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. 2022 Nov 11;2022(1):85. doi: 10.1186/s13661-022-01668-0

Dynamics and stationary distribution of a stochastic SIRS epidemic model with a general incidence and immunity

Tao Chen 1, Zhiming Li 1,
PMCID: PMC9651908  PMID: 36405431

Abstract

Infected individuals often obtain or lose immunity after recovery in medical studies. To solve the problem, this paper proposes a stochastic SIRS epidemic model with a general incidence rate and partial immunity. Through an appropriate Lyapunov function, we obtain the existence and uniqueness of a unique globally positive solution. The disease will be extinct under the threshold criterion. We analyze the asymptotic behavior around the disease-free equilibrium of a deterministic SIRS model. By using the Khasminskii method, we prove the existence of a unique stationary distribution. Further, solutions of the stochastic model fluctuate around endemic equilibrium under certain conditions. Some numerical examples illustrate the theoretical results.

Keywords: SIRS epidemic model, General incidence, Stationary distribution, Partial immunity

Introduction

Infectious diseases have been a severe threat to human health. Many disasters in history have been due to the outbreak of contagious diseases, such as the plague pandemic, smallpox, the Black Death, AIDS, SARS [1], and recently COVID-19 [2, 3]. Mathematical models are effective ways to investigate the spread of epidemics. Kermark and McKendrick [4] first studied the dynamic behaviors of epidemics by ordinary differential equations. Since then, researchers have proposed and studied many deterministic epidemic models, see [512]. Suppose the total population N(t) is divided into three classes at time t: susceptible (S), infective (I), and recovered (R) individuals, respectively. Based on the structure of compartments, researchers have proposed and studied some infectious-disease models according to the transmission characteristics and pathogenicity of the disease itself, such as SIR, SIRS, SIRI, and SIRIS models. For the SIR model, the recovered individuals have permanent immunity. However, for some diseases, the recovered individuals may lose immunity after a certain period and become susceptible individuals or relapse with reactivation of latent infection and revert to the infective class [13, 14]. The former can be described by the SIRS model, while the SIRI model can describe the latter. In recent years, much work has been carried out to study the SIRS model from all aspects, see [1520]. Let S(t), I(t), and R(t) be the number of susceptible, infectious, and recovered individuals at time t, respectively. Through ordinary differential equations, the deterministic SIRS model is usually expressed by

{S(t)=ΛρS(t)βS(t)I(t)+θR(t),I(t)=βS(t)I(t)(ρ+η+α)I(t),R(t)=ηI(t)(ρ+θ)R(t). 1

In the model (1), Λ denotes the recruitment rate of susceptible individuals, ρ and α are the natural and disease-related mortality rates, β is the contact transmission coefficient, η is the recovery rate, and θ is the immunity loss rate of recovered individuals.

In epidemic models, the incidence rate plays a vital role. It not only describes the characteristics of the disease but also measures the speed at which the disease spreads. There are two widely used incidence rates: the bilinear incidence rate βSI [2124] and the standard incidence rate βSI/N [2527]. The bilinear incidence βSI is commonly used to model communicable diseases, for example, influenza [8, 28]. The standard incidence βSI/N is more suitable for disease modeling when the total population is huge [1]. However, it is invalid to assume homogeneous mixing in a heterogeneous population. In this case, the transmission characteristics of the disease can be described through a suitable nonlinear incidence rate [8, 17, 2931]. Capasso and Serio [29] introduced a saturated nonlinear-incidence rate Sφ(I) into the epidemic model. The transmission rate between the infected and susceptible will be saturated if the number of infected individuals is larger in the population. Other nonlinear incidences are used one after another, including βIpSq, βSIp/(1+αIq), and βIpS/(1+αS). Lahrouz et al. [8] proposed an SIRS model with a general incidence rate βSI/φ(I), where φ is a positive function such that φ(0)=1 and φ0. Most of the above incidence rates are the special cases of βSI/φ(I). For instance, if φ(I)=1, then it is a bilinear incidence rate; if φ(I)=1+αIq, and the incidence rate is βSI/(1+αIq). Another advantage of the general incidence rate can be used to describe the psychological effect: the infection force may decrease with the number of infective individuals.

In the real world, there are kinds of infectious disease such as bacterial meningitis. Some infective individuals obtain immunity after recovery and become recovered individuals, but others have no immunity after recovery and become susceptible. This kind of character is called partial immunity. In the above kinds of SIRS models, there are two main limitations: (i) the classical SIRS model (1) with bilinear or standard incidence rates does not always effectively analyze the dynamic properties of the disease in a heterogeneous population; and (ii) although the SIRS model with a general incidence rate, proposed by [8], is more practical than the classical model, the partial immunity of infectious individuals has not been considered in the model. Generally, the individuals can be divided into two sections: one section of them after recovery have immunity and go to the recovered class. Another section after recovery has no immunity and returns to the susceptible class. For this reason, in the work we propose an SIRS epidemic model with a general incidence rate and partial immunity as follows

{S(t)=ΛρS(t)βS(t)I(t)φ(I(t))+(1p)ηI(t)+θR(t),I(t)=βS(t)I(t)φ(I(t))(ρ+η+α)I(t),R(t)=pηI(t)(ρ+θ)R(t), 2

where p is the immunity rate. In the model (2), (1p)ηI corresponds to the infected individuals who lost immunity after recovery, while pηI represents the infected individuals who gain immunity after recovery. In particular, if p=1 and φ(I)=1, then the model (1) is a special case of the model (2). Define the basic reproduction number as

R=Λβρ(ρ+η+α).

