Im+I)SI(μ2+γ)I+δR,dRdt=γI(μ3+δ)R, (1.1)

where Λ, μ 1, μ 2, μ 3, β 1, β 2, m, γ, δ are all positive constants, S denotes the numbers of the individuals susceptible to the disease, I denotes the infected members and R is the members who have recovered from the infection. The parameters have the following biological meanings: Λ represents the recruitment rate, μ 1, μ 2, μ 3 are the natural death rate of susceptible, infected and recovered compartments respectively. The parameter γ reflects recover rate with temporary immunity and δ represents the relapse rate. The basic reproduction number [13], [14]

R0=β1Λμ1(μ2+γδγμ3+δ)

has a great importance in epidemiology since it is a threshold quantity which determines whether an epidemic occurs or the disease dies out. The following behaviors of solutions according to the value of the threshold R0 can be given:

• If R01, then system (1.1) has only the disease-free equilibrium

E0=(Λμ1,0,0),

and it is globally asymptotically stable in the invariant set Θ.

• If R0>1, then E 0 is unstable, and there is a unique endemic equilibrium E*=(S*,I*,R*) with S* > 0, I* > 0 and R* > 0 which is globally asymptotically stable in the interior of Θ, where

Θ:={(S,I,R):S>0,I0,R0,S+I+RΛmin{μ1,μ2,μ3}}.

However, it is well established that epidemic systems are always subjected to environmental white noise and the influence of fluctuating environmental white noise is not inclusive in the deterministic models [15]. Thus, the deterministic epidemic model has some restrictions to predict the future dynamics accurately [16]. Recently, stochastic differential equation models [17], [18], [19], [20], [21], [22] have played an important role in various branches of applied sciences including infection dynamics and population dynamics, since they can provide some additional degree of realism compared to their deterministic counterparts [23]. And it is hence interesting to introduce the stochastic perturbation into the deterministic system to reveal the effect of environmental white noise on human disease [18], [21], [24], [25], [26], [27]. For example, Gray et al. [18] investigated a stochastic SIS epidemic model with constant population size and degenerate diffusion. They established conditions for extinction and persistence of the disease. Moreover, in the case of persistence, they showed the existence of a stationary distribution and obtained expressions for its mean and variance. In [21], Liu et al. studied the dynamical behavior of a stochastic SIRI epidemic model with relapse and constant population size. The authors used the Markov semigroup theory to obtain the existence of a stable stationary distribution. Caraballo [27] analyzed a stochastic epidemic model with isolation and nonlinear incidence. They established sufficient condition for extinction and obtained necessary and sufficient conditions for persistence in mean of the disease. In particular, they derived the stochastic threshold for the model. However, in the literatures [18], [21] and [27], the authors didn’t consider the effect of the media coverage. In addition, in the literatures [18] and [21], the diffusion matrix is degenerate, the authors cannot use the Has’minskii’s theory to obtain the ergodicity of a stationary distribution, while in the literature [27], although the diffusion matrix is nondegenerate, the authors didn’t studied the existence and uniqueness of an ergodic stationary distribution which implies stochastic weak stability. Accordingly, it is necessary for us to consider both of them together.

To incorporate the effect of environmental white noise, in this paper, motivated by the approach proposed by Liu and Jiang [28], we construct a stochastic differential equation model by introducing the nonlinear perturbation into each equation of system (1.1) as the stochastic perturbation may be dependent on square of the variables S, I and R, respectively. Then to make model (1.1) more reasonable and realistic, we introduce a corresponding stochastic model as follows:

{dS=[Λ(β1β2Im+I)SIμ1S]dt+(σ11S+σ12)SdB1(t),dI=[(β1β2Im+I)SI(μ2+γ)I+δR]dt+(σ21+σ22I)IdB2(t),dR=[γI(μ3+δ)R]dt+(σ31+σ32R)RdB3(t), (1.2)

subject to the initial conditions

S(0)=S0>0,I(0)=I00,R(0)=R00.

Here Bi(t) denote mutually independent standard Brownian motions defined on a complete probability space (Ω,F,{Ft}t0,P) with a filtration {Ft}t0 satisfying the usual conditions [29], i=1,2,3, σ 11 > 0, σ 12 > 0, σ 21 > 0, σ 22 > 0, σ 31 > 0 and σ 32 > 0 denote the intensities of the environmental random disturbance. Note that this model appears when we assume that the parameters μ 1, μ 2 and μ 3 are disturbed by some stochastic perturbation in each equation, that is to say, we replace μ 1, μ 2 and μ 3 by

μ1μ1(σ11S+σ12)B˙1(t),μ2μ2(σ21+σ22I)B˙2(t)andμ3μ3(σ31+σ32R),

in each equation, respectively. A large number of scholars concentrate only on media coverage and they have not considered media coverage with relapse and higher order perturbation [4], [5], [6], [7], [8], [9], [30]. Yet another group of scholars focus only on higher order perturbation [19], [28], [31], [32], [33]. Therefore, it is necessitated that we focus on them together. Investigating such problem is important and meaningful.

