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Research article

Analysis of a mathematical model for the spreading of the monkeypox virus with constant proportional-Caputo derivative operator

  • Received: 22 November 2024 Revised: 08 February 2025 Accepted: 18 February 2025 Published: 27 February 2025
  • MSC : 26A33, 34A08, 65L09, 92D25, 92D30

  • This work comprehensively analyzed the monkeypox virus utilizing a deterministic mathematical model within a constant proportional-Caputo derivative framework. The suggested model considered the interplay of human and rodent populations by incorporating certain realistic vaccination parameters. Our study was a testament to the thoroughness of this work. We explored the uniqueness result using Banach's contraction principle. The solution's positivity and boundedness were studied in detail, as were the basic reproduction number and the stability analysis of the system's equilibrium conditions. We performed a variety of Ulam's stability analyses to guarantee the solution existed. Additionally, we implemented a decomposition formula to obtain the numerical scheme. This numerical approach allowed for numerical simulation as a graphical representation for certain real data sets and different parameter values in order to understand the model's dynamic behavior.

    Citation: Jutarat Kongson, Chatthai Thaiprayoon, Weerawat Sudsutad. Analysis of a mathematical model for the spreading of the monkeypox virus with constant proportional-Caputo derivative operator[J]. AIMS Mathematics, 2025, 10(2): 4000-4039. doi: 10.3934/math.2025187

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  • This work comprehensively analyzed the monkeypox virus utilizing a deterministic mathematical model within a constant proportional-Caputo derivative framework. The suggested model considered the interplay of human and rodent populations by incorporating certain realistic vaccination parameters. Our study was a testament to the thoroughness of this work. We explored the uniqueness result using Banach's contraction principle. The solution's positivity and boundedness were studied in detail, as were the basic reproduction number and the stability analysis of the system's equilibrium conditions. We performed a variety of Ulam's stability analyses to guarantee the solution existed. Additionally, we implemented a decomposition formula to obtain the numerical scheme. This numerical approach allowed for numerical simulation as a graphical representation for certain real data sets and different parameter values in order to understand the model's dynamic behavior.



    Presently, people in many countries face a series of epidemics, each caused by a different type of emerging or reemerging virus. Monkeypox (MPOX) disease is one of these urgent situations that need to be monitored appropriately since the World Health Organization (WHO) has recently reported a resurgence of the MPOX outbreak, with the disease reemerging and spreading across multiple countries worldwide. Numerous cases and clusters have been identified simultaneously in diverse geographical areas [1]. The MPOX virus is the cause of a zoonotic illness. The spreading of this virus to humans mainly comes through bites or scratches from wild animals, such as rodents and primates. Human-to-human transmission arises through respiratory droplets or contact with body fluids when a person touches a lesion on an infected individual or their items. The symptoms of MPOX patients frequently resemble those of smallpox but are less severe. It begins with a slight fever, chills, weariness, muscle aches, exhaustion, and headache. The MPOX can cause swelling in the lymph nodes, while smallpox does not cause lymphadenopathy. The time between the onset of symptoms and the rash completely recovering typically lasts 14–28 days [2,3,4]. Currently, there is no vaccine that directly protects against MPOX disease. However, due to the similarity between the virus that causes MPOX disease and smallpox disease, vaccination against smallpox is the best choice. It effectively prevents MPOX disease by as much as 80–85 percent [5]. Mathematical models of epidemics have long been used to help us understand the effects of numerous disease transmissions in the real world. Understanding the virus and its transmission dynamics is critical for establishing efficient prevention and control strategies. Therefore, many researchers have focused on developing the MPOX epidemic model for various reasons, including potential human outbreaks. Some examples of interesting works, such as the analysis of the MPOX disease with the impact of vaccination, were studied in [6,7] A quarantine class and an enlightenment campaign were incorporated into the MPOX model, which can be found in [8], while the factor of isolated humans was added to the model, as seen in [9,10,11]. In [12], pox-like analysis was investigated under the factor of recovery with permanent immunity. Monkeypox analysis using data and statistical tools were examined in [13,14].

