Research article

Determining the global threshold of an epidemic model with general interference function and high-order perturbation

  • Received: 02 July 2022 Revised: 16 August 2022 Accepted: 26 August 2022 Published: 08 September 2022
  • MSC : 34A26, 34A12, 92D30, 37C10, 60H30

  • This research provides an improved theoretical framework of the Kermack-McKendrick system. By considering the general interference function and the polynomial perturbation, we give the sharp threshold between two situations: the disappearance of the illness and the ergodicity of the higher-order perturbed system. Obviously, the ergodic characteristic indicates the continuation of the infection in the population over time. Our study upgrades and enhances the work of Zhou et al. (2021) and suggests a new path of research that will serve as a basis for future investigations. As an illustrative application, we discuss some special cases of the polynomial perturbation to examine the precision of our outcomes. We deduce that higher order fluctuations positively affect the illness extinction time and lead to its rapid disappearance.

    Citation: Yassine Sabbar, Asad Khan, Anwarud Din, Driss Kiouach, S. P. Rajasekar. Determining the global threshold of an epidemic model with general interference function and high-order perturbation[J]. AIMS Mathematics, 2022, 7(11): 19865-19890. doi: 10.3934/math.20221088

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  • This research provides an improved theoretical framework of the Kermack-McKendrick system. By considering the general interference function and the polynomial perturbation, we give the sharp threshold between two situations: the disappearance of the illness and the ergodicity of the higher-order perturbed system. Obviously, the ergodic characteristic indicates the continuation of the infection in the population over time. Our study upgrades and enhances the work of Zhou et al. (2021) and suggests a new path of research that will serve as a basis for future investigations. As an illustrative application, we discuss some special cases of the polynomial perturbation to examine the precision of our outcomes. We deduce that higher order fluctuations positively affect the illness extinction time and lead to its rapid disappearance.



    Mathematical formulations play a central role in exploring and predicting the future of the communicable diseases [1]. For example, in the case of the coronavirus disease and of course its new mutations, many researchers have contributed to modeling the mechanisms of its spread and providing scientific recommendations to control its expansion [2,3,4,5]. It should be noted that most of the epidemiological models presented in these articles are an improved and adapted version of the SIR model [6]. This compartmentalized system was constructed by Kermack and McKendrick [7] and its philosophy is based on the idea of subdividing individuals according to their different characteristics. Explicitly, individuals are grouped into three main groups: susceptible class (C1), infected class (C2) and permanently recovered class (C3). The transmit rates among these groups are determined by the following dynamical system:

    {dC1(t)=(ΘuC1(t)bC1(t)C2(t))dt,dC2(t)=(bC1(t)C2(t)(u+a+c)C2(t))dt,dC3(t)=(cC2(t)uC3(t))dt,Ck(0)>0,k=1,2,3, (1.1)

    where Θ>0 designates the inflow rate into C1, u>0 indicates the normal death rate, b>0 is the dissemination rate of the epidemic, a>0 is the mortality ratio due to the infection, and c>0 is the cure rate. We note that the above system is one of the most straightforward epidemiological models used to depict the first wave of COVID-19 [8]. Lately, Zhou et al. [9] proposed a general version of system (1.1) by including the pre-existing immunity presumption and the nonlinear incidence function bC1(t)g(C2(t)). By mandating certain conditions on g, they introduced the following system:

    {dC1(t)=(Θ(u1+z)C1(t)bC1(t)g(C2(t)))dt,dC2(t)=(bC1(t)g(C2(t))(u2+a+c)C2(t))dt,dC3(t)=(zC1(t)+cC2(t)u3C3(t))dt,Ck(0)>0,k=1,2,3, (1.2)

    where z is the pre-existing immunity rate, and u1, u2, u3 are respectively the normal mortality rates of C1, C2, C3. The function g covers some functional responses, for instance, g(C2)=C2 [10], g(C2)=C2m+C2 (m>0) [11] and bg(C2(t))=bbcm+C2(t), where m>0 is the media intrusion rate and bc>0 is the reduced active contact rate [12].

    When dealing with epidemiological models, more characteristics can be considered such as cross-individual overlap [13]. It is worth to point out that the choice of functional response affects the prediction of illness behavior. Moreover, the previous setup of Zhou et al. [9] overlooks a large category of incidence rates that are often used in the literature. In this research, we exhibit an enhanced SIR illness system with an interference function that includes additional response examples (see Table 1). In line with this setting, the system (1.2) can be rewritten as follows:

    {dC1(t)=(Θ(u1+z)C1(t)bH(C1(t),C2(t))C2(t))dt,dC2(t)=(bH(C1(t),C2(t))C2(t)(u2+a+c)C2(t))dt,dC3(t)=(zC1(t)+cC2(t)u3C3(t))dt,Ck(0)>0,k=1,2,3. (1.3)

    We presume that the general interference response HC2(R+×R+,R+) verifies these two hypotheses:

    Assumption (a): There exists a constant ϱ>0 such that for all C1,C20,

    H(C1,C2)C20H(C1,C2)C1ϱ.

