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. 2017 Dec 5;492:2220–2236. doi: 10.1016/j.physa.2017.11.137

Stochastic persistence and stationary distribution in an SIS epidemic model with media coverage

Wenjuan Guo a,b, Yongli Cai a, Qimin Zhang b,c, Weiming Wang a,*
PMCID: PMC7125861  PMID: 32288104

Abstract

This paper aims to study an SIS epidemic model with media coverage from a general deterministic model to a stochastic differential equation with environment fluctuation. Mathematically, we use the Markov semigroup theory to prove that the basic reproduction number R0s can be used to control the dynamics of stochastic system. Epidemiologically, we show that environment fluctuation can inhibit the occurrence of the disease, namely, in the case of disease persistence for the deterministic model, the disease still dies out with probability one for the stochastic model. So to a great extent the stochastic perturbation under media coverage affects the outbreak of the disease.

Keywords: Epidemic model, Media coverage, Reproduction number, Extinction, Persistence

Highlights

  • A stochastic epidemic model with media coverage is developed.

  • The global dynamics of the deterministic model is shown.

  • The stochastic dynamics of the SDE model is given.

  • The existence of a unique stationary distribution of the SDE model is displayed.

1. Introduction

When an infectious disease appears and spreads in one place, all possible effective ways to prevent the disease will be taken by the departments for disease control and prevention. A rapid and timely measure is through the media coverage to tell people how to prevent the spread of the disease [[1], [2], [3]]. Media education plays a vital role in controlling the spread of the disease. As we know, one big characteristic of the infectious disease is the infectiousness, namely the pathogens of infectious disease, can spread from an infected person to a susceptible person through a certain way. The spread ways of the infectious disease are not the same, and its communication process is influenced by natural factors and social factors [[4], [5]]. When an infectious disease appears, if we can timely find its route of transmission, and encourage people to learn relevant publicity and education of the disease, thus can effectively control the outbreak of the disease. Media coverage may reduce the contact rate of people, which has been found during the spreading of severe acute respiratory syndrome (SARS) in 2003 [[6], [7], [8]].

Assume that the total population N is divided into two groups, susceptible (uninfected) S and infected I, i.e., N=S+I. Then the dynamics of the disease transmission can be governed by the classical SIS epidemic model with mass action incidence rate as follows:

dSdt=ΛμSβSI+γI,dIdt=βSI(μ+γ)I, (1)

where parameters Λ,μ,γ and β are all positive constants. Λ is the recruitment rate of the population, μ the natural death rate of the population, γ the recovery rate of infective individuals, β the contact transmission coefficient. The infectious force βSI in (1) plays a key role in determining the transmission of the disease.

In fact, β depends on the number as well as the pattern of the contact between the susceptible and infected individuals. When the media coverage is intervened, the contact rate may reduce if people know about the transmission way from media and then protect themselves. Generally, from the practical significance we know that the contact rate of susceptible and infectious individuals is a decreasing function. Motivated by Cui et al. [1], we adopt the contact transmission coefficient β as

β=β1β2f(I),

where β1 is the usual contact rate without taking the infected individuals into account, and β2 is the maximum reduced contact rate due to the presence of the infected individuals. However, we know that anyone cannot avoid contact with others, so we assume that β1>β2. The function f(I) satisfies

(H1) f(0)=0, f(I)0 and limIf(I)=1.

Then model (1) can be rewritten as follows:

dSdt=ΛμS(β1β2f(I))SI+γI,dIdt=(β1β2f(I))SI(μ+γ)I, (2)

whose state space is the first quadrant X={(S,I)R+2:S>0,I0}.

On the other hand, many researches have shown that environmental fluctuation has a huge influence on the development of infectious diseases [[9], [10]]. For human disease, the spread and outbreak of the infectious disease is inherently stochastic due to the unpredictability of person-to-person contacts [11] and population suffer from a continuous spectrum of perturbations [12]. Therefore, the variability and randomness of the environment are fed through to the state of the epidemic [13]. A more realistic way of modeling infectious diseases is stochastic differential equation (SDE) models in many cases [[2], [11], [12], [13], [14], [15], [16], [17], [18], [19]].

To incorporate the effect of environmental fluctuations, we formulate a stochastic differential equation (SDE) model by introducing the term multiplicative noise into the growth equations of both the susceptible and the infected populations [20] and assume that the natural death rate μ will fluctuate around some average value due to continuous environment fluctuation. And we introduce randomness into the deterministic model (2) by perturbing μ with μσζ(t):

dSdt=Λ(μσζ(t))(β1β2f(I))SI+γI,dIdt=(β1β2f(I))SI(μσζ(t)+γ)I, (3)

where ζ(t) is a Gaussian white noise and characterized by:

ζ(t)=0,ζ(t)ζ(t)=δ(tt),

where denotes ensemble average and δ() is the Dirac-δ function. σ is a real constant which measures the intensity of environmental fluctuations. And we can rewrite model (3) into the form of stochastic differential equations as follows:

dSt=[ΛμSt(β1β2f(I))StIt+γIt]dt+σStdBt,dIt=[(β1β2f(I))StIt(μ+γ)It]dt+σItdBt. (4)

where Bt is the standard one-dimensional independent Wiener process defined over the complete probability space Ω,F,{Ft}t0,Prob, and the relations between the white noise terms and Wiener process are defined by dBt=ζ(t)dt. And the state space of the SDE model (4) is X, too.

The structure of this article is as follows: In Section 2, we give the analysis of the global disease dynamics of deterministic model (2). In Section 3, we analyze the disease dynamics of stochastic model (4). Numerical investigation and simulations supporting our analytical findings are presented in Section 4. In Section 5, we discuss our new findings in the view of epidemiological implications.

