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. 2020 Feb 12;2020(1):70. doi: 10.1186/s13662-020-2521-6

A stochastic SIR epidemic model with Lévy jump and media coverage

Yingfen Liu 1, Yan Zhang 1,2,, Qingyun Wang 1
PMCID: PMC7224063  PMID: 32435266

Abstract

A stochastic susceptible–infectious–recovered epidemic model with temporary immunity and media coverage is proposed. The effects of Lévy jumps on the dynamics of the model are considered. A unique global positive solution for the epidemic model is obtained. Sufficient conditions are derived to guarantee that the epidemic disease is extinct and persistent in the mean. The threshold behavior is discussed. Numerical simulations are given to verify our theoretical results.

Keywords: Lévy jump, Temporary immunity, Threshold value, Extinction

Introduction

Epidemics have a huge impact on human life, and controlling and eradicating infectious diseases have been a vital problem that needs to be urgently solved in eco-epidemiology research. Mathematical modeling has become an important tool in analyzing the spread and control of infectious diseases. In implementing measures for preventing the spread of diseases, educating people about the correct preventions of diseases through mass media and other platforms at the first opportunity is particularly important [1]. The coverage of epidemics in the media, such as through television, newspaper, and online networks, gives an overview of the risk level and the relative need for precautions in risk areas and encourages the public to take precautionary measures, such as wearing masks, avoiding public places, and frequent hand washing [2]. Thus, in the past few years, many epidemic models integrating the effects of media coverage have been presented and analyzed [311].

Temporary immunity is another important phenomenon in the transmission of epidemic diseases, such as influenza, Chlamydia trachomatis, and Salmonella infection [12]. In the case of temporary immunity, an individual gets a fleeting immunity to a disease after recovery and then becomes susceptible again after some period. For example, after recovery from influenza, there is a long immunity to the same strain of the disease but no immunity against other strains. Many scholars have also paid close attention to the effects of temporary disease immunity on epidemic models [1318]; however, only a few have considered the effects of media coverage and temporary immunity simultaneously.

On the basis of the aforementioned discussion, a deterministic susceptible–infectious–recovered (SIR) model that considered media coverage and temporary immunity is proposed as follows:

{dSdt=ΛμS(t)(β1β2Iα+I)S(t)I(t)+γI(tτ)eμτ,dIdt=(β1β2Iα+I)S(t)I(t)(μ+γ)I(t),dRdt=γI(t)γI(tτ)eμτμR(t), 1.1

where Λ is the recruitment rate, μ denotes the natural death rate, and γ is the treatment rate. τ>0 is the length of temporary immunity period, which denotes the time from recovery to becoming susceptible again. The term I(tτ)eμτ reflects the fact that an individual has survived from natural death in a recovery pool before becoming susceptible again [13]. β=β1β2I(t)α+I(t) denotes the effective contact rate, here, β1 represents the maximal effective contact rate between susceptible and infected individuals, β2I(t)α+I(t) is the maximal reduced effective contact rate as influenced by mass media alert [5, 6]. α>0 is the effect of media coverage on contact transmission, and β1>β2.

On the other hand, epidemic models are inevitably subject to environmental noise and it is necessary to reveal how the environmental noise affects the epidemic model. In the natural world, there are various types of random noises, such as the famous white noise, Lévy jump noise which considers the motivation that the continuity of solutions may be broken under severe environmental perturbations, such as avian influenza, severe acute respiratory syndrome, volcanic eruptions, earthquakes, hurricanes [1921] and a jump process should be introduced to prevent and control diseases, and so on. In this paper, we extend the deterministic system (1.1) to the Brown motion with Lévy jumps, J(t)=0tYγ(u)N˜(ds,du), and mainly consider its effects on the effective contact rate parameter β=β1β2Iα+I such that

ββ+σB˙(t)+J˙(t).