The structure of this paper is as follows. In Section 2, we establish sufficient criteria for the existence and uniqueness of an ergodic stationary distribution of positive solutions to the stochastic system (1.2). In Section 3, we obtain sufficient criteria for extinction of the disease. In Section 4, the presented results are demonstrated and confirmed by numerical simulations. Finally, conclusion is provided to end this paper.

Throughout this paper, if G is a matrix, its transpose is denoted by GT. Moreover, we introduce the following notations:

R+d={x=(x1,,xd)Rd:xi>0,1id}andR¯+d={x=(x1,,xd)Rd:xi0,1id}.

To proceed, we should first give some condition under which system (1.2) has a unique global positive solution. Since the proof is similar to the statement of Lemma 1.1 in Liu and Jiang [28], we only state the result without proof.

Lemma 1.1

For any initial value S0 > 0, I 0 ≥ 0, R 0 ≥ 0, there is a unique solution (S(t), I(t), R(t)) to system (1.2) on t ≥ 0 and the solution will remain in R+3 with probability one, namely, (S(t),I(t),R(t))R+3 for all t ≥ 0 almost surely (a.s.).

2. Existence of ergodic stationary distribution

In this section, we will establish sufficient criteria for the existence and uniqueness of an ergodic stationary distribution of positive solutions to the stochastic system (1.2). In a biological viewpoint, the existence of a stationary distribution implies that the disease will be prevalent and persistent when the intensities of stochastic perturbations are adequately small.

Let X(t) be a regular time-homogeneous Markov process in Rd described by the stochastic differential equation

dX(t)=f(X(t))dt+r=1kgr(X(t))dBr(t).

The diffusion matrix of the process X(t) is defined as follows

A(x)=(aij(x)),aij(x)=r=1kgri(x)grj(x).

Lemma 2.1

[34]. The Markov process X(t) has a unique ergodic stationary distribution π( · ) if there exists a bounded open domain URd with regular boundary Γ, having the following properties:

A1: the diffusion matrix A(x) is strictly positive definite for all x ∈ U.

A2: there exists a nonnegative C2-function V such that LV is negative for anyRdU.

Lemma 2.2

For any x ≥ 0, the following two inequalities hold

(a).x3(x12)(x2+1);(b).x4(34x214)(x2+1).

The proofs are based on the following facts

(i)2x3(2x1)(x2+1)=2x32x32x+x2+1=(x1)20,
(ii)4x4(3x21)(x2+1)=4x43x43x2+x2+1=(x21)20.

Theorem 2.1

Assume thatR0S:=β1Λ(μ1+σ1222+2(Λσ11σ12)12+2(Λ2σ112)13)(μ2+γ+σ2122+2(Λ2σ222)13δγμ3+δ+σ3122)>1,then system(1.2)admits a unique stationary distribution π( · ) and it has the ergodic property.

Proof

To prove Theorem 2.1, we only need to verify conditions A 1 and A 2 in Lemma 2.1. We first verify the condition A 1. The diffusion matrix of system (1.2) is given by

A=((σ11S+σ12)2S2000(σ21+σ22I)2I2000(σ31+σ32R)2R2).

Obviously, the matrix A is positive definite for any compact subset of R+3, so the condition A 1 in Lemma 2.1 holds.

Now we verify the condition A 2. For any adequately small constant p ∈ (0, 1), define

R0S(p)=β1Λ(μ1+σ1222+2Λσ11σ121p+2Λ2σ112(1p)23)(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122).

Evidently, limp0+R0S(p)=R0S. Due to the continuity of the function R0S(p) and R0S>1, we can pick p adequately small such that R0S(p)>1. In view of system (1.2), we obtain

L(lnS)=ΛS+(β1β2Im+I)I+μ1+σ1222+σ11σ12S+σ1122S2ΛS+β1I+μ1+σ1222+σ11σ12S+σ1122S2, (2.1)
L(lnI)=β1S+β2SIm+IδRI+μ2+γ+σ2122+σ21σ22I+σ2222I2β1S+β2mSIδRI+μ2+γ+σ2122+σ21σ22I+σ2222I2 (2.2)

and

L(lnR)=γIR+μ3+δ+σ3122+σ31σ32R+σ3222R2. (2.3)