    Assumption (b): limC20supC1>0{|H(C1,C2)H(C1,0)|}=0.

    The properties (a) and (b) are readily satisfied by the typical examples listed in Table 1.

    Table 1.  List of some prototypes of the general interference function H.
    Name Expression Source
    Beddington-DeAngelis H(C1,C2)=C11+m1C1+m2C2 (m1,m2>0) [14]
    Crowley-Martin H(C1,C2)=C1(m1+C1)(m2+C2) (m1,m2>0) [15]
    Modified Crowley-Martin H(C1,C2)=C11+m1C1+m2C2+m3C1C2 (m1,m2,m3>0) [13]

     | Show Table
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    Substantially, the infection mechanism is random in nature at all scales [16,17,18,19,20]. From the attachment of the virus to the human cell to the encapsulation of repetitive genetic information, from the shedding of new virions to the transmission of a second individual, from individual behavior to global mobility, all the factors influence the diffusion of the infection and make it more uphill task to foretell its conduct [21,22,23]. The stochastic approach offers considerable advantages in providing insight into population dynamics under the said fluctuations [24,25,26]. To correctly describe this randomness, a series of perturbed compartmental models with different assumptions that simulate reality have been proposed [27,28,29,30,31]. Most of these models assume that random fluctuations can be modeled by integrating Brownian motions into the deterministic formulation [32]. By selecting this class of fluctuations in their linear shape, probabilistic systems are widely used in epidemiology to analyze disease prevalence [33,34,35]. In these works, the primary focus was the investigation of some biological long-run characteristics of the infection.

    Since 2017, a new form of stochastic systems has emerged where the story begins with the work proposed by Liu and Jiang in [36]. By reason of the complexity of environmental changes, they claimed that the relative linear order of the disturbance can be raised to the second. Based on this assumption, scientific papers have proposed and analyzed various real systems with second-order fluctuations [37,38]. Recently, the autrhors of [9] suggested an enhanced type of perturbation in its general representation. This frame generalizes the previously mentioned studies and offers a new line of research. Motivated by their arguments, we consider the following polynomial perturbed system:

    {dC1(t)=Deterministicpart(Θ(u1+z)C1(t)bH(C1(t),C2(t))C2(t))dt+HigherorderperturbationNh=0q1hCh+11(t)dW1(t),dC2(t)=(bH(C1(t),C2(t))C2(t)(u2+a+c)C2(t))dt+Nh=0q2hCh+12(t)dW2(t),dC3(t)=(zC1(t)+cC2(t)u3C3(t))dt+Nh=0q3hCh+13(t)dW3(t), (1.4)

    where W1(t), W2(t), W3(t) are independent Brownian motions defined on a filtered probability space ΩE,P(Ω,E,{Et}t0,P) such that {Et}t0 follows the usual assumptions, and qkh>0 (k=1,2,3,h=0,1,2,,N) are the high-order intensities of white noises.

    In [9], the authors indicated that the model (1.4) in the case of incidence bC1(t)g(C2(t)) and polynomial perturbation is well-posed mathematically and biologically, then they treated its long-run behavior. The problem is that they obtained two separate critical conditions for extinction and stationarity which is not ideal when addressing epidemiological models. Moreover, {they mention that there was} a large gap between the defined criteria; and the corresponding threshold value is still an open question (for more details see the discussion part of [9]). Compared to the results presented in [9], in this article, we address the said problem from a global angle by considering an epidemic model with a general incidence function. Taking the latter into account makes the analysis very complex, which has prompted us to innovate alternative techniques. By adding the polynomial perturbation, we present the acute threshold value between stationarity and extinction of the infection, which offers an excellent insight into the possible scenarios of epidemic status in a given population.

    Technically, we introduce an analytical method based on some long-term characteristics of an auxiliary boundary equation [39]. By using the ergodic theorem and the stochastic comparison lemma, we establish the well-defined threshold between stationarity and infection extinction. Our method differs from the one used in [9] by using the mutually exclusive possibilities lemma and other analytical tools. Specifically, we focus on the long-term characteristics of the Markov process D(t) that verifies

    {dD(t)={Θ(u1+z)D(t)}dt+Nh=0q1hDh+1(t)dW1(t),D(0)=C1(0). (1.5)

    In accordance with Lemma 5 of [9], D admits the following single stable distribution:

    πD(y)=CD(Nh=0q1hyh+1(t))2exp{2yΘu+z(Θ(u1+z)τ)(Nh=0q1hτh+1(t))2dτ},

    where CD is a specific constant that verifies R+πD(y)dy=1. From the probabilistic comparison result [40], we can compare the processes D and C1 as follows: D(t)C1(t) almost surely (a.s.). Furthermore, the time average of D(t) converges almost surely to R+yπD(dy) as t. In accordance with the above results, we clearly state that the present work aims to prove that the following quantity

    TΣ=bR+H(y,0)πD(dy)(u2+a+c)0.5q220

    is the sharp threshold between the disappearance of the illness and the ergodic characteristic of the system (1.4), and its sign provides a stellar overview of the potential scenarios of the epidemic situation. In other words, this article proposes a nice generalization of the article [9] and presents a new treatment applicable to other complex models. Importantly, we show numerically that the extreme amount of disturbance reduces the disease extinction time.