2. Global disease dynamics of deterministic model (2)

One of our purposes in this paper is to investigate the disease dynamics of deterministic model (2). The reproduction number of model (2) can be denoted as

R0=Λβ1μ(μ+γ),

which is a critical parameter to govern the disease dynamics of SIS model (2). Define a bounded set Γ as follows

Γ=(S,I)X:0<S+IΛμX.

Easy to know that model (2) has two equilibria: one is disease-free equilibrium E0=(Λμ,0) which always exists, and the other is the endemic equilibrium E=(S,I) which is a positive solution of the following equation

ΛμS(β1β2f(I))SI+γI=0,(β1β2f(I))SI(μ+γ)I=0, (5)

and S, I satisfy

S=μ+γβ1β2f(I),

and

Λμμ+γβ1β2f(I)(β1β2f(I))μ+γβ1β2f(I)I+γI=0.

Set

F(I)Λμμ+γβ1β2f(I)μI,

easy to know that F(I) is a decreasing function. Since

F(0)=Λμ(μ+γ)β1=Λβ1μ(μ+γ)β1=μ(μ+γ)β1[Λβ1μ(μ+γ)1]=μ(μ+γ)β1(R01),

if R0>1, F(I)=0 has a unique positive solution I, hence model (2) has a unique endemic equilibrium E=(S,I).

Based on the discussions above, we can give the global dynamics of model (2) as follows:

Theorem 2.1

(i) If R01 , the disease-free equilibrium E0=(Λμ,0) of model (2) is globally asymptotically stable;

(ii) If R0>1 , model (2) has a unique endemic equilibrium E=(S,I) which is globally asymptotically stable, and E0 is unstable.

Proof

(i) Define the Lyapunov function

V(S,I)=12(SΛμ)2+θI,

where θ=Λμ . Then,

dVdt=(SΛμ)(ΛμS(β1β2f(I))+γI)+θ(β1β2f(I))SI(μ+γ)I=(SΛμ)(ΛμS)(SΛμ)(β1β2f(I))SI+(SΛμ)γI+θ(β1β2f(I))SIθ(μ+γ)I.

Set

(β1β2f(I))SI=(β1β2f(I))(SΛμ)I+Λμ(β1β2f(I))I.

Then

dVdt=μ(SΛμ)2(SΛμ)2(β1β2f(I))I(SΛμ)θ((β1β2f(I)))I+(SΛμ)γI+θ((β1β2f(I)))SIθ(μ+γ)I=μ(SΛμ)2(SΛμ)2(β1β2f(I))ISθ((β1β2f(I)))I+Λμθ((β1β2f(I)))I+(SΛμ)γI+θ((β1β2f(I)))SIθ(μ+γ)I=(μ+(β1β2f(I))I)(SΛμ)2+Λ(β1β2f(I))μ(μ+γ)μθI+(SΛμ)γI.

Now we consider the term Λ(β1β2f(I))μ(μ+γ). It follows from Taylor expansion f(I)=f(0)+f(0)I+o(I) that

Λ(β1β2f(I))μ(μ+γ)=Λβ1Λβ2(f(0)+f(0)I+o(I))μ(μ+γ)=Λβ1Λβ2f(0)IΛβ2o(I)μ(μ+γ)Λβ1μ(μ+γ)Λβ2f(0)I=μ(μ+γ)(Λβ1μ(μ+γ)1)Λβ2f(0)I.

Hence,

dVdt(μ+(β1β2f(I))I)(SΛμ)2+(μ+γ)(R01)θIΛβ2f(0)θμI2+(SΛμ)γI. (6)

If R0<1, since that S,I are nonnegative, all terms of the right in (6) are nonpositive, i.e.,dVdt0, and dVdt=0 if and only if S=Λμ,I=0. Therefore, the maximal invariant set in {(S,I):dVdt=0} is a singleton {E0}.

If R0=1, we can get

dVdt(μ+(β1β2f(I))I)(SΛμ)2Λβ2f(0)θμI20

and dVdt=0 if and only if S=Λμ,I=0. By LaSalle’s invariance principle [[21], [22]], any solution of model (2) tends to B, where B{(S,I):S=Λμ,I=0} is the largest invariant subset of model (2). By the expression of model (2), B={E0} is a singleton set. So E0 is globally asymptotically stable on the set Γ if R01.

When R0>1, the Jacobian matrix of model (2) is

J=μ(β1β2f(I))Iβ2f(I)SI(β1β2f(I))S+γ(β1β2f(I))Iβ2f(I)SI+(β1β2f(I))S(μ+γ),

and

J(E0)=μβ1Λμ+γ0β1Λμ(μ+γ)

which has two eigenvalues: one is μ<0, the other is β1Λμ(μ+γ)=β1Λμ(μ+γ)μ=(μ+γ)(β1Λμ(μ+γ)1)=(μ+γ)(R01)>0. Thus the disease-free equilibrium E0 is unstable whenever R0>1. This ends the proof of (i).

(ii) The Jacobian matrix model (2) evaluated at E is

J(E)=μ(β1β2f(I))Iβ2f(I)(μ+γ)Iμ(β1β2f(I))β1β2f(I)(β1β2f(I))Iβ2f(I)(μ+γ)Iβ1β2f(I).

The characteristic polynomial of J(E) is

λ2+b1λ+b2=0,

where

b1=μ+(β1β2f(I))I+β2f(I)(μ+γ)Iβ1β2f(I)>0,b2=μ[β2f(I)(μ+γ)I+(β1β2f(I)2)I]β1β2f(I)>0.

By Routh–Hurwitz criterion, we can conclude that E is locally asymptotically stable.

Let N=S+I, it follows from (5) that

Λ=μN,μ+γ=(β1β2f(I))(NI).