Suppose φ(0)=1 and φ(t)>0 for t>0 in the model (2). Similar to [8] and [32], it is easy to obtain the dynamic properties of equilibria in the model (2) by constructing the Lyapunov function as follows:

  • (i)

    The model (2) has a unique disease-free equilibrium denoted by E0(Λρ,0,0). If R<1, the disease-free equilibrium E0 is globally asymptotically stable.

  • (ii)
    If R>1, the model (2) has a unique endemic equilibrium denoted by E(S,I,R), satisfying
    {ΛρSβSIφ(I)+(1p)ηI+θR=0,βSIφ(I)(ρ+η+α)I=0,pηI(ρ+θ)R=0.

Further, the endemic equilibrium E is globally asymptotically stable. Detailed proofs of these are provided in the Appendix.

For the deterministic SIRS model (2), an important assumption is that the disease is not affected by stochastic perturbations. In practice, some parameters of the SIRS model (2) always fluctuate due to stochastic perturbations in the environment. Thus, the stochastic epidemic model can provide more realism than the corresponding deterministic models. In the past few years, many researchers have considered stochastic epidemic models and have obtained significant results [27, 30, 3242]. For example, Jiang et al. [42] proved a global positive solution of a stochastic SIR model and investigated the asymptotic behaviors. Lahrouz and Omari [30] studied a stochastic SIRS model with a nonlinear incidence rate in a population of varying sizes. However, they did not investigate the asymptotic behavior of the solution. Zhang et al. [27] analyzed an SIRS model with a standard incidence rate under stochastic perturbations. Recently, Fatini et al. [33] analyzed a stochastic model with a nonlinear incidence and obtained the asymptotic behavior of the disease. Koufi et al. [34] considered a stochastic SIRS system with switching among different environments. Ding and Zhang [35] proposed a stochastic SIRS epidemic model with bilinear incidence. However, to the best of our knowledge, there are few reports of research about the stochastic SIRS model with general incidence and partial immunity. As an extension of the above results, we introduce various stochastic perturbations into the system (2). Then, we obtain a stochastic SIRS epidemic model with a general incidence rate and partial immunity as follows

{dS=[ΛρSβSIφ(I)+(1p)ηI+θR]dt+σ1SdB1(t)σ4SIφ(I)dB4(t),dI=[βSIφ(I)(ρ+η+α)I]dt+σ2IdB2(t)+σ4SIφ(I)dB4(t),dR=[pηI(ρ+θ)R]dt+σ3RdB3(t), 3

where Bi(t) (i=1,2,3,4) are independent standard Brownian motions defined on the complete probability space (Ω,F,{F}t0,P) with a filtration {F}t0 satisfying the usual conditions, and σi (i=1,2,3,4) are the nonnegative intensities of the standard Gaussian white noises.

The rest of the paper is organized as follows. We first review some basic concepts and useful lemmas in Sect. 2. The existence and uniqueness of the globally positive solution are proved in Sect. 3. In Sect. 4, we obtain sufficient conditions for the extinction of the disease under a stochastic system. Asymptotic behaviors of the solution are discussed around the disease-free equilibrium of the deterministic model in Sect. 5. In Sect. 6, we prove that the model (3) has a unique stationary distribution under certain conditions and discuss the asymptotic behaviors of the solution around the endemic equilibrium. A brief conclusion is provided in Sect. 7.

Preliminaries

Let Z(t) be a three-dimensional time-homogeneous Markov process described by the following stochastic differential equation (SDE)

dZ(t)=b(t,Z(t))dt+σ(t,Z(t))dB(t),

where b:[t0,+]×R3R3, σ:[t0,+]×R3R3×4 are locally Lipschitz functions in R3 and B(t)=(B1(t),B2(t),B3(t),B4(t)) is a four-dimensional standard Brownian motion. Denote R+3:={(z1,z2,z3)|zi>0,i=1,2,3}. The operator L of Z(t) is defined as

L=t+i=13bi(t,z)zi+12i=13[σT(t,z)σ(t,z)]ij2zizj.

Denote C2,1([t0,+]×R3;R+) as the family of all nonnegative functions F(t,z) defined on [t0,+]×R3 such that they are continuously once in t and twice in z. The following formula can be obtained by acting L on a function F(t,z)C2,1([t0,+]×R3;R+)

LF(t,z)=Ft(t,z)+Fz(t,z)b(t,z)+12trace[σ(t,z)Fzz(t,z)σ(t,z)],

where

Ft(t,z)=Ft,Fz(t,z)=(Fz1,Fz2,Fz3),Fzz(t,z)=(2Fzizj)3×3.

By Itô’s formula, we have dF(t,z)=LF(t,z)dt+Fz(t,z)σ(t,z)dB(t).

Lemma 1

([43])

Let Q(t),Q(t) be the quadratic variation of a continuous local martingale {Q(t):t0} with initial value Q(0)=0. Then, for almost all ωΩ, there exists a random integer k0=k0(ω) such that

Q(t)12mkQ(t),Q(t)+vlnkmk,0tnk

for all k>k0, where v>1 is a number and mk>0, nk>0 are two sequences.

Lemma 2

([44])

There exists a bounded open domain URd with regular boundary Γ, having the following properties:

  1. In the domain U and some neighborhood thereof, the smallest eigenvalue of the diffusion matrix A(z)=(aij(z)) is bounded away from zero.