    The rest of the paper is organized as follows: In Section 2, we show that the disappearance scenario occurs when TΣ<0. In Section 3, we prove that the scenario of the ergodicity of system (1.4) occurs when TΣ>0. In Section 4, we verify numerically the correctness of our outcomes. Finally, we conclude this paper in Section 5 with a discussion.

    This section aims to exhibit the criterion for the demise of the infection.

    Theorem 2.1. The disappearance of the disease occurs if TΣ<0.

    Proof. By employing Itô's lemma for drift-diffusion processes [41], we obtain

    dlnC2(t)=(bH(C1(t),C2(t))(u2+a+c)0.5(Nh=0q2hCh2(t))2)dt+Nh=0q2hCh2(t)dW2(t).

    In line with the probabilistic comparison lemma, we conclude that

    dlnC2(t)(bH(D(t),0)(u2+a+c)0.5(Nh=0q2hCh2(t))2)dt+Nh=0q2hCh2(t)dW2(t). (2.1)

    After that, we make two operations on both sides of (2.1): integration from 0 to t and division by t, then the result is

    t^{-1}\ln {\bf C}_2(t)-t^{-1}\ln {\bf C}_2(0) \leq t^{-1} \mathfrak{b} \int_0^t{\mathcal H}\big({\bf D}(\tau), 0\big){\rm{d}} \tau -(\mathfrak{u}_2+\mathfrak{a}+\mathfrak{c}) \\&\;\;\;\;+t^{-1}\\

     \underbrace{\left(\int^t_0\mathop {\mathop \sum \limits^N }\limits_{h = 0} \mathfrak{q}_{2h}{\bf C}_2^{h}(\tau){\rm{d}} {\mathbb W}_2(\tau)-0.5\int^t_0\left(\mathop {\mathop \sum \limits^N }\limits_{h = 0} \mathfrak{q}_{2h}{\bf C}_2^{h}(\tau)\right)^2{\rm{d}} \tau\right)}_{ = \mathcal{G}(t)}.
    (2.2)

    The next step is based on the use of the exponential inequality for martingales [41], which leads to

    P{supt[0,T1](t0Nh=0q2hCh2(τ)dW2(τ)0.5α1t0(Nh=0q2hCh2(τ))2dτ)>2lnT1α1}T21,

    for all 0<α1<1 and T1>0. From the Borel-Cantelli result [41], we assure the existence of T1,ω=T1(ω), ω in Ω, such that

    t0Nh=0q2hCh2(τ)dW2(τ)2lnT1α1+0.5α1t0(Nh=0q2hCh2(τ))2dτ

    holds for all T1T1,ω and T11<tT1 a.s. Therefore,

    t1G(t)2lnT1α1t+t10.5α1t0(Nh=0q2hCh2(τ))2dτt10.5t0(Nh=0q2hCh2(τ))2dτ2lnT1α1(T11)t10.5(1α1)t0(Nh=0q2hCh2(τ))2dτ2lnT1α(T11)0.5(1α1)q220.

    By taking the limitsup on two sides of (2.2), we infer that

    lim suptt1lnC2(t)blimtt1t0H(D(τ),0)dτ(u2+a+c)+limtt1G(t)bR+H(y,0)πD(dy)(u2+a+c)+limT12lnT1α(T11)0.5(1α1)q220=bR+H(y,0)πD(dy)(u2+a+c)0.5(1α1)q220a.s.

    We let α1 tends to 0+, then the obtained result is

    lim suptt1lnC2(t)TΣ<0a.s.

    That implies the stochastic extinction limtC2(t)=0 a.s. In other words, the class of individuals carrying the infection will disappear.

    This section introduces a new approach to establish the criterion of the ergodicity of our probabilistic system (1.4).

    Theorem 3.1. The single ergodic stable distribution of the probabilistic model (1.4) exists if TΣ>0.

    Proof. In order to reduce notations and provide clear mathematical writing, we set

    (Nh=0q2hCh2(t))2=2Nh=0(n+m=hq2nq2m)phCh2(t)=2Nh=0phCh2(t).