Consider the Lyapunov function

V=12(SS+II)2+k(IIIlogII),

where k is a positive constant which will be determined later. Then

dVdt=(SS+II)dNdt+kIIIdIdt=(SS+II)(ΛμN)+kIII((β1β2f(I))I(NI)(μ+γ)I)=(SS+II)(μSμS+μIμI)+k(II)[(β1β2f(I))(NI)(β1β2f(I))(NI)]=μ(SS)22μ(SS)(II)μ(II)2+k(II)[(β1β2f(I))(NI)(β1β2f(I))(NI)+(β1β2f(I))(NI)(β1β2f(I))(NI)]=μ(SS)22μ(SS)(II)μ(II)2kβ2(II)(NI)(f(I)f(I))+k(β1β2f(I))(II)(NN)k(β1β2f(I))(II)2.

Since f(I) is an increasing function, and N>I,

kβ2(II)(NI)(f(I)f(I))<0,NN=SS+II.

Thus,

dVdtμ(SS)2μ(II)2+(k(β1β2f(I))2μ)(SS)(II).

Choose k=2μβ1β2f(I), then k(β1β2f(I))2μ=0, thus,

dVdtμ(SS)2μ(II)20.

By applying the LaSalle’s asymptotic stability theorem [[21], [22]], we can obtain the endemic equilibrium E is globally asymptotically stable.  □

Remark 2.2

It is should be noted that, the difference between our model (2) with Cui’s model (2.3) in [1] is that, the incidence rate in (2) is bilinear, while in Cui’s model, the standard incidence rate.

Remark 2.3

In [1], after giving the basic reproduction number R¯0μ1d+ν+γ, the authors proved that: if R¯0<1, the disease-free equilibrium E0 is globally asymptotically stable by using Lyapunov function (Theorem 3.3 in [1]); if R¯0>1, the unique endemic equilibrium E is globally asymptotically stable by using Dulac function (Theorem 3.4 in [1]). Unfortunately, they had not given any information about the case R¯0=1. And in Theorem 2.1, we show that R0 can govern the disease dynamics: if R01, E0 is globally asymptotically stable; if R0>1, E is globally asymptotically stable. And the proving method is not Dulac function, but Lyapunov function.

3. Stochastic dynamics of SDE model (4)

3.1. Preliminaries

In this section, some definitions and results of Markov semigroup and asymptotic properties are provided to prove the main results of Theorem 3.7.

3.1.1. Markov semigroup [[14], [23], [24], [25], [26], [27]]

Let Σ=(X) be the σ-algebra of Borel subset of X, and m the Lebesgue measure on (X,Σ). D=D(X,Σ,m) denote the subset of the space L1=L1(X,Σ,m) which contains all densities, i.e. 

D={gL1:g1,g=1},

where represents the norm in L1. A linear mapping P:L1L1 is called a Markov operator if P(D)D.

Assume that k:X×X[0,+) is a measurable function such that

Xk(x,y)m(dx)=1,

for almost all yX, and

Pg(x)=Xk(x,y)g(y)m(dy)

is an integral Markov operator. The function k is called a kernel of the Markov operator P.

A family {P(t)}t0 of Markov operator is called a Markov semigroup, if {P(t)}t0 satisfies

  • (a)

    P(0)=Id;

  • (b)

    P(t+s)=P(t)P(s) for s,t0;

  • (c)

    The function tP(t)g is continuous for every gL1.

A Markov semigroup {P(t)}t0 is called integral, if for every t>0, the operator P(t) is an integral Markov operator, i.e., there is a measurable function k:(0,)×X×X[0,) such that

P(t)g(x)=Xk(t,x,y)g(y)m(dy)

for each density g.

Now we present the definition concerning the asymptotic behavior of Markov semigroup. For a Markov semigroup {P(t)}t0, a density g is called invariant, if P(t)g=g for t>0. The Markov semigroup is asymptotically stable if there exists an invariant density g such that

limtP(t)gg=0 for gD.

If the Markov semigroup {P(t)}t0 is formed by a differential equation (e.g., model (4)), the asymptotic stability of Markov semigroup implies that all the solutions of the equation start from a density converge to the invariant density.

If for every gD and a set AΣ,

limtAP(t)g(x)m(dx)=0,

then the Markov semigroup {P(t)}t0 is called sweeping with respect to A.

The following Lemma summarizes some results of asymptotic stability and sweeping.

Lemma 3.1 [[14], [15]] —

Let {P(t)}t0 be an integral Markov semigroup with a continuous kernel k(t,x,y) for t>0 , and it satisfies Xk(x,y)m(dx)=1 for any yX . If for every gD we have

0P(t)g(x)dt>0,

then the semigroup {P(t)}t0 is asymptotically stable or is sweeping with respect to compact sets.

3.1.2. Fokker–Planck equation

For any AΣ, the transition probability function is denoted by P(t,x0,y0,.) for the diffusion process (St,It), i.e., 

P(t,x0,y0,.)=Prob{(St,It)A}

with the initial value (S0,I0)=(x,y). Let (St,It) be a solution of (4) such that the distribution of (S0,I0) is absolutely continuous and has the density v(x,y). Then (St,It) has also the density U(t,x,y), where U(0,x,y)=v(x,y), and U satisfies the following Fokker–Planck equation (See [23] and pp.133–137 in [28])

Ut=12σ22(φU)x222(φU)xy+2(φU)y2(F1U)x(F2U)y, (7)

where φ(x,y)=xy and

F1(x,y)=(μ+12σ2)+Λex(β1β2f(ey))ey+γex+y,F2(x,y)=(μ+γ+12σ2)+(β1β2f(ey))ex.

Now we introduce a Markov semigroup associated with (7). Let P(t)V(x,y)=U(x,y,t) for VD. Since the operator P(t) is a contraction on D, it can be extended to a contraction on L1. Hence, the operator {P(t)}t0 generates a Markov semigroup. Denote A the infinitesimal generator of semigroup {P(t)}t0, i.e., 

AV=12σ22(φV)x222(φV)xy+2(φV)y2(F1V)x(F2V)y.