Define

V1(S)=i=12ai(S+bi)pp,V2(S,I)=c1S+c2(I+c3)pp,V1(S)=lnS+V1(S),
V2(S,I,R)=lnI+V2(S,I)+c2c3p1δμ3+δR,V3(R)=lnR+d1(σ31+σ32R)pp+σ31σ32μ3+δR,
V4(S,I,R)=(σ11S+σ12)pp+(σ21+σ22I)pp+(σ31+σ32R)pp,V5(S,I,R)=V2(S,I,R)+d2V1(S)+d3V3(R),

where a 1, a 2, b 1, b 2, c 1, c 2, c 3, d 1, d 2 and d 3 are positive constants which will be determined later. Applying Itô’s formula to V 1, we get

LV1=i=12[ai(S+bi)p1(Λ(β1β2Im+I)SIμ1S)ai(1p)2(S+bi)2p(σ11S+σ12)2S2]i=12aiΛbi1pa1(1p)b1p2σ112S42(Sb1+1)2pa2(1p)b2p2σ11σ12S3(Sb2+1)2pi=12aiΛbi1pa1(1p)b1p+2σ112(Sb1)42(Sb1+1)2a2(1p)b2p+1σ11σ12(Sb2)3(Sb2+1)2i=12aiΛbi1pa1(1p)b1p+2σ112(Sb1)44((Sb1)2+1)a2(1p)b2p+1σ11σ12(Sb2)32((Sb2)2+1)i=12aiΛbi1pa1(1p)b1p+2σ1124[34(Sb1)214]a2(1p)b2p+1σ11σ122(Sb212)=(a1Λb11p+a1(1p)b1p+2σ11216)+(a2Λb21p+a2(1p)b2p+1σ11σ124)3a1(1p)b1pσ11216S2a2(1p)b2pσ11σ122S,

where in the third inequality, we have used Lemma 2.2. Choose

a1=83(1p)b1p,a2=2(1p)b2p,b1=2Λ(1p)σ1123,b2=2Λ(1p)σ11σ12,

then we have

LV12Λσ11σ121p+2Λ2σ112(1p)23σ11σ12Sσ1122S2. (2.4)

Thus, from (2.1) and (2.4) it follows that

LV1ΛS+β1I+μ1+σ1222+σ11σ12S+σ1122S2+2Λσ11σ121p+2Λ2σ112(1p)23σ11σ12Sσ1122S2ΛS+μ1+σ1222+2Λσ11σ121p+2Λ2σ112(1p)23+β1I. (2.5)

Next, applying Itô’s formula to V 2, we have

LV2=c1(Λ(β1β2Im+I)SIμ1S)+c2(I+c3)p1[(β1β2Im+I)SI(μ2+γ)I+δR]c2(1p)2(I+c3)2p(σ21+σ22I)2I2c1Λ+(c2c3p1c1)(β1β2Im+I)SI+c2c3p1δRc2(1p)c3p22(Ic3+1)2pσ222I4c1Λ+(c2c3p1c1)(β1β2Im+I)SI+c2c3p1δRc2(1p)c3p22(Ic3+1)2σ222I4c1Λ+(c2c3p1c1)(β1β2Im+I)SI+c2c3p1δRc2(1p)c3p+2σ222(Ic3)44((Ic3)2+1)c1Λ+(c2c3p1c1)(β1β2Im+I)SI+c2c3p1δRc2(1p)c3p+2σ2224[34(Ic3)214]=c1Λ+(c2c3p1c1)(β1β2Im+I)SI+c2c3p1δR3c2(1p)c3pσ22216I2+c2(1p)c3p+2σ22216,

where in the third inequality, we have used Lemma 2.2. Choose

c1=c2c3p1,c2=83(1p)c3p,c3=2Λ(1p)σ2223,

then we obtain

LV22Λ2σ222(1p)23+c2c3p1δRσ2222I2. (2.6)

Therefore, by (2.2) and (2.6), we have

LV2β1S+β2mSIδRI+μ2+γ+σ2122+σ21σ22I+σ2222I2+2Λ2σ222(1p)23+c2c3p1δRσ2222I2+c2c3p1δμ3+δ[γI(μ3+δ)R]=β1SδRI+μ2+γ+σ2122+2Λ2σ222(1p)23+β2mSI+(σ21σ22+c2c3p1δγμ3+δ)I. (2.7)

Moreover, according to (2.3), we derive

LV3=γIR+μ3+δ+σ3122+σ31σ32R+σ3222R2+d1σ32(σ31+σ32R)p1[γI(μ3+δ)R]d1σ322(1p)2(σ31+σ32R)pR2+σ31σ32μ3+δ[γI(μ3+δ)R]γIR+μ3+δ+σ3122+σ31σ32γμ3+δI+σ3222R2+d1σ32σ31p1γId1σ322(1p)σ31p2R2.