  2. If zRdU, the mean time τ at which a path issuing from z reaches the set U is finite, and supzKEτ< for every compact subset KRd.

If (A.1) and (A.2) hold, then the Markov process Z(t) has a stationary distribution π(). Further,

P{1T0Tf(Z(t))dtTRdf(y)π(dy)}=1

for all zRd, where f(z) be a function integrable concerning measure π.

In Lemma 2, Assumption (A.1) can be verified by the existence of a positive number M such that i,j=1daij(z)ζiζjM|ζ|2, zU, ζRd. To verify Assumption (A.2), it is sufficient to prove that there is a nonnegative C2-function ψ such that for some θ>0, Lψ(z)<θ, zRdU (see [45]).

Existence and uniqueness of a positive solution

In this section, we first prove that the solution of the stochastic model (3) satisfies the following properties.

Theorem 1

For any given initial value (S(0),I(0),R(0))R+3 in the model (3), there exists a unique positive solution (S(t),I(t),R(t)) for t0. The solution remains in R+3 with probability one, that is to say, (S(t),I(t),R(t))R+3 for all t0 almost certainly.

Proof

Since the coefficients of model (3) are locally Lipschitz continuous, there exists a unique local solution (S(t),I(t),R(t)) on t[0,τe] for any given initial value (S(0),I(0),R(0))R+3, where τe is the explosion time. The solution is global if we can prove that τe=+ a.s. To do this, define the stopping time as

τ+=inf{t[0,τe]:S(t)0 or I(t)0 or R(t)0}.

Set inf=+ as usual, where ∅ represents the empty set. Obviously, τ+τe. We now only need to prove τ+= a.s. If τ+<, there must exist a positive constant C satisfying P(τ+<C)>0. Define a function V:R+3R+ as

V(S(t),I(t),R(t))=ln(S(t)I(t)R(t)).

By Itô’s formula, we have

dV(S(t),I(t),R(t))=LV(S(t),I(t),R(t))dt+σ1dB1(t)+σ2dB2(t)+σ3dB3(t)+σ4S(t)I(t)φ(I(t))dB4(t),

where

LV(S(t),I(t),R(t))=1S(t)[ΛρS(t)βS(t)I(t)φ(I(t))+(1p)ηI(t)+θR(t)]+1I(t)[βS(t)I(t)φ(I(t))(ρ+η+α)I(t)]+1R(t)[pηI(t)(ρ+θ)R(t)]12[σ12+σ22+σ32+σ42(I(t)φ(I(t)))2+σ42(S(t)φ(I(t)))2]ρβI(t)(ρ+η+α)(ρ+θ)12[σ12+σ22+σ32+σ42(I(t)φ(I(t)))2+σ42(S(t)φ(I(t)))2]:=G(S(t),I(t)). 4

The inequality (4) holds since φ(I(t))1. Then,

dV(S(t),I(t),R(t))G(S(t),I(t))+σ1dB1(t)+σ2dB2(t)+σ3dB3(t)+σ4S(t)I(t)φ(I(t))dB4(t).

Integrate both sides of dV(S(t),I(t),R(t)) from 0 to t, to yield

V(S(t),I(t),R(t))V(S(0),I(0),R(0))+0tG(S(s),I(s))ds+σ1B1(t)+σ2B2(t)+σ3B3(t)+0tσ4S(s)I(s)φ(I(s))dB4(s). 5

From the definition of τ+, we have limtτ+V(S(t),I(t),R(t))=. Hence, it follows that (5) satisfies

V(S(0),I(0),R(0))+0τ+G(S(s),I(s))ds+σ1B1(τ+)+σ2B2(τ+)+σ3B3(τ+)+0τ+σ4S(s)I(s)φ(I(s))dB4(s) 6

for tτ+. On the other hand, V(S(0),I(0),R(0))=ln(S(0)I(0)R(0))> since (S(0),I(0),R(0))R+3. Then,

V(S(0),I(0),R(0))+0τ+G(S(s),I(s))ds+σ1B1(τ+)+σ2B2(τ+)+σ3B3(τ+)+0τ+σ4S(s)I(s)φ(I(s))dB4(s)>. 7

Combining (6) with (7), we have

V(S(0),I(0),R(0))+0τ+G(S(s),I(s))ds+σ1B1(τ+)+σ2B2(τ+)+σ3B3(τ+)+0τ+σ4S(s)I(s)φ(I(s))dB4(s)>.

Obviously, this is a contradiction. Therefore, τ+=+. The proof is complete. □

Extinction of a disease

The extinction of a disease has always been a concern. In the deterministic model (2), the disease will be extinct if R<1. That is to say, the disease-free equilibrium E0(Λρ,0,0) is globally asymptotically stable. However, the condition of disease extinction in model (3) is different from that of the model (2). Define a parameter

Rs=β22σ42(ρ+η+α+12σ22).

Theorem 2

For any initial value (S(0),I(0),R(0))R+ in model (3), if Rs<1, then the disease I(t) will die out exponentially with probability one; that is,

lim supt+lnI(t)t(ρ+η+α+12σ22)(Rs1)<0a.s.

Proof

Through Itô’s formula, we have

dlnI(t)=[1I(t)(βS(t)I(t)φ(I(t))(ρ+η+α)I(t))12σ2212σ42(S(t)φ(I(t)))2]dt+σ2dB2(t)+σ4S(t)φ(I(t))dB4(t).