Considering the effects of temporary immunity and media coverage on a stochastic susceptible–infectious–recovered (SIR) epidemic model driven by Lévy noise:

{dS=[ΛμS(t)(β1β2Iα+I)S(t)I(t)+γI(tτ)eμτ]dtdS=(β1β2Iα+I)S(t)I(t)(σdB(t)+Yγ(u)N˜(dt,du)),dI=[(β1β2Iα+I)S(t)I(t)(μ+γ)I(t)]dt+(β1β2Iα+I)S(t)I(t)(σdB(t)dI=+Yγ(u)N˜(dt,du)),dR=[γI(t)γI(tτ)eμτμR(t)]dt. 1.2

The initial conditions are

S(0)=S00,I(ξ)=ϕ1(ξ)0,ϕ1(0)>0,ξ[τ,0],ϕ1C([τ,0];R+), 1.3

where τ>0 is the length of the temporary immunity period, which covers the time from recovery phase to being the susceptible ones again; and σ2(t) denotes the intensity of white noise. B(t) is a standard Brownian motion that is defined on a complete probability space (Ω,F,P) with filtration {Ft}tR+ satisfying the usual conditions ({Ft}tR+ is right continuous and increasing while F0 contains all P-null sets) [2226]. N is a Poisson counting measure with compensator Ñ and characteristic measure λ on a measurable subset Y of (0,) which satisfies λ(Y)<; λ is assumed to be a Lévy measure, such that N˜(dt,du)=N(dt,du)λN˜(du)dt; γ:Y×ΩR is bounded and continuous with respect to λ and is B(Y)×Ft-measurable, where B(Y) is a σ-algebra with respect to the set Y. In this paper, B and N are assumed to be independent of each other.

As the first two equations of models (1.2) do not depend on the third one, then the following equations should be considered:

{dS=[ΛμS(t)(β1β2Iα+I)S(t)I(t)+γI(tτ)eμτ]dtdS=(β1β2Iα+I)S(t)I(t)(σdB(t)+Yγ(u)N˜(dt,du)),dI=[(β1β2Iα+I)S(t)I(t)(μ+γ)I(t)]dt+(β1β2Iα+I)S(t)I(t)(σdB(t)dI=+Yγ(u)N˜(dt,du)). 1.4

Moreover, we make the following assumption.

Assumption (H1)

γ(u) is a bounded function, 1+γ(u)>0 and |Λμγ(u)|δ, uY.

Remark 1

This assumption means that the intensities of Lévy noises are not infinite.

The outline of this paper is as follows. In Sect. 2, a unique positive solution for system (1.4) is obtained. The conditions are derived for the extinction and persistence in the mean of diseases. The threshold behavior is obtained and discussed. In Sect. 3, some numerical simulations are presented to verify our theoretical results of system (1.4).

Main results

Existence and uniqueness of the global solution

In the following, we discuss the existence and uniqueness of the positive solution of system (1.4).

Theorem 2.1

If Assumption (H1)holds, then, for any initial value(S(0),I(0))L1([τ,0];R+2), a unique solution(S(t),I(t))R+2of system (1.4) exists ontτand the solution will remain inR+2with probability one.

Proof

According to the local Lipschitz condition of system (1.4), we see that, for any initial value X0=(S(0),I(0))R+2, a unique local solution (S(t),I(t)) exists on [τ,τe), herein, τe represents the explosion time. To prove that the solution is global, one is required to obtain τe= a.s. Then we suppose that k01 is sufficiently large such that S(0) and I(0) lie within the interval [1/k0,k0]. For each integer k>k0, we define the stopping time τk=inf{t[τ,τe]:S(t)(1/k,k),or I(t)(1/k,k)}. Then τk increases as k. Denote τ=limk+τk, thus ττe. In the following, we need to show that τ=. If not, there are constants T>0 and ε(0,1) satisfying P{τ<}>ε. Thus, an integer k1k0 exists such that P{τkT}ε, for all k>k1. Construct a C2-function V:R+2R+ by