Choose

d1=1(1p)σ31p,

then

LV3γIR+μ3+δ+σ3122+(σ31σ32γμ3+δ+d1σ32σ31p1γ)I. (2.8)

Analogously, we have

LV4=σ11(σ11S+σ12)p1(Λ(β1β2Im+I)SIμ1S)σ1122(1p)(σ11S+σ12)pS2+σ22(σ21+σ22I)p1×((β1β2Im+I)SI(μ2+γ)I+δR)σ2222(1p)(σ21+σ22I)pI2+σ32(σ31+σ32R)p1×(γI(μ3+δ)R)σ3222(1p)(σ31+σ32R)pR2σ11σ12p1Λ1p2σ11p+2Sp+2+σ22σ21p1β1SI+σ22σ21p1δR1p2σ22p+2Ip+2+σ32σ31p1γI1p2σ32p+2Rp+2. (2.9)

Consequently, in view of (2.5), (2.7) and (2.8), we obtain

Proof

Choose

d2=β1Λ(μ1+σ1222+2Λσ11σ121p+2Λ2σ112(1p)23)2,d3=δγ(μ3+δ+σ3122)2,

then we obtain

LV5β1Λμ1+σ1222+2Λσ11σ121p+2Λ2σ112(1p)23+μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122+β2mSI+(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I=(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122)(R0S(p)1)+β2mSI+(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I, (2.10)

where

R0S(p):=β1Λ(μ1+σ1222+2Λσ11σ121p+2Λ2σ112(1p)23)(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122).

Define a C 2-function V¯:R+3R in the following form

V¯(S,I,R)=MV5(S,I,R)lnSlnR+V4(S,I,R),

where M > 0 is a sufficiently large number satisfying the following condition

M(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122)(R0S(p)1)+J13 (2.11)

and

J1=sup(S,I,R)R+3{1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122}<.

In addition, notice that V¯(S,I,R) is not only continuous, but also tends to ∞ as (S, I, R) approaches the boundary of R+3. So it should be lower bounded and achieve this lower bound at a point (S 0, I 0, R 0) in the interior of R+3. Then we define a C 2-function V:R+3R¯+ as follows

V(S,I,R)=MV5(S,I,R)lnSlnR+V4(S,I,R)V¯(S0,I0,R0).

From (2.1), (2.3), (2.9) and (2.10) it follows that

LVM(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122)(R0S(p)1)+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)IΛSγIR1p2σ11p+2Sp+21p2σ22p+2Ip+21p2σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122. (2.12)

Now we are in the position to construct a bounded open domain U ϵ such that the condition A 2 in Lemma 2.1 holds. Define a bounded open set as follows

Uϵ={(S,I,R)R+3:ϵ<S<1ϵ,ϵ2<I<1ϵ2,ϵ3<R<1ϵ3},

where 0 < ϵ < 1 is a small enough number. In the set R+3Uϵ, we can select ϵ small enough such that the following conditions hold

Λϵ+J21, (2.13)
σ11p+2(1p)4ϵp+2+J21, (2.14)
ϵmMβ2, (2.15)
ϵ21M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22), (2.16)
γϵ+J21, (2.17)
σ22p+2(1p)4ϵ2(p+2)+J21, (2.18)
σ32p+2(1p)4ϵ3(p+2)+J21, (2.19)

where J 2 is a positive constant which will be given explicitly in expression (2.21). For the sake of convenience, we can divide R+3Uϵ into six domains,

U1={(S,I,R)R+3:Sϵ},U2={(S,I,R)R+3:S1ϵ},U3={(S,I,R)R+3:S<1ϵ,Iϵ2},
U4={(S,I,R)R+3:I>ϵ2,Rϵ3},U5={(S,I,R)R+3:I1ϵ2},U6={(S,I,R)R+3:R1ϵ3}.

Evidently, Uϵc=R+3Uϵ=U1U2U3U4U5U6. Next, we will show that LV(S,I,R)1 for any (S,I,R)Uϵc, which is equivalent to verifying it on the above six domains, respectively.

Case 1. For any (S, I, R) ∈ U 1, in view of (2.12), we obtain

LVΛS+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122ΛS+J2Λϵ+J21, (2.20)

which follows from (2.13) and

J2:=sup(S,I,R)R+3{Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122}<. (2.21)

Case 2. For any (S, I, R) ∈ U 2, from (2.12) it follows that

LV1p4σ11p+2Sp+2+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ31221p4σ11p+2Sp+2+J2σ11p+2(1p)4ϵp+2+J21, (2.22)

which follows from (2.14).