Integrating both sides of the above equation from 0 to t leads to

lnI(t)=lnI(0)+0t[βS(s)φ(I(s))(ρ+η+α)12σ2212σ42(S(s)φ(I(s)))2]ds+σ2B2(t)+0tσ4S(s)φ(I(s))dB4(s).

Denote Q(t)=0tσ4S(s)φ(I(s))dB4(s). Obviously, Q(t) is a continuous local martingale, and the quadratic variation satisfies

Q(t),Q(t)=σ420t(S(s)φ(I(s)))2ds.

Based on Lemma 1, take mk=m<1, nk=k and v=2. Hence, it follows that

Q(t)12mσ420t(S(s)φ(I(s)))2ds+2lnkm,0tk. 8

Then,

lnI(t)lnI(0)+0t[βS(s)φ(I(s))(ρ+η+α+12σ22)12(1m)σ42(S(s)φ(I(s)))2]ds+σ2B2(t)+2mlnk.

Through calculation, we have

βSφ(I)(ρ+η+α+12σ22)12(1m)σ42(Sφ(I))2=12(1m)σ42(Sφ(I)β(1m)σ42)2+β22(1m)σ42(ρ+η+α+12σ22)β22(1m)σ42(ρ+η+α+12σ22)=(ρ+η+α+12σ22)(11mRs1).

Hence,

lnI(t)lnI(0)+0t(ρ+η+α+12σ22)(11mRs1)ds+σ2B2(t)+2mlnk=lnI(0)+(ρ+η+α+12σ22)(11mRs1)t+σ2B2(t)+2mlnk.

Dividing the inequality by t (t[k1,k]), we obtain

lnI(t)tlnI(0)t+(ρ+η+α+12σ22)(11mRs1)+σ2B2(t)t+2mlnkt.

From the strong law of large numbers, when k+, i.e., t+, this yields

lim suptlnI(t)t(ρ+η+α+12σ22)(11mRs1).

The desired inequality holds by letting m0. The proof is complete. □

Example 1

Let φ(I)=1+I2 in the models (2) and (3).

  • (i)

    Take (S(0),I(0),R(0))=(150,10,2), (Λ,β,ρ,p,η,θ,α)=(6,0.0009,0.04,0.97,0.1,0.001,0.01), and (σ1,σ2,σ3,σ4)=(0.0016,0.0032,0.0022,0.039). After direct calculation, R=0.9<1 and Rs=0.0018<1. Figure 1 shows that the disease will become extinct in both a random and deterministic environment.

  • (ii)

    Let β=0.009; other parameters and initial values are the same as those in (i). After direct calculation, R=9>1 and Rs=0.1775<1. Figure 2 shows that the disease will become extinct in a random environment but persist in a deterministic environment.

Figure 1.

Figure 1

Dynamical curves of compartments: (a) S, (b) I, and (c) R under R<1 and Rs<1

Figure 2.

Figure 2

Dynamical curves of compartments: (a) S, (b) I, and (c) R under R>1 and Rs<1

Asymptotic behavior around the disease-free equilibrium

In the model (2), the disease-free equilibrium E0(Λρ,0,0) is globally asymptotically stable when R<1. However, E0 is no longer the equilibrium of model (3) due to the stochastic perturbations. Thus, it is interesting to study the asymptotic behavior of the solution of model (3) around E0.

Theorem 3

If R1 and σ12<ρ2, σ22<ρ+2α+2pηη2p2ρ, σ32<ρ+2θ2θ2ρ, then the solution of model (3) satisfies

lim supt1tE0t[(S(s)Λρ)2+I2(s)+R2(s)]dsσ12Λ2Mρ2

for any given initial value (S(0),I(0),R(0))R+3, where

M=min{ρ2σ12,ρ2+α+pηη2p22ρσ222,ρ2+θσ322θ2ρ}.

Proof

Let x=S(t)Λ/ρ, y=I(t) and z=R(t). Substituting these variables into the model (3), one can obtain the following equations

{dx=[Λρ(x+Λρ)β(x+Λ/ρ)φ(y)y+(1p)ηy+θz]dtdx=+σ1(x+Λρ)dB1(t)σ4x+Λ/ρφ(y)ydB4(t),dy=[β(x+Λ/ρ)φ(y)y(ρ+η+α)y]dt+σ2ydB2(t)+σ4x+Λ/ρφ(y)ydB4(t),dz=[pηy(ρ+θ)z]dt+σ3zdB3(t).

Denote Φ1=12(x+y)2, Φ2=y and Φ3=12z2. Define a function Φ=Φ1+2ρ+α+pηβΦ2+Φ3. Then,

dΦ=dΦ1+2ρ+α+pηβdΦ2+dΦ3,

where

dΦ1=LΦ1dt+(x+y)[σ1(x+Λρ)]dB1(t)+(x+y)σ2ydB2(t),dΦ2=LΦ2dt+σ2ydB2(t)+σ4x+Λ/ρφ(y)ydB4(t),dΦ3=LΦ3dt+σ3z2dB3(t).