V(S,I)=(SaalnSa)+(I1lnI)+γeμτtτtI(s)ds, 2.1

where a is a constant that will be given later. By virtue of Itô’s formula, we have

dV(S,I)=(1aS)[(ΛμS(β1β2Iα+I)SI+γI(tτ)eμτ)dtσSI(β1β2Iα+I)dB1(t)]+aσ2S2I22S2(β1β2Iα+I)2dtaY[ln(1γ(u)(β1β2Iα+I)I)+γ(u)I(β1β2Iα+I)]λ(du)dtY[aln(1γ(u)(β1β2Iα+I)I)+γ(u)SI(β1β2Iα+I)]N˜(dt,du)+(11I)[((β1β2Iα+I)SI(μ+γ)I)dt+σ(β1β2Iα+I)SIdB(t)]Y[ln(1+γ(u)(β1β2Iα+I)S)γ(u)(β1β2Iα+I)S]λ(du)dt+σ2S2I22I2(β1β2Iα+I)2dt+Y[γ(u)(β1β2Iα+I)SIln(1+γ(u)(β1β2Iα+I)S)]N˜(dt,du)+γIeμτdtγI(tτ)eμτdt=(1aS)[(ΛμS(β1β2Iα+I)SI+γI(tτ)eμτ)]dt+[aσ2S2I22S2(β1β2Iα+I)2aY[ln(1γ(u)(β1β2Iα+I)I)+γ(u)(β1β2Iα+I)I]λ(du)]dt+[(11I)((β1β2Iα+I)SI(μ+γ)I)+σ2S2I22I2(β1β2Iα+I)2]dtY[ln(1+γ(u)(β1β2Iα+I)S)γ(u)(β1β2Iα+I)S]λ(du)dt+γIeμτ2γI(tτ2)eμτ2)dtσ(1aS)(β1β2Iα+I)SIdB(t)+σ(11I)(β1β2Iα+I)SIdB(t)Y[aln(1γ(u)(β1β2Iα+I)I)+γ(u)SI(β1β2Iα+I)]N˜(dt,du)+Y[γ(u)(β1β2Iα+I)SIln(1+γ(u)(β1β2Iα+I)S)]N˜(dt,du)=LV(S,I)dtσ(1aS)(β1β2Iα+I)SIdB(t)+σ(11I)(β1β2Iα+I)SIdB(t)Y[aln(1γ(u)(β1β2Iα+I)I)+γ(u)SI(β1β2Iα+I)]N˜(dt,du)+Y[γ(u)(β1β2Iα+I)SIln(1+γ(u)(β1β2Iα+I)S)]N˜(dt,du). 2.2

Here, LV:R+2R+ is defined as follows:

LV(S,I)=(1aS)[(ΛμS(β1β2Iα+I)SI+γI(tτ)eμτ)]+[aσ2S2I22S2(β1β2Iα+I)2aY[ln(1γ(u)(β1β2Iα+I)I)+γ(u)(β1β2Iα+I)I]λ(du)]+[(11I)((β1β2Iα+I)SI(μ+γ)I)+σ2S2I22I2(β1β2Iα+I)2]Y[ln(1+γ(u)(β1β2Iα+I)S)γ(u)(β1β2Iα+I)S]λ(du)+γIeμτ2γI(tτ2)eμτ2(Λ+μa+μ+γ)aΛS+[aβ2Iα+Iμγ(1eμτ)]I+aσ2S2I22S2(β1β2Iα+I)2+σ2S2I22I2(β1β2Iα+I)2aY[ln(1γ(u)(β1β2Iα+I)I)+γ(u)(β1β2Iα+I)I]λ(du)Y[ln(1+γ(u)(β1β2Iα+I)S)γ(u)(β1β2Iα+I)S]λ(du)(Λ+μa+μ+γ)aΛS+[aβ2Iα+Iμγ(1eμτ)]I+aσ2S2I22S2(β1β2Iα+I)2+σ2S2I22I2(β1β2Iα+I)2+aYφ1λ(du)+Yφ2λ(du), 2.3

where φ1=ln(1γ(u)(β1β2Iα+I)I)γ(u)(β1β2Iα+I)I, φ2=ln(1+γ(u)(β1β2Iα+I)S)+γ(u)(β1β2Iα+I)S and choose a=μ+γ(1eμτ)β2.