Case 3. For any (S, I, R) ∈ U 3, by (2.12), we have

LVM(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122)(R0S(p)1)+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122M(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122)(R0S(p)1)+Mβ2mSI+J1+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)IM(μ2+γ+σ2122+2Λ2σ222(1p)23δγμ3+δ+σ3122)(R0S(p)1)+Mβ2m1ϵϵ2+J1+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)ϵ23+1+1=1, (2.23)

which follows from (2.11), (2.15) and (2.16) and

J1=sup(S,I,R)R+3{1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122}<.

Case 4. For any (S, I, R) ∈ U 4, according to (2.12), we get

LVγIR+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ3122γIR+J2γϵ2ϵ3+J2=γϵ+J21, (2.24)

which follows from (2.17).

Case 5. For any (S, I, R) ∈ U 5, by (2.12), we derive

LV1p4σ22p+2Ip+2+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ31221p4σ22p+2Ip+2+J2σ22p+2(1p)4ϵ2(p+2)+J21, (2.25)

which follows from (2.18).

Case 6. For any (S, I, R) ∈ U 6, from (2.12) it follows that

LV1p4σ32p+2Rp+2+Mβ2mSI+M(c2c3p1δγμ3+δ+d2β1+d3σ31σ32γμ3+δ+d1d3σ32σ31p1γ+σ21σ22)I1p4σ11p+2Sp+21p4σ22p+2Ip+21p4σ32p+2Rp+2+σ1122S2+σ3222R2+σ22σ21p1β1SI+σ11σ12S+(β1+σ32σ31p1γ)I+(σ31σ32+σ22σ21p1δ)R+μ1+μ3+δ+σ11σ12p1Λ+σ1222+σ31221p4σ32p+2Rp+2+J2σ32p+2(1p)4ϵ3(p+2)+J21, (2.26)

which follows from (2.19).

Accordingly, from (2.20), (2.22), (2.23), (2.24), (2.25) and (2.26) it follows that for a small enough ϵ,

LV1forall(S,I,R)R+3Uϵ.

Hence the condition A 2 in Lemma 2.1 also holds. By Lemma 2.1, we derive that system (1.2) admits a unique stationary distribution π( · ) and it has the ergodic property. This completes the proof. □

Remark 2.1

From the expression of R0S, we can obtain that if there is no stochastic perturbation in system (1.2), then R0S=R0, so R0S>1 is a generalized result determining the persistence of the disease. In addition, if we only consider the linear perturbation, i.e., σ11=σ22=σ32=0, then

R0S:=R0S=β1Λ(μ1+σ1222)(μ2+γ+σ2122δγμ3+δ+σ3122).

Therefore, R0S>1 can be regarded as a generalized result of Caraballo et al. [10].

3. Extinction

In this section, we will obtain sufficient criteria for extinction of the disease. To this end, we establish the following theorem.

Theorem 3.1

Let (S(t), I(t), R(t)) be the solution to system (1.2) with any initial value S 0 > 0, I 0 ≥ 0, R 0 ≥ 0, then for almost ω ∈ Ω, the solution has the following property:

lim supt1tln(ω1μ2+γβ1Λμ1I(t)+ω2μ3+δR(t))νa.s., (3.1)

where

R0=β1Λμ1(μ2+γδγμ3+δ),ω1=γμ3+δ,ω2=δγ(μ3+δ)(μ2+γβ1Λμ1),
ν:=β10|xΛμ1|π(x)dx+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}12(σ212+σ312).

In particular, if ν < 0, then the disease I will die out exponentially with probability one, i.e.,

limtI(t)=0a.s.

In addition, the distribution of S(t) converges weakly to the measure which has the density

π(x)=Qx22(2Λσ11+μ1σ12)σ123(σ11x+σ12)2+2(2Λσ11+μ1σ12)σ123e2σ12(σ11x+σ12)(Λx+2Λσ11+μ1σ12σ12),x(0,),

where Q is a constant such that 0π(x)dx=1 .

Proof

Consider the following auxiliary logistic equation with stochastic perturbation

dX=[Λμ1X]dt+(σ11X+σ12)XdB1(t), (3.2)

with initial value X0=S0>0.

From Theorem 3.1 of Liu and Jiang [28], we can obtain that system (3.2) has the ergodic property and the invariant density is given by

π(x)=Qx22(2Λσ11+μ1σ12)σ123(σ11x+σ12)2+2(2Λσ11+μ1σ12)σ123e2σ12(σ11x+σ12)(Λx+2Λσ11+μ1σ12σ12),x(0,),

where Q is a constant such that

0π(x)dx=1.