Through calculation, we have

LΦ1=(x+y)[ρxβ(x+Λ/ρ)φ(y)y+(1p)ηy+θz]+(x+y)[β(x+Λ/ρ)φ(y)y(ρ+η+α)y]+σ12(x+Λ/ρ)2+σ22y22=(x+y)[ρx(ρ+α+pη)y+θz]+σ12(x+Λ/ρ)2+σ22y22=ρx2(ρ+α+pη)y2(2ρ+α+pη)xy+θxz+θyz+σ12(x+Λ/ρ)2+σ22y22=ρx2(ρ+α+pη)y2(2ρ+α+pη)xy+θρzρx+θρzρy+σ12(x+Λ/ρ)2+σ22y22ρx2(ρ+α+pη)y2(2ρ+α+pη)xy+θ22ρz2+ρ2x2+θ22ρz2+ρ2y2+σ12x2+σ12(Λρ)2+σ22y22 9
=(ρ2σ12)x2(ρ2+α+pησ222)y2+θ2ρz2+σ12Λ2ρ2(2ρ+α+pη)xy,LΦ2=β(x+Λ/ρ)φ(y)y(ρ+η+α)yβxy+(βΛρ(ρ+η+α))yβxy, 10
LΦ3=z(pηy(ρ+θ)z)+12σ32z2=pηyz(ρ+θσ322)z2=ηpρyρz(ρ+θσ322)z2η2p22ρy2(ρ2+θσ322)z2. 11

The inequalities (9) and (11) follow from the fact that ab(a2+b2)/2 and (a+b)22a2+2b2 for any a,bR. The inequality (10) holds due to R<1. Combining these equations, we have

LΦ(ρ2σ12)x2(ρ2+α+pηη2p22ρσ222)y2(ρ2+θσ322θ2ρ)z2+σ12Λ2ρ2. 12

Hence,

dΦ[(ρ2σ12)x2(ρ2+α+pηη2p22ρσ222)y2(ρ2+θσ322θ2ρ)z2+σ12Λ2ρ2]dt+(x+y)[σ1(x+Λρ)]dB1(t)+σ2y(x+y+2ρ+α+pηβ)dB2(t)+σ3z2dB3(t).

Integrating both sides of the inequality from 0 to t, and taking the expectation yields

0E[Φ(t)]E[Φ(0)]+E0t[(ρ2σ12)x2(s)(ρ2+α+pηη2p22ρσ222)y2(s)(ρ2+θσ322θ2ρ)z2(s)+σ12Λ2ρ2]ds,

which implies

E0t[(ρ2σ12)x2(s)+(ρ2+α+pηη2p22ρσ222)y2(s)+(ρ2+θσ322θ2ρ)z2(s)+σ12Λ2ρ2]dsE[Φ(0)]+σ12Λ2ρ2t.

Therefore,

lim supt1tE0t[(ρ2σ12)x2(s)+(ρ2+α+pηη2p22ρσ222)y2(s)+(ρ2+θσ322θ2ρ)z2(s)+σ12Λ2ρ2]dsσ12Λ2ρ2.

Then,

lim supt1tE0t(x2(s)+y2(s)+z2(s))dsσ12Λ2Mρ2,

i.e.,

lim supt1tE0t[(S(s)Λρ)2+I2(s)+R2(s)]dsσ12Λ2Mρ2.

The result follows. □

Remark 1

Theorem 3 shows that if R1 and σi (i=1,2,3) satisfy certain conditions, the solution (S(t),I(t),R(t)) of model (3) oscillates around E0, and the intensity of the oscillation is determined by σi (i=1,2,3). Further, when σi (i=1,2,3) decrease, the solution (S(t),I(t),R(t)) of model (3) is close to the disease-free equilibrium E0. If σ1=0, (12) is simplified as

LΦρ2(SΛρ)2(ρ2+α+pηη2p22ρσ222)I2(ρ2+θσ322θ2ρ)R2,

which is negative-definite when σ22<ρ+2α+2pηη2p2ρ, σ32<ρ+2ρ2ρ2ρ. Therefore, the disease-free equilibrium E0 of model (3) is stochastically asymptotically stable.

Example 2

Assume that (S(0),I(0),R(0))=(0.4,0.1,0.3), (Λ,β,ρ,p,η,θ,α)=(0.3,0.4,0.2,0.97,0.31,0.01,0.1), and (σ1,σ2,σ3,σ4)=(0.03,0.08,0.04,0.12). After calculation, one can see that R=0.9836<1 and σ12<ρ2, σ22<ρ+2α+2pηη2p2ρ, σ32<ρ+2θ2θ2ρ, satisfying the conditions of Theorem 3. Figure 3 shows the trajectories of models (2) and (3). The disease-free equilibrium E0(1.5,0,0) is global asymptotically stable. The solution of model (3) is around the solution of model (2).

Figure 3.

Figure 3

(a) Time-series phases of solutions (S(t), I(t), R(t)) for model (2); (b) Time-series phases of solutions (S(t), I(t), R(t)) for model (3). The parameters are taken from Example 2

Existence of the stationary distribution

In this section, we mainly study two properties: (i) the asymptotic behavior of the solution of the model (3) around the endemic equilibrium E(S,I,R) of the model (2), and (ii) the existence and uniqueness of the stationary distribution of the solution for the model (3). Denote

κ1=ρ2σ12,κ2=ρ2+α+pηp2η22ρσ22,κ3=ρ2+θθ2ρσ32,W=σ12S2+σ22(I2+2ρ+α+pη2βIφ(I))+σ32R2.

Theorem 4

If R>1 and 0<W<min{κ1S2,κ2I2,κ3R2}, then

lim supt1tE0t[κ1(S(s)S)2+κ2(I(s)I)2+κ3(R(s)R)2]dsW. 13

Further, there is a unique stationary distribution π for the solution of model (3).