    The Itô differential operator L associated with the stochastic equation of C2(t) is given by

    L(lnC2(t))=bH(C1(t),C2(t))+(u2+a+c)+0.5(Nh=0q2hCh2(t))2=bH(D(t),0)+bH(D(t),0)bH(C1(t),0)+bH(C1(t),0)bH(C1(t),C2(t))+(u2+a+c)+0.5q220+q20q21C2(t)+0.52Nh=2phCh2(t).

    From Assumption (a), we have

    L(lnC2(t))bH(D(t),0)+(u2+a+c)+0.5q220+bϱ(D(t)C1(t))+bH(C1(t),0)bH(C1(t),C2(t))+q20q21C2(t)+0.52Nh=2phCh2(t). (3.1)

    Now, the application of L on (lnD(t)lnC1(t)) gives

    L(lnD(t)lnC1(t))A(D1(t)C11(t))+bH(C1(t),C2(t))C2(t)C11(t)0.5(Nh=0q1hDh(t))2+0.5(Nh=0q1hCh1(t))2.

    Since D(t)C1(t) a.s., we obtain

    L(lnD(t)lnC1(t))q10q11(D(t)C1(t))+bϱC2(t). (3.2)

    We define the function Φ(t) as follows:

    Φ(t)=lnC2(t)+bϱq10q11(lnD(t)lnC1(t)).

    Based on (3.1) and (3.2), we get

    LΦ(t)bH(D(t),0)+(u2+a+c)+0.5q220+(q20q21+b2ϱ2q10q11)C2(t)+0.52Nh=2phCh2(t)+bH(C1(t),0)bH(C1(t),C2(t)). (3.3)

    We add and subtract at the same time the quantity bR+H(y,0)πD(dy) in (3.3) as follows:

    LΦ(t)bR+H(y,0)πD(dy)+(u2+a+c)+0.5q220+b(R+H(y,0)πD(dy)H(D(t),0))+(q20q21+b2ϱ2q10q11)C2(t)+0.52Nh=2phCh2(t)+bH(C1(t),0)bH(C1(t),C2(t)).

    To eliminate the term associated with C2(t), we set

    ΦΘ(t)=lnC2(t)+bϱq10q11(lnD(t)lnC1(t))+ΘC2(t),

    where the positive constant Θ verifies

    Θ(u2+a+c)(q20q21+b2ϱ2q10q11).

    The application of L on ΦΘ(t) gives

    LΦΘ(t)=TΣbR+H(y,0)πD(dy)+(u2+a+c)+0.5q220+b(R+H(y,0)πD(dy)H(D(t),0))+ΘbH(C1(t),C2(t))C2(t)+0.52Nh=2phCh2(t)+bH(C1(t),0)bH(C1(t),C2(t)).

    In the same vein, we apply L on the function ζ1(1+C1(t))ζ+ζ1Cζ2(t), ζ(0,1), then

    L(ζ1(1+C1(t))ζ+ζ1Cζ2(t))=(1+C1(t))ζ1(Θ(u1+z)C1(t)bH(C1(t),C2(t))C2(t))+0.5(ζ1)(1+C1(t))ζ2(Nh=0q1hCh+11(t))2+Cζ12(t)(bH(C1(t),C2(t))C2(t)(u2+a+c)C2(t))+0.5(ζ1)Cζ22(t)(Nh=0q2hCh+12(t))2.

    Accordingly, we derive that

    L(ζ1(1+C1(t))ζ+ζ1Cζ2(t))A0.5(1ζ)q211Cζ+21(t)+bϱC1(t)Cζ2(t)((u2+a+c)+0.5(1ζ)q220)Cζ2(t)+(1ζ)q20q21Cζ+12(t)0.5(1ζ)q221Cζ+22(t)0.5(1ζ)2Nh=2phCh+ζ2(t)Θ0.5(1ζ)q211Cζ+21(t)+bϱ(ζ+1)1Cζ+11(t)+bϱζ(ζ+1)1Cζ+12(t)0.5(1ζ)q221Cζ+22(t)0.5(1ζ)2Nh=2phCh+ζ2(t).

    Now, we define a new function ΦΘ,ζ as follows:

    ΦΘ,ζ(C1(t),C2(t))=SΦΘ(t)+ζ1(1+C1(t))ζ+ζ1Cζ2(t),

    where S>0 satisfies that STΣ+Z+20 and Z is given by

    Z=max{sup(C1,C2)R2+,{Θ+bϱ(ζ+1)1Cζ+11(t)0.25(1ζ)q211Cζ+21(t)+bϱζ(ζ+1)1Cζ+12(t)0.25(1ζ)q221Cζ+22(t)+0.52Nh=2phCh2(t)0.5(1ζ)2Nh=2phCh+ζ2(t)},1}.

    Clearly, the function ΦΘ,ζ reaches its minimum value at a point (C1,C2). For this reason, we will consider a new non-negative function defined as follows:

    ΦΣΘ,ζ(C1(t),C2(t))=SΦΘ(t)+ζ1(1+C1(t))ζ+ζ1Cζ2(t)ΦΘ,ζ(C1,C2).