    Fractional calculus is an area of pure mathematics that generalizes the concepts of differentiation and integration involving non-integer derivatives and integrals. It is a valuable and efficient tool for describing complex dynamical systems and simulating real-world problems, particularly in epidemiology, since it has hereditary properties and describes memory in the context of numerous diseases. Besides, fractional models provide a more realistic illness trajectory. Fractional differential operators enhance epidemiological modeling by combining memory, heterogeneity, and nonlocal dynamics. This leads to more accurate predictions, a better understanding of diseases, and improved control strategies for illnesses such as monkeypox, COVID-19, HIV, and so on. Fractional derivatives, which can take any real number as an order, are highly flexible and nonlocal. These characteristics make them more dependable than classical derivatives for approximating real data since they take into account global interactions and memory effects. Researchers have defined the many forms of fractional derivative operators in fractional calculus. Each form is created to capture distinct characteristics of the fractional derivative idea. For instance, Riemann-Liouville (RL, one of the original definitions of fractional derivative), Caputo [15,16], Caputo-Katugampola [17], Caputo-Fabrizio [18,19], Atangana-Baleanu [18,19], Hilfer [20], constant proportional-Caputo (CPC) [21], and (k,ψ)-Hilfer proportional [22]. The CPC derivative is a modern development in the fractional derivative, which is designed in [21]. It is a hybrid concept between Caputo's type and the proportional derivatives to gain a novel type of fractional calculus and potential applications for modeling actual data from various problems. In addition, the CPC operator is a more comprehensive framework than the Caputo fractional derivative operator, for which supporting research can be found in [23,24]. This operator offers a significant advantage by effectively addressing current challenges in different issues that traditional operators cannot adequately evaluate. Several studies [25,26,27] highlight that the CPC operator provides a more practical and accurate approach for examining mathematical models applied to real-world problems using real data compared to classical and fractional-order operators.

    The application of fractional calculus to mathematical modeling is a novel approach that has captured the interest of many researchers across diverse scientific domains. It is particularly intriguing due to the memory effect, a unique and powerful characteristic of fractional-order models, which remains supereminent over the classical models due to the diverse properties of fractional operators that yield more accurate and reliable data. Many fractional models consist of differential equations carefully designed by researchers to address the pressing problems within the global environment. Extensive research has been conducted on studying and analyzing fractional-order models for disease transmission dynamics. El-Mesady et al. [28] designed a fractional-order vaccination mathematical model for tuberculosis incorporating a susceptible class with an underlying ailment. Peter et al. [29] developed a fractional mathematical model for studying measles infection with double-dose vaccination. The work [30] constructed a mathematical model under the Atangana-Baleanu-Caputo derivative to examine meningitis with treatment and vaccination dynamics. The authors [31] presented the pneumococcal pneumonia infection model using fractional-order derivatives in the sense of the Caputo-Fabrizio operator. Peter [32] studied the transmission dynamics of a Brucellosis model under the Caputo-Fabrizio fractional operator. Additionally, MPOX virus infection is one of the research areas that has gotten a lot of attention and produced some fascinating results since the disease resurfaced after a long hiatus. We refer the reader to several previously interesting works about the MPOX fractional model. For example, Peter et al. [33] presented and established the dynamical behavior of the MPOX virus model by using both classical and differential equations via the Caputo-Fabrizio fractional derivative. Ngungu et al. [34] studied the dynamics of the MPOX virus spreading with a non-pharmaceutical intervention using real-time data with the Caputo-Fabrizio operator. Wireko et al. [35] used fractal-fractional operators (FFOs) to explore the biological behavior of the MPOX disease. Sudsutad et al. [36] investigated the theoretical analysis for the transmission of the MPOX virus fractional model under the FFOs involving the Atangana-Baleanu sense. The study by El-Mesady et al. [37] looked into how the MPOX virus spreads in human hosts and rodent populations using a Caputo fractional-order nonlinear model. The MPOX virus is established by applying a deterministic mathematical model in the context of the Atangana-Baleanu fractional derivative that depends on the generalized Mittag-Leffler kernel [38]. Zhang et al. [39] studied a deterministic Caputo fractional-order mathematical model of Marburg-MPOX virus co-infection transmission. Liu et al. [40] analyzed the dynamics of a MPOX disease with the impact of vaccination utilizing a fractional mathematical model. For more works, we refer readers to see [41,42]. However, even though many researchers employ fractional differential systems to understand real-world phenomena, finding exact solutions to such systems through manual methods is still a formidable challenge. Hence, several efficient techniques are produced to find the approximated solution of fractional differential systems, such as the predictor-corrector [43,44], Adams-Bashforth [43,45], Newton polynomial [43,45], and the decomposition formula method [46,47]. The last introduced powerful knowledge is Ulam stability, an essential technique in mathematical analysis and other related sciences. Ulam stability is vital to maintaining the stability and reliability of solutions under minor variations. It ensures that solutions remain valid and usable even though conditions change marginally. There are various kinds of Ulam stability commonly used, like Ulam-Hyers (UH) stability and Ulam-Hyers-Rassias (UHR) stability; see the history and its application in [48,49,50,51].