Proof

We first prove the inequality (13). Since R>1, model (2) has a unique endemic equilibrium E(S,I,R) satisfying

pηI=(ρ+θ)R,βSφ(I)=ρ+η+α,Λ=ρS+βSIφ(I)(1p)ηIθR.

Let Ψ1=12(S+ISI)2, Ψ2=IIIlnII and Ψ3=12(RR)2. Define a function

Ψ=Ψ1+2ρ+α+pηβφ(I)Ψ2+Ψ3.

Then,

dΨ=dΨ1+2ρ+α+pηβφ(I)dΨ2+dΨ3.

By Itô’s formula, we have

dΨ1=LΨ1dt+(S+ISI)(σ1SdB1(t)+σ2IdB2(t)),dΨ2=LΨ2dt+(II)σ2dB2(t)+(II)σ4SIφ(I)dB4(t),dΨ3=LΨ3dt+(RR)Rσ3dB3(t),

where

LΨ1=(S+ISI)[ΛρS(ρ+α+pη)I+θR]+σ122S2+σ222I2=(S+ISI)[ρS+(ρ+α+pη)IθRρS(ρ+α+pη)I+θR]+σ122(SS+S)2+σ222(II+I)2(SS+II)[ρ(SS)(ρ+α+pη)(II)+θ(RR)]+σ12(SS)2+σ12S2+σ22(II)2+σ22I2 14
=(ρσ12)(SS)2(ρ+α+pησ22)(II)2(2ρ+α+pη)×(SS)(II)+θρ(RR)ρ(SS)+θρ(RR)ρ(II)+σ12S2+σ22I2(ρσ12)(SS)2(ρ+α+pησ22)(II)2(2ρ+α+pη)×(SS)(II)+θ22ρ(RR)2+ρ2(II)2+θ22ρ(RR)2+ρ2(SS)+σ12S2+σ22I2 15
=(ρ2σ12)(SS)2(ρ2+α+pησ22)(II)2+θ2ρ(RR)2(2ρ+α+pη)(SS)(II)+σ12S2+σ22I2,LΨ2=(1II)[βSIφ(I)(ρ+η+α)I]+12Iσ22=(II)[βS(φ(I)φ(I))φ(I)φ(I)+β(SS)φ(I)]+12Iσ22β(SS)(II)φ(I)+12Iσ22, 16
LΨ3=(RR)[pηI(ρ+θ)R]+12σ32R2=(RR)[pηI+(ρ+θ)R+pηI(ρ+θ)R]+12σ32(RR+R)2(RR)[pη(II)(ρ+θ)(RR)]+σ32(RR)2+σ32R2 17
=ρ(RR)pηρ(II)(ρ+θσ32)(RR)2+σ32R2ρ2(RR)2+p2η22ρ(II)2(ρ+θσ32)(RR)2+σ32R2=(ρ2+θσ32)(RR)2+p2η22ρ(II)2+σ32R2. 18

The inequalities (15) and (18) hold because aba2/2+b2/2, (14) and (17) hold because (a+b)22a2+2b2, while (16) holds because of the fact that βS(II)(φ(I)φ(I))φ(I)φ(I)>0. Combined with the above inequalities, one can obtain

LΨ=LΨ1+2ρ+α+pηβφ(I)LΨ2+LΨ3(ρ2σ12)(SS)2(ρ2+α+pηp2η22ρσ22)(II)2(ρ2+θθ2ρσ32)(RR)2+σ12S2+σ22(I2+2ρ+α+pη2βIφ(I))+σ32R2=κ1(SS)2κ2(II)2κ3(RR)2+W. 19

Note that

dΨ=LΨdt+(S+ISI)(σ1SdB1(t)+σ2IdB2(t))+2ρ+α+pηβφ(I)(II)σ2dB2(t)+(RR)Rσ3dB3(t).

Integrating both sides of dΨ from 0 to t, and taking the expectations, from (19), this yields

0EΨ(S(t),I(t),R(t))EΨ(S(0),I(0),R(0))E0t[κ1(S(s)S)2κ2(I(s)I)2κ3(R(s)R)2]ds+Wt.

Dividing both sides by t and letting t, we have

lim supt1tE0t[κ1(S(s)S)2+κ2(I(s)I)2+κ3(R(s)R)2]dsW.

Then, (13) has been proved.

On the other hand, we only prove Assumptions (A.1) and (A.2) for the existence and uniqueness of the stationary distribution. Consider the ellipsoid κ1(SS)2κ2(II)2κ3(RR)2+W=0, i.e.,

(SS)2(Wκ1)2+(II)2(Wκ2)2+(RR)2(Wκ3)2=1.

If S>W/κ1, I>W/κ2 and R>W/κ3, i.e., W<min{κ1S2,κ2I2,κ3R2}, then the ellipsoid is fully contained in R+3. Let U be the neighborhood of the ellipsoid such that UR+3. Thus,

κ1(SS)2κ2(II)2κ3(RR)2+W<0

for any (S,I,R)R+3U, i.e. LΨ<0 for any (S,I,R)R+3U. Assumption (A.2) is then satisfied. We rewrite the model (3) as

d[S(t)I(t)R(t)]=[ΛρSβSIφ(I)+(1p)ηI+θRβSIφ(I)(ρ+η+α)IpηI(ρ+θ)R]dt+[σ1S00σ4SIφ(I)0σ2I0σ4SIφ(I)00σ3R0][dB1(t)dB2(t)dB3(t)dB4(t)].