Let X(t) be the solution to (3.2) with initial value X0=S0>0, then employing the comparison theorem of 1-dimensional stochastic differential equation [35], we obtain S(t) ≤ X(t) for any t ≥ 0 a.s.

On the other hand, by Theorem 1.4 of [36], p.27, we can derive that there exists a left eigenvector of

M0=(0δμ2+γβ1Λμ1γμ3+δ0)

corresponding to ρ(M0)=δγ(μ3+δ)(μ2+γβ1Λμ1) (the spectral radius of M 0), which is denoted as (ω1,ω2)=(γμ3+δ,δγ(μ3+δ)(μ2+γβ1Λμ1)), i.e.,

δγ(μ3+δ)(μ2+γβ1Λμ1)(ω1,ω2)=(ω1,ω2)M0.

Define a C 2-function V˜:R+2R+ by

V˜(I,R)=α1I+α2R,

where α1=ω1μ2+γβ1Λμ1, α2=ω2μ3+δ. Applying Itô’s formula [29] to lnV˜, we obtain

d(lnV˜)=L(lnV˜)dt+α1(σ21+σ22I)IV˜dB2(t)+α2(σ31+σ32R)RV˜dB3(t), (3.3)

where

L(lnV˜)=α1V˜[(β1β2Im+I)SI(μ2+γ)I+δR]+α2V˜[γI(μ3+δ)R]α12(σ21+σ22I)2I22V˜2α22(σ31+σ32R)2R22V˜2α1V˜[β1SI(μ2+γ)I+δR]+α2V˜[γI(μ3+δ)R]α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ322R42V˜2=α1β1V˜(SΛμ1)I+α1V˜[β1Λμ1I(μ2+γ)I+δR]+α2V˜[γI(μ3+δ)R]α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ322R42V˜2α1β1V˜(XΛμ1)I+1V˜{ω1μ2+γβ1Λμ1[β1Λμ1I(μ2+γ)I+δR]+ω2μ3+δ[γI(μ3+δ)R]}α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ332R42V˜2α1β1V˜|XΛμ1|I+1V˜(ω1,ω2)(M0(I,R)T(I,R)T)α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ322R42V˜2=α1β1V˜|XΛμ1|I+1V˜(δγ(μ3+δ)(μ2+γβ1Λμ1)1)(ω1I+ω2R)α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ322R42V˜2=α1β1V˜|XΛμ1|I+1V˜(δγ(μ3+δ)(μ2+γβ1Λμ1)1)[(μ2+γβ1Λμ1)α1I+(μ3+δ)α2R]α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ322R42V˜2β1|XΛμ1|+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}α12σ212I2+α12σ222I42V˜2α22σ312R2+α22σ322R42V˜2.

In addition, by Cauchy inequality, we have

V˜2=(α1σ21I1σ21+α2σ31R1σ31)2(α12σ212I2+α22σ312R2)(1σ212+1σ312). (3.4)

Therefore

L(lnV˜)β1|XΛμ1|+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}12(σ212+σ312)α12σ222I42V˜2α22σ322R42V˜2. (3.5)

In view of (3.3), (3.4) and (3.5), we obtain

d(lnV˜)[β1|XΛμ1|+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}12(σ212+σ312)α12σ222I42V˜2α22σ322R42V˜2]dt+α1(σ21+σ22I)IV˜dB2(t)+α2(σ31+σ32R)RV˜dB3(t). (3.6)

Integrating (3.6) from 0 to t and then dividing by t on both sides, we get

lnV˜(t)tlnV˜(0)t+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}12(σ212+σ312)+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}+β1t0t|X(s)Λμ1|ds1t0tα12σ222I4(s)2V˜2(s)ds1t0tα22σ322R4(s)2V˜2(s)ds+1t0tα1σ21I(s)V˜(s)dB2(s)+1t0tα1σ22I2(s)V˜(s)dB2(s)+1t0tα2σ31R(s)V˜(s)dB3(s)+1t0tα2σ32R2(s)V˜(s)dB3(s)=lnV˜(0)t+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}12(σ212+σ312)+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}+β1t0t|X(s)Λμ1|ds1t0tα12σ222I4(s)2V˜2(s)ds1t0tα22σ322R4(s)2V˜2(s)ds+M1(t)t+M2(t)t+M3(t)t+M4(t)t, (3.7)

where

M1(t):=0tα1σ21I(s)V˜(s)dB2(s),M2(t):=0tα2σ31R(s)V˜(s)dB3(s),
M3(t):=0tα1σ22I2(s)V˜(s)dB2(s),M4(t):=0tα2σ32R2(s)V˜(s)dB3(s)

are local martingales whose quadratic variations are respectively

M1,M1(t)=0t(α1σ21I(s)V˜(s))2dsσ212t,M2,M2(t)=0t(α2σ31R(s)V˜(s))2dsσ312t,
M3,M3(t)=0t(α1σ22I2(s)V˜(s))2dsandM4,M4(t)=0t(α2σ32R2(s)V˜(s))2ds.