On the other hand, notice that d(S+I+γeμttτteμSI(s)ds)=[ΛγIμ(S+I+γeμttτteμSI(s)ds)]dt. Then

S+I+γeμttτteμSI(s)dsΛμ+eμt[S(0)+I(0)+γτ0eμSI(s)dsΛμ]{Λμ,if S(0)+I(0)+γτ0eμSI(s)dsΛμ,S(0)+I(0)+γτ0eμSI(s)ds,if S(0)+I(0)+γτ0eμSI(s)ds>ΛμK.

Then applying the Taylor formula to the function ln(1t) where t=(β1β2Iα+I)Iγ(u) and Assumption (H1) to φ1, we have

φ1=ln(1γ(u)(β1β2Iα+I)I)γ(u)(β1β2Iα+I)I=γ(u)(β1β2Iα+I)I+((β1β2Iα+I)Iγ(u))22(1θγ(u)(2β1β2)I)2γ(u)(β1β2Iα+I)I(2β1β2)2δ22(1(2β1β2)δ)2,

where θ(0,1) is an arbitrary number. Similarly,

φ2=Y[ln(1+γ(u)(β1β2Iα+I)S)γ(u)(β1β2Iα+I)S]λ(du)(2β1β2)2δ22(1(2β1β2)δ)2.

Then

LV(S,I)(Λ+μa+μ+γ)+aσ2K22(2β1β2)2+σ2K22(2β1β2)2+(a+1)δ22(2β1β2)22(1δ(2β1β2))2K˜.

Therefore, we obtain

dV(S,I)K˜dtσ(1aS)(β1β2Iα+I)SIdB(t)+σ(11I)(β1β2Iα+I)SIdB(t)Y[aln(1γ(u)(β1β2Iα+I)I)+γ(u)SI(β1β2Iα+I)]N˜(dt,du)+Y[γ(u)(β1β2Iα+I)SIln(1+γ(u)(β1β2Iα+I)S)]N˜(dt,du). 2.4

Taking the integral on the above inequality from 0 to τkT,

0τkTdV(S,I)0τkTK˜dt0τkTσ(1aS)(β1β2Iα+I)SIdB(t)+0τkTσ(11I)(β1β2Iα+I)SIdB(t)0τkTY[aln(1γ(u)(β1β2Iα+I)I)+γ(u)SI(β1β2Iα+I)]N˜(ds,du)+0τkTY[γ(u)(β1β2Iα+I)SIln(1+γ(u)(β1β2Iα+I)S)]N˜(ds,du), 2.5

where τkT=min{τk,T}. Consequently,

EV(S(τkT),I(τkT))V(S(0),I(0))+K˜E(τkT)V(S(0),I(0))+K˜T.

Let Ωk={τkT}, then P(Ωk)ε. For each ωΩk, S(τk,ω), or I(τk,ω), equals either k or 1/k, and

V(S(τk,ω),I(τk,ω))min{k1lnk,1/k1+lnk}.

Thus,

V(S(0),I(0))+KTE[1Ωk(ω)V(S(ω),I(ω))]εmin{k1lnk,1/k1+lnk}, 2.6

where 1Ωk is the indicator function of Ωk. Letting k, we obtain the contradiction.

The proof is completed. □

The extinction of diseases of system (1.4) with Lévy jumps

In this section, we define

R0=Λ(2β1β2)μ(μ+γ),

and denote x(t)=1t0tx(s)ds, then the extinction of the disease will be discussed in the following.

Theorem 2.2

Suppose(S(t),I(t))be any solution of system (1.4) with an initial value (1.3). Thus:

  1. ifσˆ2>(2β1β2)24(μ+γ), then
    lim suptlnI(t)t(2β1β2)24σˆ2(μ+γ)<0a.s.;
  2. ifR01<Λ2σˆ2μ2(μ+γ)andσˆ2μ(2β1β2)2Λ, then
    lim suptlnI(t)t(μ+γ)(R01Λ2σˆ2μ2(μ+γ))<0a.s.,

whereσˆ2=β12α2σ22(α+N0)2+Yγ2(u)β1αα+N02(1+(2β1β2)δ)2λ(du).