The adjoint operator of A is as follows

AV=12σ2φ2Vx222Vxy+2Vy2+(F1V)x+(F2V)y.

3.2. Existence and boundedness of the global positive solution

Another purpose in this paper is to investigate the disease dynamics of stochastic model (4). We first illustrate the existence of unique positive global solution of model (4).

Theorem 3.2

There exists a unique positive solution (St,It) of model (4) on t0 with any given initial value (S0,I0)X , and will remain in X with probability one.

The proof of this Theorem 3.2 is rather standard and hence is omitted.

Lemma 3.3

Let Nt=St+It be the total population size in system (4) for an initial value (S0,I0)X . Then we have

limt1t0tN(u)du=Λμ a.s.. (8)

The proof of Lemma 3.3 is similar to Theorem 4 in [16]. So we omit it.

3.3. Stochastic extinction

Denote

R0s=R0σ22(μ+γ),

which can be seen as a threshold of the stochastic extinction (i.e., disease-free) or persistence (i.e., endemic) of disease for SDE model (4). And we now give the stochastic extinction of the SDE model (4) as follows:

Theorem 3.4

Let (St,It) be a solution of SDE model (4) for any given initial value (S0,I0)Γ . If

R0s<1, (9)

then (St,It) has the following property:

limsuptlogIttc<0a.s.limt1t0tSsds=Λμa.s. (10)

where c(μ+γ)(1R0s)>0 .

Proof

By Itô formula, we have

dlogIt=((β1β2f(I))S(μ+γ)σ22)dt+σdBt(β1S(μ+γ)σ22)dt+σdBt.

Hence,

logIttlogI0t+β1t0tS(u)du(μ+γ)σ22σBtt. (11)

From Lemma 3.3, we have

limtsup1t0tS(u)dulimtsup1t0tN(u)du=Λμa.s. (12)

By the strong law of large numbers, we have

limtBtt=0a.s. (13)

Then combining (11), (12), (13), we get

limtsuplogIttβ1Λμ(μ+γ)σ22=(μ+γ)(β1Λμ(μ+γ)σ22(μ+γ)1)=(μ+γ)(R0s1)c.

If R0s<1, limtsuplogItt<c<0 a.s. Thus for any sufficiently small ϵ>0(ϵ<c), there exists T=T(ω) such that

logIt(ω)t<c+ϵ,tT,

that is,

It(ω)e(c+ϵ)t,tT.

By integration,

01t0tIs(ω)ds1t0te(c+ϵ)sds=1t(c+ϵ)(e(c+ϵ)t1)0,(t) (14)

Considering (8), we have

limt1t0tNsds=limt1t0t(Ss+Is)ds=Λμ. (15)

It follows from (14), (15) that

limt1t0tSsds=Λμa.s.

This completes the proof.  □

3.4. Stochastically asymptotic stability and stationary distribution

Before showing the main results of this section, we firstly give some useful lemmas.

Lemma 3.5

For every point (x0,y0)X and t>0 , the transition probability function P(t,x0,y0,.) has a continuous density k(t,x,y;x0,y0)C(R+,X,X) .

Proof

Set X(t)=lnSt,Y(t)=lnIt. By Itô formula, X(t) and Y(t) can satisfy the stochastic system

dX(t)=F1(X(t),Y(t))dt+σdBt,dY(t)=F2(X(t),Y(t))dt+σdBt,

where

F1(x,y)=(μ+12σ2)+Λex(β1β2f(ey))ey+γex+y,F2(x,y)=(μ+γ+12σ2)+(β1β2f(ey))ex.

Set

a(x,y)=F1(x,y)F2(x,y), and b(x,y)=σσ.

The Lie bracket [a,b] can be calculated as follows:

[a,b]=σΛex+β2f(ey)ey(β1β2f(ey))ey(β1β2f(ey))exβ2f(ey)ex+y.

Hence, for any (x,y)X, [a,b](x,y) and b(x,y) are linearly independent, so vector [a,b] and b span the space X. Based on Hörmander theorem (See Theorem 8 in [23]), the transition probability function P(t,x0,y0,.) has a continuous density k(t,x,y;x0,y0)C(R+,X,X).  □

In order to check the positivity of k, we show a method based on support theorems (see, [[29], [30]]). Fix a point (x0,y0)X and a function φC([0,T],R), consider the following integral equations system

x˙φ(t)=σφ(t)+F1(xφ(t),yφ(t)),y˙φ(t)=σφ(t)+F2(xφ(t),yφ(t)), (16)

with the initial value xφ(0)=x0, yφ(0)=y0 and denote Dx0,y0,φ the derivative of the function hxφ+h(T)yφ+h(T) from C([0,T];R) to R2. If the rank of Dx0,y0,φ is 2 for some φC([0,T];R), then k(t,x,y;x0,y0)>0 for x=xφ(T) and y=yφ(T). Let E(t)=f(xφ(t),yφ(t)), where f is the Jacobian matrix of f=F1F2 . For all 0t0tT, set Q(t,t0) is the matrix function such that Q(t0,t0)=I, Q(t,t0)t=E(t)Q(t,t0), v=σσ, then,

Dxo,y0,φh=0TQ(T,s)vh(s)ds. (17)

Lemma 3.6

For each (x0,y0)X , and for every (x,y)X , there exists T>0 such that k(t,x,y;x0,y0)>0 .

Proof

Step 1: We first verify that Dxo,y0,φ has rank 2. Let ϵ(0,T), and h=1[Tϵ,T]. Since Q(T,s)=IE(T)(Ts)+o(Ts), from (17) we have

Dxo,y0,φh=ϵv12ϵ2E(t)v+o(ϵ2),

where

E(t)v=σΛex+β2f(ey)ey(β1β2f(ey))ey(β1β2f(ey))exβ2f(ey)ex+y.