    From the above calculation, we obtain

    LΦΣΘ,ζ(t)STΣ+SΘbϱC1(t)C2(t)+bS(H(C1(t),0)H(C1(t),C2(t)))+0.52Nh=2phCh2(t)+Θ0.5(1ζ)q211Cζ+21(t)+bϱ(ζ+1)1Cζ+11(t)+bϱζ(ζ+1)1Cζ+12(t)0.5(1ζ)q221Cζ+22(t)0.5(1ζ)2Nh=2phCh+ζ2(t)+b(R+H(y,0)πD(dy)H(D(t),0))=Ψ(C1(t),C2(t))+b(R+H(y,0)πD(dy)H(D(t),0)).

    Now, we define five sets:

    Ja,a={(C1(t),C2(t))R2,+|aC1(t)a1,aC2(t)a1},Ja,1={(C1(t),C2(t))R2,+|0<C1(t)<a},Ja,2={(C1(t),C2(t))R2,+|0<C2(t)<a},Ja,3={(C1(t),C2(t))R2,+|C1(t)>a1},Ja,4={(C1(t),C2(t))R2,+|C2(t)>a1}.

    Here, R2,+={(x,y):x>0,y>0}, a=min{a,a}, where a>0 verifies (3.9), and a>0 is chosen carefully such that

    SΘbϱa+bSϱa+ζSΘbϱaζ+2(2SΘbϱa0.25(ζ+2)(1ζ)q221)2ζ110, (3.4)
    SΘbϱa+ζSΘbϱaζ+2(2SΘbϱa0.25(ζ+2)(1ζ)q211)2ζ11<0, (3.5)
    STΣ+U0.25(1ζ)q211aζ2+10, (3.6)
    STΣ+U0.25(1ζ)q221aζ2+10, (3.7)

    where

    U=sup(C1,C2)R2,+{0.5SΘbϱC21(t)+0.5SΘbϱC22(t)+SbϱC1(t)+Θ+bϱ(ζ+1)1Cζ+11(t)+bϱζ(ζ+1)1Cζ+12(t)0.25(1ζ)q211Cζ+21(t)0.25(1ζ)q221Cζ+22(t)+0.52Nh=2phCh2(t)0.5(1ζ)2Nh=2phCh+ζ2(t)}.

    Plainly, Jca,a=R2,+Ja,a=Ja,1Ja,2Ja,3Ja,4. In the following, we will verify that

    Ψ(C1(t),C2(t))+10, (3.8)

    for any (C1(t),C2(t))Jca,a which is equivalent to showing it on Ja,1, Ja,2, Ja,3 and Ja,4, respectively. For this reason, we have the following situations:

    (1) Assume that (C1(t),C2(t))Ja,1. From (3.4), we obtain

    Ψ(C1(t),C2(t))STΣ+SΘbϱa+bSϱa+SΘbϱaC22(t)0.25(1ζ)q211Cζ+21(t)+0.52Nh=2phCh2(t)+Θ+bϱ(ζ+1)1C1(t)ζ+1+bϱζ(ζ+1)1Cζ+12(t)0.25(1ζ)q221Cζ+22(t)0.25(1ζ)q221Cζ+22(t)0.5(1ζ)2Nh=2phCh+ζ2(t)STΣ+Z+SΘbϱa+bSϱa+ζSΘbϱaζ+2(2SΘbϱa0.25(ζ+2)(1ζ)q221)2ζ11.

    (2) Here, we use the uniform continuity at C2=0 of the function H(C1(t),C2(t)). By Assumption (b), a>0 such that as 0<C2a,

    SΘbϱa+ζSΘbϱaζ+2(2SΘbϱa0.25(ζ+2)(1ζ)q211)2ζ1+bS(H(C1(t),0)H(C1(t),C2(t)))<1. (3.9)

    Consequently, if C2<a=min{a,a}, we get from (3.5) that

    Ψ(C1(t),C2(t))STΣ+SΘbϱa+SΘbϱaC21(t)0.25(1ζ)q211Cζ+21(t)+0.52Nh=2phCh2(t)+Θ+bS(H(C1(t),0)H(C1(t),C2(t)))+bϱ(ζ+1)1C1(t)ζ+1+bϱζ(ζ+1)1Cζ+12(t)0.25(1ζ)q221Cζ+22(t)0.5(1ζ)2Nh=2phCh+ζ2(t)STΣ+Z+SΘbϱa+ζSΘbϱaζ+2(2SΘbϱa0.25(ζ+2)(1ζ)q211)2ζ1+bS(H(C1(t),0)H(C1(t),C2(t)))1.