Proof

Applying Itô’s formula, we derive that

dlnI(t)=[(β1β2Iα+I)S(μ+γ)σ2S22(β1β2Iα+I)2]dt+σ(β1β2Iα+I)SdB(t)+Y[ln(1+(β1β2Iα+I)Sγ(u))(β1β2Iα+I)Sγ(u)]λ(du)+Yln(1+(β1β2Iα+I)Sγ(u))N˜(dt,du). 2.7

Then

lnI(t)t=lnI(0)t+(β1β2Iα+I)S(μ+γ)σ22(β1β2Iα+I)2S2+M1(t)t+M2(t)t+1t0tY[ln(1+(β1β2Iα+I)Sγ(u))(β1β2Iα+I)Sγ(u)]λ(du)ds(2β1β2)S(μ+γ)β12α22(α+N0)2σ2S2+M1(t)t+M2(t)t+lnI(0)t+Yγ2(u)β1αα+N02(1+(2β1β2)δ)2λ(du)S2. 2.8

Here, M1(t)=0tσ(β1β2Iα+I)SdB(s) and M2(t)=0tYln(1+γ(u)(β1β2Iα+I)S)N˜(ds,du).

On the other hand, we have

d(S+I+γeμτtτtI(s)ds)=[ΛμS(μ+γ(1eμτ))I]dt. 2.9

Then

S+I+γeμτtτtI(s)dstS(0)+I(0)+γeμττ0I(s)dst=ΛμS(t)(μ+γ(1eμτ))I(t). 2.10

Therefore,

S(t)=Λμμ+γ(1eμτ)μI(t)ϕ(t), 2.11

and here, ϕ(t)=S+I+γeμτtτtI(s)dsμtS(0)+I(0)+γeμττ0I(s)dsμt, thus limtϕ(t)=0. According to (2.11), we obtain

lnI(t)t(2β1β2)S(t)(μ+γ)σˆ2S2(t)+M1(t)t+M2(t)t+lnI(0)t(2β1β2)[Λμμ+γ(1eμτ)μI(t)ϕ(t)](μ+γ)σˆ2[Λμμ+γ(1eμτ)μI(t)ϕ(t)]2+lnI(0)t+M1(t)+M2(t)t=(μ+γ)(Λ(2β1β2)μ(μ+γ)1Λ2σˆ2μ2(μ+γ))μ+γ(1eμτ)μ((2β1β2)2σˆ2Λμ)I(t)+M1(t)t+M2(t)t+ψ(t), 2.12

where

ψ(t)=(2β1β2)ϕ(t)+2σˆ2Λμϕ(t)σˆ2(μ+γ(1eμτ)μI(t)+ϕ(t))2+lnI(0)t.

In addition,

M1,M1t=σ20t(β1β2Iα+I)2S2ds,M2,M2t=0tY(ln(1+(β1β2Iα+I)Sγ(u)))2λ(du)ds,

and

ln(1+β1αα+N0θ)ln(1+(β1β2Iα+I)Sγ(u))ln(1+(2β1β2)θ).

Then we have

M2,M2tmax{(ln(1+(2β1β2)θ))2,(ln(1+β1αα+N0θ))2}λ(Y)t

and

lim suptM1,M1tt=σ2lim supt1t0t(β1β2Iα+I)2S2dsσ2(2β1β2)2(Λμ)2lim suptM1,M1tt<a.s.,lim suptM2,M2ttmax{(ln(1+(2β1β2)θ))2,(ln(1+β1αα+N0θ))2}λ(Y)lim suptM2,M2tt<,a.s.

Thus,

lim suptMi(t)t=0(i=1,2)andlim suptψ(t)=0. 2.13

By virtue of the condition (2) and (2.12), we obtain

lim suptlnI(t)t(μ+γ)(R01Λ2σˆ2μ2(μ+γ))<0a.s.