Hence, E(t)v and v are linearly independent. So Dxo,y0,φ has rank 2.

Next we show that for any two points (x0,y0)X and (x,y)X, there exist a control function φ and T>0 such that the solution of system (16) satisfies xφ(0)=x0,yφ(0)=y0,xφ(T)=x,yφ(T)=y. Set zφ=yφxφ, and system (16) becomes

x˙φ(t)=σφ(t)+g1(xφ(t),zφ(t)),z˙φ(t)=g2(xφ(t),zφ(t)), (18)

where

g1(x,z)=(μ+12σ2)+Λex(β1β2f(ez))ez+γex+z,g2(x,z)=γ+(β1β2f(ez))exΛex+(β1β2f(ez))ezγex+z.

Step 2: Now we check that for any (z0,z)R2 such that z0z there exists a xˆ sufficiently large, a control functionφ, T>0 and a solution (xφ(t),zφ(t)) of system (18) with the value as follows

zφ(0)=z0,zφ(t)=z,xφ(t)=xˆ.

Case 2–1: Since limxf(x)=1 , then β1β2f(ez)β1β2. If z0<z, let xˆ large enough such that

γ+(β1β2)exˆΛexˆγex+z>0.

Let z(t) of the initial problem

z˙(t)=g2(xˆ,z(t)),z(0)=z(0),

in the maximal interval [0,τ). We choose the control function φ(t)=1σg1(xˆ,z(t)), (xφ(t),zφ(t))=(xˆ,z(t)) is the solution of system (18), and there exists τ1>0 such that z(τ1)[z0,z]. If not, z(t) will be bounded. Hence, τ=. On the other hand, for all t0, we obtain

z˙(t)=g2(xˆ,z(t))γ+(β1β2)exˆΛexˆγex+z>0.

Hence z(t)(t). But this contradict the assumption that z(t) is bounded. Then we discuss our true assertion as follows:

  • If z(0)=z0<z<z(τ1), we can find a T(0,τ1) such that zφ(T)=z.

  • If z(τ1)<z0<z, by the mean value theorem, there exists τ2(0,τ1) such that
    z˙(τ2)=z(τ1)z0τ1<0. (19)
    Then z<z(τ2), if not, z(τ2)z. Since
    z˙(t)=g2(xˆ,z(t))γ+(β1β2)exˆΛexˆγex+z(τ2)γ+(β1β2)exˆΛexˆγex+z>0,
    which contradict (19). Then z(0)=z0<z<z(τ2) and there exists T(0,τ2) such that zφ(T)=z.

Case 2–2: If z<z0, let xˆ sufficiently small such that

γ+β1exˆΛexˆ+β1ez<0.

By an analogical argument applied above, we obtain the conclusion of case 1.

Step 3: In this step we check that for any (x0,x)R2 such that x0x and for all z0R, there exists a z0ˆ(z0ϵ,z0+ϵ), a control function φ, T>0 and a solution (xφ(t),zφ(t)) of system (18) where

xφ(0)=x0,xφ(T)=x,zφ(0)=z0,zφ(T)=zˆ0.

Case 3–1: If x0<x, we choose l>0 sufficiently large such that x<x0+12l. Let

m=max{|g1(x,z)|+|g2(x,z)|:(x,z)[x0l,x0+l]×[z0l,z0+l]}.

Let ϵ>0 sufficiently small such that ϵ<12l and τ0>0 such that τ0<ϵm. Then we choose a constant such that the control function satisfies

lτ0+mσφl2τ0m.

Note the condition τ0<l4m, and the control function φ surely exists. Since (xφ(t),zφ(t)) is the solution of the following initial problem:

x˙φ(t)=σφ(t)+g1(xφ(t),zφ(t)),xφ(0)=x0,z˙φ(t)=g2(xφ(t),zφ(t)),zφ(0)=z0,

then for all tτ0 and ϵ we have

|xφ(t)x0|=|σφt+0tg1(xφ(u),zφ(u))du|σ|φ|τ0+0t|g1(xφ(u),zφ(u))|du(σ|φ|+m)τ0l,

and

|zφ(t)z0|=|0tg2(xφ(u),zφ(u))du|mτ0ϵ. (20)

Furthermore,

xφ(τ0)=x0σφτ0+0τ0g1(xφ(u),zφ(u))dux0σφτ0mτ0x0+12l.

Therefore, x(0)=x0<x<x0+12lxφ(τ0) and there exists T(0,τ0) such that xφ(T)=x. In addition, from (20) we exclude the existence of zˆ0(z0ϵ,z0+ϵ) such that zφ(t)=zˆ0.

Case 3–2: If x<x0, we choose l>0 sufficiently large such that 12l<x<x0. We define m and τ0 as in case 1, then we choose a constant such that the control function satisfies

l2τ0+mσφlτ0m.

By an analogical argument applied in Case 3–1, we have

xφ(τ0)x012l<x<x0=xφ(0),

and we can get the same conclusion in Case 3–1.

Step 4: Now we check that for any (x0,x)R2 such that x0x and for all z0R, there exists a zˆ0(z0ϵ,z0+ϵ) , a control functionφ, T>0 and a solution (xφ(t),zφ(t)) of system (18) where

xφ(0)=x0,xφ(T)=x,zφ(0)=zˆ0,zφ(T)=z0. (21)

From Step 2, we know that there exists a constant control function φ, T>0 and zˆ0(z0ϵ,z0+ϵ) such that the solution of the system

x~˙φ(t)=σφ(t)g1(x~φ(t),z~φ(t)),z~˙φ(t)=g2(x~φ(t),z~φ(t))

verifies

x~φ(0)=x,x~φ(T)=x0,z~φ(0)=z0,z~φ(T)=zˆ0.

Hence, (xφ(t),zφ(t)) such that xφ(t)=x~φ(Tt) and zφ(t)=z~φ(Tt) is the solution of (18) that satisfies the properties in (21).