    After composing all of the stories and being motivated by the above discussions, the CPC operator is particularly interesting in this aspect because it is a recent operator, and there has been little literature-based research on its application. Also, to the best of our current understanding, no studies using the proposed derivative operator have been conducted or published in the existing literature on the dynamics of the monkeypox virus as well as the benefit of using the CPC operator, as mentioned above, to address memory and hereditary properties for resulting in more accurate prediction and translation. Therefore, this study takes a comprehensive approach to analyzing the behavior of the MPOX model and investigating the factors influencing population changes, which may help control the monkeypox outbreak. We have developed a deterministic MPOX model by extending the works [9,33] in terms of incorporating the vaccinated-individuals compartment into the model and yielding a unique classical model. Later, we transform the model into a fractional-order system using the CPC operator to gain a better understanding of the virus dynamics. Our focus is on studying the dynamic behavior of this model, a task we accomplish by leveraging the well-known fixed-point theory of Banach's type to prove the solution's existence and uniqueness. We investigate the stability of equilibrium points with the help of the basic reproduction number. Moreover, we ensure the solutions exist by analyzing their stability via various Ulam stability. A decomposition formula for the CPC derivative technique is derived to obtain the numerical scheme, and some graphics in the numerical simulation are shown to visualize the system's behavior analysis. This work will help to fill the gap in the study of monkeypox transmittance using fractional derivatives and expand the scope of this study to benefit disease control.

    The remaining sections of the paper are as follows: Section 2 introduces some concepts of the CPC operators. The MPOX model construction is presented in Section 3. Section 4 is dedicated to investigating model analysis, including the solution's positiveness and boundedness, the basic reproduction number, and the local stability analysis of the equilibrium points. Section 5 explores the existence theory for the proposed model; that is, the uniqueness result is verified using Banach's fixed-point theorem. Section 6 verifies various Ulam's type stability and their generalization. The numerical scheme derived from a decomposition formula for the CPC derivative is determined in Section 7. Finally, the results are discussed via some examples, and the summation of this discussion is given in the final part.

    This section provides some fundamental definitions and properties of fractional calculus, which will be used to analyze the system throughout this work.

    Definition 2.1. ([52]). The Caputo fractional order derivative of a function f with order α(0,1) is provided by

    CDα0,tf(t)=1Γ(1α)t0f(s)(ts)αds.

    Definition 2.2. ([52]). Assume f(t) is an integrable function. The RL-integral of α>0 is given by

    RLIα0,tf(t)=1Γ(α)t0f(s)(ts)α1ds,a<t.

    Definition 2.3. ([21]). A proportional-Caputo (CP) is a hybrid operator that combines the proportional operator and the Caputo fractional derivative as:

    CPDα0,tf(t)=1Γ(1α)t0(K1(α,s)f(s)+K0(α,s)f(s))(ts)αds=(K1(α,t)f(t)+K0(α,t)f(t))×tαΓ(1α),

    where K0(α,t)=αC2αt1α and K1(α,t)=(1α)tα, for C is constant and α(0,1).

    Moreover, as defined in the particular case where K0 and K1 are depending only on α, the CPC operator can be defined by

    CPCDα0,tf(t)=1Γ(1α)t0(K1(α)f(s)+K0(α)f(s))(ts)αds=K1(α)RLI1α0,tf(t)+K0(α)CDα0,tf(t),

    where K0(α) and K1(α) are constants with respect to t.

    Here, this study uses the specific case when K0(α)=αC2αQ1α and K1(α)=(1α)Qα where C and Q are constants.

    Definition 2.4. ([21]). The inverse operator of the CPC fractional derivative operator is provided by:

    CPCIα0,tf(t)=1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))f(s)ds,

    which satisfies the relation below:

    CPCIα0,t[CPCDα0,tf(t)]=f(t)e(K1(α)K0(α)t)f(0).

    In this subsection, we formulate a deterministic model of the dynamics of MPOX transmission across two groups: humans denoted by Nh and rodents denoted by Nr. The human population has six different compartments: the susceptible (Sh), exposed (Eh), infectious (Ih), clinically ill (Ch), recovered (Rh), and vaccinated individuals (Vh). The rodent population has three compartments: the susceptible (Sr), exposed (Er), and infectious (Ir). Thus, the total populations of humans and rodents are given by Nh(t)=Sh(t)+Eh(t)+Ih(t)+Ch(t)+Rh(t)+Vh(t) and Nr(t)=Sr(t)+Er(t)+Ir(t), respectively. The transmission diagram of the population flow among these compartments is displayed in Figure 1.

    Figure 1.  Transmission chart of the suggested MPOX model.