Moreover, according to (2.12), we have

lnI(t)t(2β1β2)S(t)(μ+γ)σˆ2S(t)2+M1(t)t+M2(t)t+lnI(0)t=σˆ2[S(t)2(2β1β2)σˆ2S(t)](μ+γ)+M1(t)t+M2(t)t+lnI(0)t=σˆ2(S(t)(2β1β2)2σˆ2)2+(2β1β2)24σˆ2(μ+γ)+M1(t)t+M2(t)t+lnI(0)t(μ+γ)+(2β1β2)24σˆ2+M1(t)t+M2(t)t+lnI(0)t. 2.14

According to the condition (1) and (2.14), we obtain

lim suptlnI(t)t(μ+γ)+(2β1β2)24σˆ2<0,a.s.

That is, limtI(t)=0. Moreover, we have

limtS(t)=Λμμ+γ(1eμτ)μlimtI(t)limtϕ(t)=Λμ.

The conclusion is proven. □

Persistence in the mean of system (1.4)

Now we are in a position to discuss the persistence in the mean of the disease and before that some notations are presented in the following.

For convenience, we denote

R1=β1αΛ(μ+γ)μ(α+N0),σ˜=σ22(β1αα+N0)2N02+Y(2β1β2)2δ22(1δ(2β1β2))2λ(du),λ=(μ+γ)(R01σˆ2Λ2μ2(μ+γ)),λ0=μ+γ(1eμτ)μ((2β1β2)2σˆ2Λμ),I=λλ0,I˜=μ(α+N0)((μ+γ)(R11)σ˜)β1α(μ+γ(1eμτ)).

Theorem 2.3

Suppose that Assumption (H1)holds andR11>σ˜2μ+γ, then, for the solution(S(t),I(t))of model (1.4), we have

lim suptI(t)I,lim inftI(t)I˜.

Proof

By virtue of (2.12), we have

lnI(t)t(μ+γ)(R01Λ2σˆ2μ2(μ+γ))μ+γ(1eμτ)μ((2β1β2)2σˆ2Λμ)I(t)+M1(t)t+M2(t)t+ψ(t). 2.15

Then

lnI(t)λtλ00tI(s)ds+F(t), 2.16

here, F(t)=M1(t)+M2(t)+ψ(t)t.

Considering limtF(t)t=0, then, for an arbitrary ζ>0, there exist a T1=T1(ω)>0 and a set Ωk such that F(t)tζ and P(Ωk)1ζ for all tT1, ωΩk. Let Tˆ=max{T,T1}, then according to Lemma 2.2 and Theorem 3 in Ref. [19], we obtain

lim suptI(t)λλ0I. 2.17

On the other hand, by (2.8) and (2.11), we obtain

lnI(t)t=(β1β2Iα+I)S(μ+γ)σ22(β1β2Iα+I)2S2+M1(t)t+M2(t)t+lnI(0)t+1t0tY[ln(1+(β1β2Iα+I)Sγ(u)(β1β2Iα+I)Sγ(u)]λ(du)dsβ1αα+N0S(t)(μ+γ)σ˜+M1(t)t+M2(t)t+lnI(0)t=β1αα+N0[Λμμ+γ(1eμτ)μI(t)ϕ(t)](μ+γ)σ˜+M1(t)+M2(t)+lnI(0)t=(μ+γ)[β1αΛμ(α+N0)(μ+γ)1]σ˜β1α(μ+γ(1eμτ))μ(α+N0)I(t)β1αα+N0ϕ(t)+M1(t)+M2(t)+lnI(0)t=(μ+γ)[R11]σ˜β1α(μ+γ(1eμτ))μ(α+N0)I(t)β1αα+N0ϕ(t)+M1(t)+M2(t)+lnI(0)t. 2.18

As 0<S+IN0, then we derive that <lnI(t)<ln(N0). Thus,

I(t)μ(α+N0)β1α(μ+γ(1eμτ))((μ+γ)(R11)σ˜β1αα+N0ϕ(t)+M1(t)+M2(t)tln(N0)lnI(0)t). 2.19