The diffusion matrix of model (3) is

A=[σ12S2+σ42S2I2f2(I)σ42S2I2f2(I)0σ42S2I2f2(I)σ22I2+σ42S2I2f2(I)000σ32R2].

Suppose M=min(S,I,R)UR+3{σ12S2,σ22I2,σ32R2}. Then, for any (S,I,R)U and ζ=(ζ1,ζ2,ζ3)R+3, we have

i,j=13aij(S,I,R)ζiζj=(σ12S2+σ42S2I2f2(I))ζ122σ42S2I2f2(I)ζ1ζ2+(σ22I2+σ42S2I2f2(I))ζ22+σ32R2ζ32=σ12S2ζ12+σ22I2ζ22+σ32R2ζ32+σ42S2I2f2(I)(ζ12ζ22)σ12S2ζ12+σ22I2ζ22+σ32R2ζ32M|ζ|2,

which meets Assumption (A.1). Therefore, model (3) has a unique stationary distribution π. □

Remark 2

Theorem 4 shows that the solution (S(t),I(t),R(t)) of model (3) oscillates around E if R1 when σi (i=1,2,3) and some parameters satisfy certain conditions.

Example 3

Let φ(I)=1+I2, (S(0),I(0),R(0))=(150,10,2), (Λ,β,ρ,p,η,θ,α)=(6,0.02,0.04,0.97,0.1,0.001,0.01), and (σ1,σ2,σ3,σ4)=(0.0016,0.0032,0.0022,0.0085), one can obtain that R=Λβρ(ρ+η+α)=20>1, κ1=ρ2σ12=0.02>0, κ2=ρ2+α+pηp2η22ρσ22=0.0094>0, and κ3=ρ2+θθ2ρσ32=0.021>0. Then, Theorem 4 shows that there exists a unique stationary distribution π of model (3). Figures 4(a), (b), and (c) reflect the dynamical population of the susceptible, infective, and recovered individuals in model (2) and model (3), respectively. In Figs. 4(d), (e), and (f), we provide the frequency histogram and corresponding marginal density function curves of compartments S, I, and R, respectively. These two kinds of figures indicate that there exists a unique stationary distribution for model (3).

Figure 4.

Figure 4

Dynamical curves of compartments: (a) S, (b) I, (c) R. The frequency histograms and marginal density functions of compartments: (d) S, (e) I, (f) R

The following numerical example focuses on the effect of the partial immunization rate p on the dynamics of disease transmission.

Example 4

Let (S(0),I(0),R(0))=(0.4,0.1,0.3), (Λ,β,ρ,η,θ,α)=(0.3,0.9,0.2,0.31,0.01,0.1), and (σ1,σ2,σ3,σ4)=(0.03,0.01,0.04,0.1). We analyze the effect of partial immunity p on the dynamic behavior of model (3). Take p=0.03,0.32,0.64, and 0.97. The corresponding curves of I(t) are shown in Figs. 5(a) and (b), respectively. As the value of p increases, the growth rate and stability level of I(t) will decrease. This indicates that a large partial immunity rate can better control the epidemic than a small one. Thus, it is effective to increase the immunity rate and control the outbreak of the disease.

Figure 5.

Figure 5

The effect of partial immunity on compartment I: (a) model (2) and (b) model (3)

Based on the models (2) and (3), Figs. 6 and 7 show the sensitivity of partial immunity rate on S(t), I(t), and R(t) in three-dimensional changes in time, respectively. As the increases of p in [0,1], the value of S(t) becomes smaller, and I(t) reduces faster than others. However, R(t) increases with the increase of p.

Figure 6.

Figure 6

The effect of partial immunity p with respect to time t for compartments: (a) S, (b) I, and (c) R in model (2)

Figure 7.

Figure 7

The effect of partial immunity p with respect to time t for compartments: (a) S, (b) I, and (c) R in model (3)

Conclusion

In this paper, we propose a stochastic SIRS model with partial immunity and noninear incidence. Through a theoretical derivation, the following results are obtained for the kind of models: (i) By constructing a suitable function, the SIRS model has a unique global positive solution starting from the positive initial value (see Theorem 1). (ii) If Rs<1, the disease will become extinct under the stochastic system (see Theorem 2). The result reveals that the large stochastic perturbations may lead to disease extinction. (iii) If R1 and some parameter limits are satisfied, the solution of model (3) oscillates around E0. Significantly, the disease-free equilibrium E0 of model (3) is stochastically asymptotically stable when σ1=0 (see Theorem 3 and Remark 1). (iv) A sufficient condition is given for the existence of the stationary distribution by using the Khasminskii method. Under this sufficient condition, the solution of model (3) will oscillate around E (see Theorem 4).

The numerical simulations are provided to illustrate the theoretical analysis. Take φ(I)=1+I2. Four examples are given according to the following aspects: (i) Effects of the stochastic perturbations on the extinction of the infectious disease. (ii) Asymptotic behavior around the disease-free equilibrium. (iii) The existence of the stationary distribution. (iv) Effect of the partial immunization rate p on the disease-transmission dynamics. Through these numerical simulations, we observe that: (i) The sufficient condition for the extinction of the disease in model (3) is Rs<1. Also, large perturbations may lead to the extinction of the disease even though it will be persistent in model (2). (ii) A large partial immunity rate can better control the epidemic than a small one.