Step 5: Let (x0,z0)R2, (x,z)R2 and ϵ>0 small enough, and we assume that z0<z.

  • From Step 2, there exists xˆR sufficiently large, xˆx0 and xˆx, a control function φ1, T1>0 such that
    zφ1(0)=z0ϵ,zφ1(T1)=z+ϵ,xφ(t)=xˆ.
  • From Step 3, there exists zˆ0(z0ϵ2,z0+ϵ2), a control function φ2, T2>0 such that
    xφ2(0)=x0,xφ(T2)=xˆ,zφ2(0)=z0,zφ2(T2)=zˆ0.
    Since zˆ0(z0ϵ2,z0+ϵ2)(zφ1(0),zφ1(T1)), there exists t1(0,T1) such that zˆ0=zφ1(t1).
  • From Step 4, there exists zˆ(zϵ2,z+ϵ2), a control function φ3, T3>0 such that
    xφ3(0)=xˆ,xφ(T3)=x,zφ3(0)=zˆ,zφ3(T3)=z.
    Since zˆ(z0ϵ2,z0+ϵ2)(zφ1(0),zφ1(T1)), there exists t2(0,T1) such that zˆ=zφ1(t2).

Next we assume that t1t2 without loss of generality, consider the control function φ defined by

φ(t)=φ2(t),0tT2φ1(tT2+t1),T2<tT2+t2t1φ3(tT2t2+t1),T2+t2t1<tT,

where T=T2+t2t1+T3. Then we have

xφ(0)=x0,zφ(0)=z0,xφ(T)=x,zφ(T)=z.

Hence,

xφ(0)=x0,yφ(0)=y0,xφ(T)=x,yφ(T)=y.

This claims that k(t,x,y;x0,y0)>0.  □

Following, we give the main results of this section of the SDE model (4) as follows:

Theorem 3.7

Let (St,It) be a solution of the SDE model (4) for any given initial value (S0,I0)Γ . If

R0s>1andσ2<2μmin{1,A} (22)

hold, then the semigroup {P(t)}t0 is asymptotically stable, where

A=min{S2,I2}S2+I22μσ22μλI,λ=2μβ1β2f(I).

Proof

According to Lemma 3.5, it follows that {P(t)}t0 is an integral Markov semigroup with a continuous kernel k(t,x,y,x0,y0) . Then from Lemma 3.6 for every fD, we have

0P(t)fdt>0a.s.

By virtue of Lemma 3.1, it follows that the semigroup {P(t)}t0 is asymptotically stable or sweeping with respect to compact sets. In order to exclude the sweeping case, we shall construct a non-negative C2 -function V and a closed set OΣ such that

sup(S,I)XOAV<0.

In fact, when R0s>1, R0=R0s+σ22(μ+γ)>1, from (5) we know model (2) has an endemic equilibrium E. Then we know

Λ=μS+(β1β2f(I))SIγI,(β1β2f(I))SI=(μ+γ)I,

then we have

Λ=μS+μI.

Set

V=12(SS+II)2+λ(IIIlnII)V1+λV2,

where λ is defined as in Theorem 3.7. Then

AV1=(SS+II)(ΛμSμI)+12σ2S2+12σ2I2=μ(SS)2μ(II)22μ(SS)(II)+12σ2S2+12σ2I2,
AV2=(II)((β1β2f(I))S(μ+γ))+12σ2I=(II)((β1β2f(I))S(β1β2f(I))S+(β1β2f(I))S(β1β2f(I))S)+12σ2I=(β1β2f(I))(SS)(II)β2(f(I)f(I))(II)S+12σ2I,
AV=AV1+λAV2μ(SS)2μ(II)2+(λ(β1β2f(I))2μ)(SS)(II)+12σ2S2+12σ2I2+λ2σ2I.

Set λ(β1β2f(I))2μ=0, and λ=2μβ1β2f(I). Then we have

AVμ(SS)2μ(II)2+12σ2S2+12σ2I2+λ2σ2I=(μσ22)(S2μ2μσ2S)2(μσ22)(I2μ2μσ2I)2+μσ22μσ2(S2+I2)+λ2σ2Ib1(Sb2S)2b1(Ib2I)2+b3.

Under conditions (22), we can obtain

μσ22μσ2(S2+I2+2μσ22μλI)<2μ22μσ2min{S2,I2}.

From what has been discussed above, the ellipsoid

b1(Sb2S)2b1(Ib2I)2+b3=0

lies entirely in X. Hence there exists a closed set OΣ which contains the ellipsoid and c>0 such that

sup(S,I)XOAVc<0.

The proof is hence completed.  □

Remark 3.8

By virtue of Theorem 3.7, the stochastic process (St,It) has a unique stationary distribution with density v(x,y).

4. Applications

In this section, we apply the analytical results above to an SIS model.

4.1. An example

As an example, we choose the function f(I) as

f(I)=IM+I,

which was proposed by Cui et al. [1]. And model (2) becomes

dSdt=ΛμS(β1β2IM+I)SI+γI,dIdt=(β1β2IM+I)SI(μ+γ)I, (23)

and the stochastic version (4) is

dSt=[ΛμSt(β1β2ItM+It)StIt+γIt]dt+σStdBt,dIt=[(β1β2ItM+It)StIt(μ+γ)It]dt+σItdBt. (24)

It is easy to verify that f(I) satisfy the Assumption (H1). Then model (23) has a disease-free equilibrium E0=(Λμ,0) and an endemic equilibrium E=(S,I) when R0>1:

S=(μ+γ)(M+I)β1(M+I)β2I,I=(M+I)(Λβ1μ(μ+γ))Λβ2Iμ(β1(M+I)β2I).

From Theorem 2.1, Theorem 3.7, we can obtain the following results.