From the strong large numbers theorem it follows that

limtMi(t)t=0a.s.,i=1,2. (3.8)

Furthermore, in view of the exponential martingales inequality [29], for any positive constants T, α and β, we have

P{sup0tT[Mj(t)α2Mj,Mj(t)]>β}eαβ,j=3,4.

Choose T=k, α=1, β=2lnk, we obtain

P{sup0tk[Mj(t)12Mj,Mj(t)]>2lnk}1k2,j=3,4.

By the Borel-Cantelli Lemma [29], we obtain that for almost all ω ∈ Ω, there is a random integer k0=k0(ω) such that for k ≥ k 0, we derive

sup0tk[Mj(t)12Mj,Mj(t)]2lnk,j=3,4.

That is

M3(t)2lnk+12M3,M3(t)=2lnk+120t(α1σ22I2(s)V˜(s))2ds (3.9)

and

M4(t)2lnk+12M4,M4(t)=2lnk+120t(α2σ32R2(s)V˜(s))2ds (3.10)

for all 0 ≤ t ≤ k, k ≥ k 0 a.s. Substituting (3.9) and (3.10) into (3.7) leads to

lnV˜(t)tlnV˜(0)t+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}12(σ212+σ312)+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}+β1t0t|X(s)Λμ1|ds+M1(t)t+M2(t)t+4lnkt

for all 0 ≤ t ≤ k, k ≥ k 0 a.s. In other words, we have shown that for 0k1tk,

lnV˜(t)tlnV˜(0)t+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}12(σ212+σ312)+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}+β1t0t|X(s)Λμ1|ds+M1(t)t+M2(t)t+4lnkk1. (3.11)

Since X(t) is ergodic and 0xπ(x)dx< a.s., we have

limt1t0t|X(s)Λμ1|ds=0|xΛμ1|π(x)dx. (3.12)

Taking the superior limit on both sides of (3.11) and combining with (3.8) and (3.12), we obtain

lim suptlnV˜(t)tβ10|xΛμ1|π(x)dx+min{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R01}+max{μ2+γβ1Λμ1,μ3+δ}(δγ(μ3+δ)(μ2+γβ1Λμ1)1)1{R0>1}12(σ212+σ312):=νa.s.,

which is the required assertion (3.1). In addition, if ν < 0, we can easily obtain that

lim suptlnI(t)t<0andlim suptlnR(t)t<0a.s.,

which implies that limtI(t)=0 and limtR(t)=0 a.s. In other words, the disease I will die out exponentially with probability one.

Therefore, for any small ϵ > 0 there are t 0 and a set Ωϵ ⊂ Ω such that P(Ωϵ)>1ϵ and (β1β2Im+I)SIβ1SI>β1ϵS for t ≥ t 0 and ω ∈ Ωϵ. Now from

[Λμ1Sβ1ϵS]dt+(σ11S+σ12)SdB1(t)dS[Λμ1S]dt+(σ11S+σ12)SdB1(t),

it follows that the distribution of the process S(t) converges weakly to the measure with the density π. This completes the proof. □

Remark 3.1

From Theorem 3.1, we can derive that if R0>1, σ212 and σ312 are sufficiently large such that ν < 0, then the disease will die out exponentially a.s. However, as far as we know, in the deterministic system (1.1), if R0>1, then the endemic equilibrium E* is globally asymptotically stable. This shows that the disease will prevail and persist in the long term. Hence our result is very different from the one of the deterministic system (1.1). This shows that large white noise will lead to the eradication of the infectious disease.

4. Numerical simulations

In this section, we will present a realistic example to illustrate our theoretical results, that is Herpes simplex virus type 2. As far as we know, Herpes simplex virus type 2 (HSV-2) is a human disease transmitted by close sexual or physical contact. The virus usually infects the oral mucosa or genital tract. An individual with herpes remains infected for life and the virus reactivate regularly producing a relapse period of infectiousness [10]. For herpes an SIRI model is appropriate. In the following examples we will present some numerical simulations to demonstrate the case of HSV-2. We use the same parameters given by Blower [2]. The detailed values of the parameters are presented in Table 1.

Table 1.

List of parameters.