    (3) Assume that (C1(t),C2(t))Ja,3. From (3.6), we have

    Ψ(C1(t),C2(t))STΣ0.25(1ζ)q211Cζ+21(t)+0.5SΘbϱC21(t)+0.5SΘbϱC22(t)+SbϱC1(t)+Θ+bϱ(ζ+1)1C1(t)ζ+1+bϱζ(ζ+1)1Cζ+12(t)0.25(1ζ)q211Cζ+21(t) 0.25(1ζ)q221Cζ+22(t)+0.52Nh=2phCh2(t)0.5(1ζ)2Nh=2phCh+ζ2(t)STΣ+U0.25(1ζ)q211aζ21.

    (4) Assume that (C1(t),C2(t))Ja,4. From (3.7), we get

    Ψ(C1(t),C2(t))STΣ0.25(1ζ)q221Cζ+22(t)+0.5SΘbϱC21(t)+0.5SΘbϱC22(t)+SbϱC1(t)+Θ+bϱ(ζ+1)1C1(t)ζ+1+bϱζ(ζ+1)1Cζ+12(t)0.25(1ζ)q211Cζ+21(t) 0.25(1ζ)q221Cζ+22(t)+0.52Nh=2phCh2(t)0.5(1ζ)2Nh=2phCh+ζ2(t)STΣ+U0.25(1ζ)q221aζ21.

    In summary, the assertion (3.8) is obtained. On the other hand, we can easily show that O>0 such that Ψ(C1,C2)O, for all (C1,C2)R2,+. Accordingly, we get

    t0E(Ψ(C1(τ),C2(τ)))dτ+SϱE(t00H(y,0)πD(dy)dτt0H(D(τ),0)dτ)t0E(LΦΣΘ,ζ(t)(C1(τ),C2(τ)))dτ=E(ΦΣΘ,ζ(t)(C1(t),C2(t)))E(ΦΣΘ,ζ(t)(C1(0),C2(0)))E(ΦΣΘ,ζ(t)(C1(0),C2(0))).

    By using the ergodic property of D(t), we conclude that

    0lim inftt1t0(EΨ(C1(τ),C2(τ))1{(C1(τ),C2(τ))Jca,a}+EΨ(C1(τ),C2(τ))1{(C1(τ),C2(τ))Ja,a})dτlim inftt1t0(P((C1(τ),C2(τ))Jca,a)+OP((C1(τ),C2(τ))Jϵ,ϵ))dτ=1+(1+O)lim inftt1t0P((C1(τ),C2(τ))Ja,a)dτ.

    Consequently,

    lim inftt1t0P((C1(τ),C2(τ))Za,a)dτ(1+O)1>0.

    Hence,

    lim inftt1t0P((C1(0),C2(0),C3(0));τ,Ja,a)ds>0,(C1(0),C2(0),C3(0))R3,+,

    where R3,+={(x,y,z):x>0,y>0,z>0}. From Lemma 3.2 of [42] and also the mutually exclusive possibilities lemma [43], we confirm the existence of a single invariant distribution πΣ.

    Remark 3.1. From Theorem 3.1 of this paper and also Theorem 2.6 of [44], we can deduce interesting indications on the stochastic permanence of the Markovian processes C1, C2 and C3. Explicitly, we obtain that

    limtt1t0C1(τ)dτ=R3,+c1πΣ(dc1,dc2,dc3)<,limtt1t0C2(τ)dτ=R3,+c2πΣ(dc1,dc2,dc3)<,limtt1t0C3(τ)dτ=R3,+c3πΣ(dc1,dc2,dc3)<.

    By way of illustration, this indicates the persistence of the infection over time.

    In this section, we exhibit some simulations to shed some light on the exactitude of our global threshold. For that purpose, we present three situations of system (1.4), and in each case, we explore the complex long-run behavior of the illness. We will consider general saturated interference function introduced in Table 1. The model parameters are theoretically selected according to well audit the outcomes of this paper. By using the high-order discrete Milstein method, the associated discretization equations of our system are directly obtained as follows:

    {C1,k+1=C1,k+[Θ(u1+z)C1,kbH(C1,k,C2,k)C2,k]Δt+Nh=0q1hCh+11,kΔtξk+12(Nh=0q1hCh+11,k)(Nh=0q1h(h+1)Ch1,k)(ξ21)Δt,C2,k+1=C2,k+[bH(C1,k,C2,k)C2,k(u2+a+c)C2,k]Δt+Nh=0q2hCh+12,kΔtζk+12(Nh=0q2hCh+12,k)(Nh=0q2h(h+1)Ch2,k)(ζ21)Δt,C3,k+1=C3,k+[zC1,k+cC2,ku3C3,k]Δt+Nh=0q3hCh+13,kΔtαk+12(Nh=0q3hCh+13,k)(Nh=0q3h(h+1)Ch3,k)(α21)Δt,

    where the time increment Δt>0. ξk, ζk and αk are three independent random variables which follow the Gaussian distribution N(0,1). (C1,k,C2,k,C3,k) is the corresponding value of the k-th iteration.