In this work, we focus on using white noise to describe the randomness of the SIRS model. Other interesting topics for further work should be considered, such as a stochastic SIRS model with regime switching or Lévy Jumps. In recent years, the application of fractional differential equations in biological and epidemic models has increased significantly. Combined with the theory of fractional differential equations [46], the model can be extended to a fractional SIRS epidemic model. In addition, the partial-immune mechanism studied may also exist in some cells or viruses, which can be described by branching process [47]. We leave these for further investigation.

Acknowledgements

The authors are grateful to the editor and referees for their helpful comments.

Appendix

The proofs of the results (i) and (ii) of model (2) are provided as follows.

Proof of (i)

The disease-free equilibrium E0(Λρ,0,0) can be directly obtained by setting I=0 in model (2). Next, we prove that if R<1, the disease-free equilibrium E0 is globally asymptotically stable.

For convenience, we replace (S,I,R) with (N,I,R). Through model (2), this yields

dN=d(S+I+R)=ΛρNαI.

Obviously, model (2) is equivalent to the following model

{dNdt=ΛρNαI,dIdt=βIφ(I)(NIR)(ρ+η+α)I,dRdt=pηI(ρ+θ)R. 20

Thus, the global stability of equilibria can be discussed by the model (20). Construct a function as

V1=β2α(NΛρ)2+0Iφ(s)ds+β2pηR2.

Clearly, V1 is a positive-definite function. The first-order derivative V1˙ of V1 with respect to t is

V1˙=V1NdNdt+V1IdIdt+V1RdRdt=βα(NΛρ)[ρ(NΛρ)αI]+φ(I)[βIφ(I)(NRI)(ρ+η+α)I]+βpηR[pηI(ρ+θ)R]=βρα(NΛρ)2β(ρ+θ)pηR2βI2(ρ+η+α)Iφ(I)+ΛρβI=βρα(NΛρ)2β(ρ+θ)pηR2βI2(ρ+η+α)I(φ(I)R).

The fact that φ(0)=1 and f(I)0 implies φ(I)1. Under R1, one can easily obtain that V1˙ is negative-definite. By the Lyapunov asymptotic theorem, E0 is globally asymptotically stable. □

Proof of (ii)

To obtain the endemic equilibrium E, let the right sides of (2) be equal to zero, i.e.,

{ΛρSβSIφ(I)+(1p)ηI+θR=0,βSIφ(I)(ρ+η+α)I=0,pηI(ρ+θ)R=0.

Since φ(0)=1 and f(I)0, these equations can be simplified as

{S=ρ+η+αβφ(I),R=pηρ+θI,ΛρS(ρ+η+α)I+(1p)ηI+θR=0.

Substitute the first two equations into the third equation, i.e.,

Λρ(ρ+η+α)βφ(I)(ρ+η+α)I+(1p)ηI+θpηρ+θI=0.

Define

T(I)=Λρ(ρ+η+α)βφ(I)(ρ+α+pηρρ+θ)I.

Thus, T(I)=0, that is, I is the solution of the equation T(I)=0. Differentiating T(I) with respect to I, we have

T(I)=ρ(ρ+η+α)βφ(I)(ρ+α+pηρρ+θ).

Note that φ(I)0, we have T(I)<0. Thus, T(I) decreases for I[I(0),). Based on the existence theorem of zero, Moreover, T(I)Λ(ρ+α+pηρρ+θ)I, which leads to limIT(I)=. In addition,

T(0)=Λρ(ρ+η+α)β=ρ(ρ+η+α)β(R1).

According to the existence theorem of the zero point, T(I)=0 has a unique positive solution if and only if T(0)>0, i.e., R>1. In other words, a unique endemic equilibrium E(S,I,R) exists in model (2).

Let n=NN, i=II, and r=RR. Substituting these variables into model (20), one can obtain the following equations

{dndt=ρnαi,didt=β(i+I)φ(i+I)[nir+S(1φ(i+I)φ(I))],drdt=pηi(ρ+θ)r. 21

Next, we only need to prove that the trivial solution of model (21) is globally asymptotically stable. Define

V2=β2αn2+φ(I)[iIln(1+iI)]+Ii+I(φ(s)φ(I))(sI)sds+β2pηr2.

Obviously, V2 is a positive-definite function and

V2˙=V2ndndt+V2ididt+V2rdrdt=βαn(ρnαi)+φ(i+I)i+Ii[β(i+I)φ(i+I)(nir+S(1φ(i+I)φ(I)))]+βpηr[pηi(ρ+θ)r]=βραn2βi2β(ρ+θ)pηr2βiφ(I)S(φ(i+I)φ(I)).

Recall that f0, one has φ(i+I)φ(I)0. Evidently, V2˙ is negative-definite. Thus, V2 is a Lyapunov function for model (21). By the Lyapunov asymptotic stability theorem, the trivial solution of model (21) is globally asymptotically stable. That is to say, the endemic equilibrium state E(S,I,R) is globally asymptotically. □

Author contributions

Chen conducted the theoretical results, simulation, analyzed the examples and drafted the manuscript. Li supervised the work and revised the manuscript.

Funding

This work is supported by the National Natural Science Foundation of China (No: 12061070) and the Natural Science Foundation of Xinjiang Uygur Autonomous Region of China (Nos: 2021D01E13).

Availability of data and materials

Not applicable.

Declarations

Competing interests

The authors declare no competing interests.

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