By virtue of the conclusion limtϕ(t)=0, we derive that

lim inftI(t)μ(α+N0)[(μ+γ)(R11)σ˜]β1α(μ+γ(1eμτ))I˜. 2.20

This completes the proof. □

Discussions and numerical simulations for system (1.4)

In this paper, we propose a stochastic SIR epidemic model that incorporate the effects of temporary immunity and media coverage. Some theoretical results are obtained with the influence of Lévy jumps. We prove that the system has a unique global solution at first. Then the conditions for extinction and persistence of the disease is derived. The results reveal that the intensity of Lévy noises can greatly influence the extinction and persistence of the disease.

In the following, we give some numerical simulations to support our obtained theoretical results of model (1.4) through the Milstein method [27] and Euler numerical approximation [28].

Example 3.1

Choose the parameter values in model (1.2) as follows:

Λ=0.6,β1=0.3,β2=0.2,μ=0.15,γ=0.2,α=1.8,γ(u)=0.07,σ=0.03,S(0)=2,I(0)=0.5,Y=(0,+),λ(Y)=1,

then we have

R1=1.064>1+σ˜2μ+γ=1.0251,

and the condition of Theorem 2.3 is satisfied. Thus, the disease I is persistent with probability one and Fig. 1 confirms it. The red lines, the green lines and the blue lines are solutions of system (1.4), the corresponding deterministic system and the system with white noise, respectively.

Figure 1.

Figure 1

The populations are persistent in the mean for system (1.4)

Example 3.2

Let the parameters be as follows:

Λ=0.3,β1=0.002,β2=0.001,μ=0.6,γ=0.1,α=0.1,σ=0.3,γ(u)=0.6,S(0)=0.5,I(0)=2,Y=(0,+),λ(Y)=1,

then R0=0.0021<1+Λ2σˆ2μ2(μ+γ)1 and σˆ2=1.3023105μ(2β1β2)2Λ=2.7104. Applying the conditions (2) in Theorem 2.2, we derive that the infective population I(t) will be extinct with probability one (see Fig. 2).

Figure 2.

Figure 2

The disease goes to extinction

Example 3.3

In model (1.4), set

Λ=0.3,β1=0.002,β2=0.001,μ=0.15,γ=0.01,α=0.01.

The initial value is (S(0),I(0))=(0.5,0.1). To show the effects of noise to the system (1.4), two cases are considered as follows: (1) σ=0.1, γ(u)=0.1, (2) σ=0.1, γ(u)=0.7, and we obtain Fig. 3, where the green lines, the blue lines the red lines, and the rose lines denote solutions of the deterministic system, the system with white noise, system (1.4) with γ(u)=0.1 and γ(u)=0.7, respectively. We derive that jumps have negative effects for the prevailing of diseases (see Fig. 3).

Figure 3.

Figure 3

The effects of jumps to system (1.4)

At last, some interesting issues merit further investigations. In this paper, the threshold behavior is discussed and two threshold expressions R0 and R1 are obtained. However, the threshold value cannot be derived according to the complex expression of the contact rate and it is an interesting issue left for further work. Moreover, in this paper, we consider the effects of white noise and the Lévy jumps to the model behavior, however, if we also take other perturbations, such as the regime-switching [2931] to the proposal of epidemic model, what will happen? We will also investigate this question in our future work.

Acknowledgments

Acknowledgements

The authors would like to express their sincere thanks to the anonymous referees and associated editor for his/her careful reading of the manuscript.

Availability of data and materials

All data generated or analysed during this study are included in this published article.

Authors’ contributions

All authors contributed substantially to this paper, participated in drafting and checking the manuscript. All authors read and approved the final manuscript.

Funding

This work is supported by The National Natural Science Foundation of China (11901110, 11961003), The National Natural Science Foundation of Jiangxi (20192BAB211003, 20192ACBL20004) and The Foundation of Education Committee of Jiangxi (GJJ160929, GJJ170824).

Competing interests

The authors declare that they have no competing interests regarding the publication of this paper.

Footnotes

Publisher’s Note

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