    In this example, we will deal with the following stochastic system:

    {dC1(t)=(Θ(u1+z)C1(t)bC1(t)C2(t)1+m1C1(t)+m2C2(t))dt+q10C1(t)dW1(t),dC2(t)=(bC1(t)C2(t)1+m1C1(t)+m2C2(t)(u2+a+c)C2(t))dt+q20C2(t)dW2(t),dC3(t)=(zC1(t)+cC2(t)u3C3(t))dt+q30C3(t)dW3(t),C1(0)=0.5,C2(0)=0.3,C3(0)=0.2, (4.1)

    associated with the following auxiliary process:

    dD(t)=(Θ(u1+z)D(t))dt+q10D(t)dW1(t),D(0)=0.5.

    We choose Θ=0.23, u1=0.2, u3=0.19, z=0.02, u2=0.2, m1=0.1, m2=0.1, a=0.2, c=0.02, q10=0.11, q20=0.112 and q30=0.1. {By setting} b=0.4 and considering a large time T, we get

    TΣ=limTT1T0bD(τ)1+m1D(τ)dτ(u2+a+c)0.5q2200.0478<0.

    From Theorem 2.1, we can infer the disappearance of the illness. Numerically, it can be seen in Figure 1 that the disease disappears after 230 days in the population with a strong permanence of classes 1 and 3. Now, we select b=0.55 to switch from the case of extinction to the case of persistence. Then,

    TΣ=limTT1T0bD(τ)1+m1D(τ)dτ(u2+a+c)0.5q2200.0879>0.
    Figure 1.  Computer illustration of the trajectories of the probabilistic model (4.1) with linear white noise.

    In accordance with Theorem 3.1, we infer that the properties of stationarity and ergodicity hold. From Figure 2, we offer a good illustration of these two statistical characteristics. Clearly, in this situation, the continuation of all classes is strongly happening which is depicted in Figure 3.

    Figure 2.  The 3D graphs and associated upper views of the joint probability density at time t=600 of the classes C1, C2 and C3.
    Figure 3.  Computer simulation of the solution of the stochastic model (4.1) with linear white noises.

    In this example, {we deal with} the following stochastic system:

    {dC1(t)=(Θ(u1+z)C1(t)bC1(t)C2(t)1+m1C1(t)+m2C2(t))dt+q10C1(t)dW1(t)+q11C21(t)dW1(t),dC2(t)=(bC1(t)C2(t)1+m1C1(t)+m2C2(t)(u2+a+c)C2(t))dt+q20C2(t)dW2(t)+q21C22(t)dW2(t),dC3(t)=(zC1(t)+cC2(t)u3C3(t))dt+q30C3(t)dW3(t)+q31C23(t)dW3(t),C1(0)=0.5,C2(0)=0.3,C3(0)=0.2, (4.2)

    associated with the following auxiliary process:

    dD(t)=(Θ(u1+z)D(t))dt+q10D(t)dW1(t)+q11D2(t)dW1(t),D(0)=0.5.

    For the comparison objective, we keep the same parameter values as the first case and we select q11=0.022, q21=0.013 and q31=0.011. As the above case, we select b=0.4. Then, we get

    TΣ=limTT1T0bD(τ)1+m1D(τ)dτ(u2+a+c)0.5q2200.0520<0.

    Apparently, the condition of Theorem 2.1 holds. Numerically, the extinction phenomenon of the illness is illustrated in Figure 4. Classes 1 and 3 still persist. Now, we choose b=0.55 to move from the case of extinction to the case of persistence. Then,

    TΣ=limTT1T0bD(τ)1+m1D(τ)dτ(u2+a+c)0.5q2200.0896>0.
    Figure 4.  Computer simulation of the trajectories of the probabilistic model (4.2) with quadratic white noises.

    Based on Theorem 3.1, The last value implies that the system (4.2) admits a stable distribution. From Figure 5, we get an insight into the stationarity of the model (4.2). Furthermore, we offer Figure 6 to clarify the continuation of all classes C1, C2 and C3.

    Figure 5.  The 3D graphs and associated upper views of the joint probability density at time t=600 of the classes C1, C2 and C3.
    Figure 6.  Computer illustration of the solution of the probabilistic model (4.2) with quadratic white noises.