Theorem 4.1

(a) For the deterministic model (23) ,

(a-1) If R01 , the disease-free equilibrium E0=(Λμ,0) is globally asymptotically stable and unstable if R0>1 ;

(a-2) If R0>1 , the endemic equilibrium E=(S,I) is globally asymptotically stable.

(b) For the stochastic model (24) ,

(b-1) if R0s=R0σ22(μ+γ)<1 , the disease dies out with probability one;

(b-2) If R0s>1 and σ2<2μmin{1,min{S2,I2}S2+I22μσ22μ2μβ1I} hold, the semigroup {P(t)}t0 is asymptotically stable, and the system exhibits stationary distribution.

4.2. Numerical simulations and dynamics comparisons

In this subsection, in order to show different dynamical results of the deterministic model (23) and its stochastic description (24) under the same condition of parameter values, we present some numerical simulations. We use the Milstein’s method [17] to simulate the stochastic model (24). The numerical scheme for stochastic model (24) is given by:

Sk+1=Sk+[ΛμSk(β1β2IkM+Ik)SkIk+γIk]Δt+σSkΔtξk+σ22Sk(ξk21)Δt,Ik+1=Ik+[(β1β2IkM+Ik)SkIk(μ+γ)Ik]Δt+σIkΔtξk+σ22Ik(ξk21)Δt,

where ξk(k=1,2,,n) are independent Gaussian random variables N(0,1).

For the deterministic model (23) and its stochastic description (24), the parameter values are taken as in Table 1.

Table 1.

Parameter values of numerical simulations.

Parameters and the epidemiological meaning Value References
Λ: The recruitment rate of the population 0.2 Estimated
μ: The natural death rate 0.05 [2]
β1: The contact rate without infections individuals 0.15 [[1], [2]]
β2: The maximum reduced contact rate 0.1 [2]
γ: The recovery rate of I 0.05 [31]
M: A constant such that f(I) satisfies (H1) 10 [[1], [2]]

Note that R0s=R0σ22(μ+γ)<R0, if R0<1, then R0s<1. We can know that if I(t) goes to extinction for the deterministic model (23), from Theorem 4.1, for the stochastic (24), I(t) almost surely tends to zero exponentially with probability one. Therefore, we only consider the case of R0>1.

With the parameters in Table 1, we can obtain that R0=Λβ1μ(μ+γ)=6.0>1, and deterministic model (23) has a unique endemic equilibrium E=(0.7953,3.2047) which is globally stable for any initial values (S0,I0) according to Theorem 4.1 (a-2)(see Fig. 2).

Fig. 2.

The paths of St,It of SDE model (24) with initial (S0,I0)=(5,1) under different noise intensities σ=0.03(a), σ=0.05(b), and σ=0.07(c), respectively. Other parameters are given in Table 1.

Fig. 2(a).

Fig. 2(a)

(a) σ=0.03,R0s=5.9955.

Fig. 2(b).

Fig. 2(b)

(b) σ=0.05,R0s=5.9875.

Fig. 2(c).

Fig. 2(c)

(c) σ=0.07,R0s=5.9755.

Next we focus on the role of noise strength in the resulting dynamics for the SDE model (24).

4.2.1. Stochastic endemic dynamics

We first choose the environment fluctuations intensity σ=0.03, then R0s=5.9955>1 and σ2=0.0009<0.1×min{1,0.0720}. Thus from Theorem 4.1 (b-2), we can conclude that the disease is almost surely persistent, and the numerical results are shown in Fig. 2 (a). From Fig. 2 (a), we can see that, after some initial transients the solutions St and It of the SDE model (24) fluctuate around the deterministic steady state values S=0.7953 and I=3.2047 of the deterministic model (23), respectively. To see the increased level of non-equilibrium fluctuation in the system dynamics with the increasing noise intensity, we increase σ to 0.05, R0s=5.9875>1, σ2=0.0025<0.1×min{1,0.0717}; when σ increase to 0.07, R0s=5.9755>1, σ2=0.0049<0.1×min{1,0.0713}. The similar outcomes of Fig. 2 (a) of the paths of St and It are presented in Figs. 2 (b) and 2 (c).

For the sake of learning the effects of the noise on the disease dynamics further, we have repeated the simulation 10000 times keeping all parameters fixed and never observing any extinction scenario up to t=100. In Fig. 3, by virtue of Theorem 4.1 and Remark 3.8, we show the existence of the unique stationary distributions for St and It of model (24) at t=300, where the smooth curves are the probability density functions of St and It, respectively, and the numerical method for them can be found in Appendix B in [12]. From Fig. 3, one can find that, the solutions (St,It) to the SDE model (24) for higher σ (e.g., σ2=0.07) that the amplitude of fluctuation is remarkable and the distribution of the solution is skewed, while for lower σ (e.g., σ=0.03), the amplitude of fluctuation is slight and the oscillations are more symmetrically distributed. More precisely, when σ=0.03, the distribution appears closer to a normal distribution (See Fig. 3 (a)), but as σ2 increases to 0.5, the distribution is positively skewed (See Fig. 3 (c)). Obviously, in all these three persistent cases, the SDE model (24) has a stationary distribution.

Fig. 3.

Histogram of the probability density function of S(100) (left column) and I(100) (right column) population for the stochastic model (24) with three different values of σ: σ=0.03 (upper panel), 0.05 (middle panel) and 0.07 (lower panel), the smoothed curves are the probability density functions of St and It, respectively. Other parameters are given in Table 1.

Fig. 3(a).

Fig. 3(a)

(a) σ=0.03.

Fig. 3(b).

Fig. 3(b)

(b) σ=0.05.

Fig. 3(c).

Fig. 3(c)

(c) σ=0.07.