Parameters Description Values Source
Λ Recruitment rate 0.1 [2], [10]
β1 Contact rate before media alert 0.2 [2], [10]
β2 Reduction of the contact rate 0.15 [2], [10]
m Half-saturation constant 1 [2], [10]
μ1 Natural death rate of susceptible compartments 0.05 [2], [10]
μ2 Natural death rate of infected compartments 0.05 [2], [10]
μ3 Natural death rate of recovered compartments 0.05 [2], [10]
γ Recover rate with temporary immunity 0.2857 [2], [10]
δ Relapse rate 0.2857 [2], [10]

For the numerical simulations, we use Milstein’s Higher Order Method mentioned in [37] to obtain the corresponding discretization transformation of system (1.2)

{Sk+1=Sk+[Λ(β1β2Ikm+Ik)SkIkμ1Sk]Δt+(σ11Sk+σ12)SkΔtξk+Sk2(2σ112Sk2+3σ11σ12Sk+σ122)×(ξk21)Δt,Ik+1=Ik+[(β1β2Ikm+Ik)SkIk(μ2+γ)Ik+δRk]Δt+(σ21+σ22Ik)IkΔtηk+Ik2(σ212+3σ21σ22Ik+2σ222Ik2)×(ηk21)Δt,Rk+1=Rk+[γIk(μ3+δ)Rk]Δt+(σ31+σ32Rk)RkΔtζk+Rk2(σ312+3σ31σ32Rk+2σ322Rk2)(ζk21)Δt,

where the time increment Δt > 0, ξk, ηk, ζk are mutually independent Gaussian random variables which follow the distribution N(0, 1) for k=0,1,2,,n.

Example 4.1. In this example, we choose initial values S0=0.2; I0=0.3; R0=0.1 and time step Δt=0.001, σ11=0.01, σ12=0.004, σ212=0.09672245, σ22=0.01, σ312=0.1286, σ322=0.08. Direct calculation leads to that

R0S=β1Λ(μ1+σ1222+2(Λσ11σ12)12+2(Λ2σ112)13)(μ2+γ+σ2122+2(Λ2σ222)13δγμ3+δ+σ3122)1.3512>1.

That is to say, the condition of Theorem 2.1 holds. In view of Theorem 2.1, we derive that system (1.2) admits a unique ergodic stationary distribution π( · ). See Fig. 1 .

Fig. 1.

Fig. 1

The left column shows the paths of S(t), I(t) and R(t) of system (1.2) with initial values S0=0.2; I0=0.3; R0=0.1 under the noise intensities σ11=0.01,σ12=0.004,σ212=0.09672245,σ22=0.01,σ312=0.1286 and σ322=0.08. Other parameter values are given in Table 1. The blue lines represent the solution to system (1.2) and the red lines represent the solution to the corresponding undisturbed system (1.1). The right column displays the histogram of the probability density functions of S, I, R populations. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Example 4.2. In this example, we choose initial values S0=0.2; I0=0.3; R0=0.1 and time step Δt=0.001, σ112=1.6, σ122=1.8, σ212=2, σ222=4, σ312=2, σ322=6. By a simple computation, we obtain

R0=β1Λμ1(μ2+γδγμ3+δ)0.03702<1

and

ν:=β10|xΛμ1|π(x)dxmin{μ2+γβ1Λμ1,μ3+δ}(1δγ(μ3+δ)(μ2+γβ1Λμ1))12(σ212+σ312)0.08583<0.

Thus, the condition of Theorem 3.1 is satisfied. That is to say, the disease will be extinct a.s. Fig. 2 illustrates this.

Fig. 2.

Fig. 2

The column shows the paths of S(t), I(t) and R(t) of system (1.2) with initial values S0=0.2; I0=0.3; R0=0.1 under the noise intensities σ112=1.6,σ122=1.8,σ212=2,σ222=4,σ312=2 and σ322=6. Other parameter values are given in Table 1. The blue lines represent the solution to system (1.2) and the red lines represent the solution to the corresponding undisturbed system (1.1). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

5. Conclusion

In this paper, we have studied the salient features of a higher order stochastically perturbed SIRI epidemic model with relapse and media coverage. We first establish sufficient criteria for the existence and uniqueness of an ergodic stationary distribution of positive solutions to the stochastic system (1.2) by constructing a suitable stochastic Lyapunov function. Then we make up adequate conditions for complete eradication and wiping out of the infectious disease. In a biological viewpoint, the existence of a stationary distribution implies that the disease will be prevalent and persistent in the long term. Moreover, it is a meaningful topic to study whether or not the method used in this paper can be also applicable to other stochastic multi-dimensional epidemic models, such as rabies transmission model, malaria transmission model and syphilis transmission model. These works could be hopping taken up by the future studies and aptly solved.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Acknowledgments

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

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