    In this part, we numerically prove that TΣ is the sill of the system (1.4) in the special case of cubic perturbation. So, we firstly introduce this probabilistic model:

    {dC1(t)=(Θ(u1+z)C1(t)bC1(t)C2(t)1+m1C1(t)+m2C2(t))dt+q10C1(t)dW1(t)+q11C21(t)dW1(t)+q12C31(t)dW1(t),dC2(t)=(bC1(t)C2(t)1+m1C1(t)+m2C2(t)(u2+a+c)C2(t))dt+q20C2(t)dW2(t)+q21C22(t)dW2(t)+q22C32(t)dW2(t),dC3(t)=(zC1(t)+cC2(t)u3C3(t))dt+q30C3(t)dW3(t)+q31C23(t)dW3(t)+q32C33(t)dW3(t),C1(0)=0.5,C2(0)=0.3,C3(0)=0.2, (4.3)

    associated with the following auxiliary process:

    dD(t)=(Θ(u1+z)D(t))dt+q10D(t)dW1(t)+q11D2(t)dW1(t)+q12D3(t)dW1(t),D(0)=0.5.

    Here, we select q12=0.014, q22=0.0135, q32=0.012 and we keep the other coefficient values as the above two cases. Again, if we select b=0.4, then the result is

    TΣ=limTT1T0bD(τ)1+m1D(τ)dτ(u2+a+c)0.5q2200.0616<0.

    Theoretically, we have the disappearance of the illness according to Theorem 2.1. It remains to verify it numerically. From Figure 7, the disease will clear up in about 70 days with long-term persistence of categories 1 and 3. Now, we opt b=0.55. Then,

    TΣ=limTT1T0bD(τ)1+m1D(τ)dτ(u2+a+c)0.5q2200.0905>0.
    Figure 7.  Trajectories of the probabilistic model (4.3) with cubic white noises.

    From Theorem 3.1, we establish that there is a single stable distribution for (4.3) which is depicted in Figure 8. The persistence of all classes is depicted in Figure 9.

    Figure 8.  The 3D graphs and associated upper views of the joint probability density at time t=600 of the classes C1, C2 and C3.
    Figure 9.  Computer simulation of the solution of the probabilistic model (4.3) with cubic white noises.

    Mathematical formulation plays a major role in understanding epidemics and also in supporting public health decision-making. The regularly used models provide deterministic predictions, that is to say, a strict behavior of the system studied, thus ignoring individual and environmental variations. Actually, we group these unpredictable variations under the name of stochasticity (or randomness), and the present study is devoted to the analysis of an epidemic strewing under heavy stochasticity. The non-linearity and the complexity of the fluctuations pushed us to consider a general form of the probabilistic part. Focusing on these motivations, we have offered an improved generalization of the recent paper [9]. In the following, we present our substantial enhancements of the mentioned research.

    In [9], the authors considered a nonlinear prevalence function of the form: bC1(t)g(C2(t)). This type of function has certain limitations and is not suitable for covering certain well-known functional responses. By assuming mutual interference between classes C1 and C2, we have proposed a general function H which includes all the existing functional incidences.

    In [9], the authors presented two distinct criteria to classify the asymptotic attitude of system (1.4) with the incidence function bC1(t)g(C2(t)). Explicitly, they obtained the following results:

    (1) The sufficient condition of the disease disappearance is

    RC0=bg(0)R+yπD(dy)(u2+a+c+0.5q220)<0.

    (2) The sufficient condition of the ergodicity is

    RS0=Θbg(0)(u1+z+0.5q210+2Nh=1h+122h1i+j=hq1iq1jΘh)(u2+a+c+0.5q220)>0.

    However, in this article, we have unified the criterion of the above-mentioned characteristics by providing the following acute threshold value:

    TΣ=bR+H(y,0)πD(dy)(u2+a+c)0.5q220.

    Specifically,

    (1) The condition of the disease disappearance is TΣ<0.

    (2) The condition of the ergodicity is TΣ>0.

    As a special case, we mention that the sharp threshold of the perturbed model studied in [9] is exactly RC0.

    Numerically, we have chosen the first three values of h, that are, linear, quadratic and cubic perturbations. In all cases, we have confirmed that TΣ is the global sill among disappearance of infection and ergodicity. From Figure 10, we infer that when we raise the perturbation order, the illness disappears swiftly. This indicates that the intense environmental variations have a negative effect on the illness duration. This remark requires further theoretical clarification and explanation. We will deal with this interesting question in our future work.

    Figure 10.  Stochastic paths of infected class C2 in the case of N=3 (q13=0.0116, q23=0.012, q33=0.0108); in the case of N=4 (q14=0.016, q24=0.024, q34=0.038) and in the case of N=5 (q15=0.06, q25=0.08, q35=0.017). The other coefficients are selected above.

    Some fascinating topics deserve more attention. For example, we can consider our model with fractal-fractional differentiation. This framework is an attractive branch of applied mathematics that deals with derivatives and integrals of non-integer order. Due to its amazing features, it is preferred for describing and simulating real-world problems in various fields such as biological mechanisms, material science, hydrological modeling, economic phenomena. We will address this idea in our future work.

    This research was sponsored by the Guangzhou Government Project under Grant No. 62216235, also supported by SERB of India (EEQ/2021/001003).

    The authors declare no conflicts of interest.



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