From the figures above we can see, when σ=0.03, σ=0.05 or σ=0.07, as long as the condition of Theorem 4.1 (b-2) is satisfied, the stochastic model (4) has a stationary distribution. The stationary distribution of (St,It) are showed from 10,000 simulation runs under the three different noise intensities at t=100. Numerical simulation reflect that the distribution at t=100 remains stable in the future time. From Fig. 3 we know that the smoothed curves are the probability density functions of St and It. The distributions of Fig. 3 reflect the stationary distribution has a big change with the increasing value of σ. It means the mean values and the skewness of the distribution for St and It vary as the increasing magnitude of σ. Namely, when σ=0.03, the distribution is close to a standard distribution, and when σ=0.07, the distribution is positively skewed.

4.2.2. Stochastic disease-free dynamics

During the numerical experiments for the SDE model (24), the values of It are not equals to zero, and we assume that 10,000 individuals are deemed to be 1 unit susceptible or infected population approximately in this paper. In other words, if the value of It is less than 0.0001, the infected population can be regarded as extinction.

As an example, we choose the white noise intensity σ=1.01, and R0s=0.8995<1. That is, according to the results of Theorem 4.1 (b-1), the disease exponentially goes to extinction almost surely, i.e. It tends to zero exponentially a.s. (see Fig. 4 (a)). In order to understand the effect of the noise intensity σ, we choose three different values of σ as 1.03 (see Fig. 4 (b)), 1.05 (see Fig. 4 (c)) and 1.07 (see Fig. 4 (d)). For σ=1.03 and 1.05, R0s=0.6955 and 0.4875, respectively. Furthermore, if we repeat 10,000 numerical simulations with these three different values of σ, we can know that the average extinction time of It is 20.196, 19.3475 and 18.1035, respectively. We may conclude that the average extinction time decreases with the increase of noise intensity σ.

Fig. 4.

The paths of It of SDE model (24) with initial (S0,I0)=(5,1) and other parameters are taken as Table 1.

Fig. 4(a).

Fig. 4(a)

(a) σ=1.01.

Fig. 4(b).

Fig. 4(b)

(b) σ=1.03.

Fig. 4(c).

Fig. 4(c)

(c) σ=1.05.

5. Conclusions and remarks

The outbreak of the epidemic diseases has brought great damage and loss to people. Many scholars are devoted to reduce the outbreak of the disease for a long time, and many prevention strategies such as media coverage have been used to control and suppress the outbreak of infectious diseases. However, the effects of environmental fluctuation on the epidemic cannot be ignored. In our present paper, we research the influence of environment noise on the dynamics behavior of the disease. There are two aspects in our research significances:

Mathematically, we study the global dynamics of deterministic epidemic model (2) and its corresponding stochastic version (4). For the deterministic case (2), we introduce the basic reproductive number R0 as a threshold parameter to determine whether there is an endemic: if R01, the disease-free equilibrium E0 is globally asymptotically stable; while if R0>1, the endemic equilibrium E is globally asymptotically stable. And for the stochastic case (4), by using the Markov semigroup theory, we prove that we can use the corresponding basic reproduction number R0s to govern the stochastic dynamics: If R0s1, almost all solutions of model (4) tend to the absorbing set E0, that is, the disease will go extinct with probability one; while if conditions

R0s>1andσ2<2μmin{1,A}

hold, the disease will break out with probability one. It should be noted that the condition above is a sufficient condition for the persistence of disease, not a necessary and sufficient condition.

Epidemiologically, we partially provide the effects of the environment fluctuations on the disease spreading to the SDE model (4). We summarize our main findings as follows:

  • 1.

    Large environment fluctuations can suppress the disease outbreak: Theorem 3.4 indicates that the extinction of disease in the stochastic model (4) occurs if the basic reproduction number R0s<1. Theorem 2.1 shows that the deterministic model (2) admits a unique endemic equilibrium E which is globally asymptotically stable if its basic reproduction number R0>1. Notice that R0s=R0σ22(μ+γ)<R0, and hence there may exist a fact that R0s<1<R0. This is the case when the deterministic model (2) has an endemic (see Fig. 1) while the stochastic model (4) has disease extinction with probability one (see Fig. 4). This implies that large environment fluctuations under media coverage in I-class can suppress the outbreak of disease.

  • 2.

    The stationary distribution exists in the case of R0s>1: As suggested in Theorem 3.7, Remark 3.8 and Fig. 3, the stochastic model (4) has a stationary distribution if R0s>1 (c.f., Fig. 3), which leads to the stochastic persistence of the disease.

Fig. 1.

Fig. 1

The time-series plots of St,It for the deterministic model (23) with initial (S0,I0)=(5,1), and other parameters are taken as Table 1, R0=6.0>1.

It isshould be pointed out that, although our SDE model (4) is similar to that in [2] (one incidence rate is bilinear, the other is standard [2]), the proving methods for stochastically disease dynamics are very different. In [2], the authors used the method of stochastic stability, and here, we use the Markov semigroup theory to prove stochastically asymptotic stability of model (4). On the other hand, in [2], the authors proved that if R0s<1, under an extra conditions of σ, the disease goes to extinct with probability one (Theorem 3.1 in [2]); and in Theorem 3.4, we show that only when R0s<1, does the disease die out almost surely, regardless of the intensity of environmental fluctuations σ. This point may show the different effect on the stochastic dynamics between the bilinear incidence rate with the standard incidence rate.

Acknowledgments

The research was supported in part by the Natural Science Foundation of China (61672013, 11661064, 11601179, 11461053 and 61772017) and the Natural Science Foundation of the Jiangsu Higher Education Institutions of China (16 kJB110003).

Contributor Information

Wenjuan Guo, Email: wenjuanguowj@sina.com.

Yongli Cai, Email: yonglicai@hytc.edu.cn.

Qimin Zhang, Email: zhangqimin@nxu.edu.cn.

Weiming Wang, Email: wangwm_math@hytc.edu.cn.

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