    Here, the descriptions of the population changes of each group are presented in the following:

    Human groups: The amount of susceptible humans changes due to recruitment through birth rate or immigration Λh. The vaccinated population further increased the number in this class after the induced immunity waned at the rate η. This population class is rejected by the natural death per capital rate μh and by the population gaining infection after contact with infected humans or infected rodents at the rate b1 or b2, respectively. It is also reduced by vaccinating at the rate λ. The amount of exposed humans grows with the force of infection in the term of ϕh=(b1Ih(t)+b2Ir(t))/Nh(t) and declines by the disease progression rate a1 and the natural death per capital rate μh. The amount of infected individuals increases after transitioning from the exposed class with the disease progression rate a1. The natural recovery rate ω reduces the population in the infectious class due to immunity. This population is also reduced by the natural death rate μh, the disease-induced death rate δ1, and the clinically ill rate a2 after moving to a clinically ill class of humans. The number of clinically ill humans grows due to those who seek medical assistance after becoming sick with a clinically ill rate a2. These individuals are decreased by disease-induced death rate δ2 and natural death rate μh. Moreover, moving to the recovered class at the rate ν can reduce the population in this class. The group in the recovered compartment increases with the recovery rate of clinically ill humans ν and the natural recovery rate due to immunity ω, while it declines with the natural death rate μh. The susceptible individuals enter into the vaccinated class with a rate λ. The vaccinated individuals are declined by the natural death rate and the waning induced immunity with a rate η.

    Rodent groups: The amount of susceptible rodents changes due to recruitment through birth rate Λr. These individuals are decreased by interaction with infected rodents at a rate b3 and natural death per capital rate of rodents μr. The amount of exposed rodents grows with the force of infection in the term ϕr=b3Ir(t)/Nr(t). It is declined by the natural death rate μr and the progression rate a3, which transit from exposed rodents to infected rodents. The amount of infected rodents increases from the exposed rodent's transit to infectious rodents at the rate a3. The infected rodents are reduced due to the natural death rate μr.

    Therefore, based on the above description, a nonlinear system of the integer-order of the MPOX model corresponding with nine ordinary differential equations, the so-called MPOX model, is shown below:

    {dSh(t)dt=Λh(b1Ih(t)+b2Ir(t)Nh(t)+μh+λ)Sh(t)+ηVh(t),dEh(t)dt=(b1Ih(t)+b2Ir(t)Nh(t))Sh(t)(μh+a1)Eh(t),dIh(t)dt=a1Eh(t)(ω+a2+μh+δ1)Ih(t),dCh(t)dt=a2Ih(t)(ν+μh+δ2)Ch(t),dRh(t)dt=νCh(t)+ωIh(t)μhRh(t),dVh(t)dt=λSh(t)(μh+η)Vh(t),dSr(t)dt=Λr(b3Ir(t)Nr(t)+μr)Sr(t),dEr(t)dt=b3Ir(t)Sr(t)Nr(t)(a3+μr)Er(t),dIr(t)dt=a3Er(t)μrIr(t), (3.1)

    where the positive initial conditions are Sh(0)=Sh0, Eh(0)=Eh0, Ih(0)=Ih0, Ch(0)=Ch0, Rh(0)=Rh0, Vh(0)=Vh0, Sr(0)=Sr0, Er(0)=Er0, and Ir(0)=Ir0. The details of each all positive parameter are included and displayed in Table 1.

    Table 1.  The details of dependent parameters of the MPOX model (3.1).
    Parameters Description
    Λh, Λr The recruitment rate for susceptible humans and rodents, respectively.
    b1, b2, b2 Contact rate between infected humans and susceptible humans, rodents and susceptible humans, and rodents and susceptible rodents, respectively.
    a1 Disease progression rate from exposed humans to infected humans.
    a2 Clinically ill rate.
    a3 Progression rate from exposed rodents to infected rodents.
    ω Natural recovery rate due to immunity.
    ν The rate of recovery for clinically ill humans.
    η Waning induced immunity.
    λ Vaccinated against monkeypox.
    δ1, δ2 Disease-induced death rate for infectious and clinically ill humans, respectively.
    μh, μr Natural death per capital rate of humans and rodents, respectively.

     | Show Table
    DownLoad: CSV

    As we know, fractional infectious models have specific hereditary properties and describe memory regarding disease dynamics because they employ fractional derivatives with a higher degree of freedom to account for more complex diseases and provide knowledge into the behavior and control of epidemic diseases. Consequently, this subsection further develops the integer order MPOX model (3.1) utilizing the CPC derivative operator as follows:

    {CPCDα0,tSh(t)=F1(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tEh(t)=F2(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tIh(t)=F3(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tCh(t)=F4(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tRh(t)=F5(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tVh(t)=F6(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tSr(t)=F7(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tEr(t)=F8(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)),CPCDα0,tIr(t)=F9(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)), (3.2)

    where Fj=Fj(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)), for j=1,2,,9 and Fj for the suggested model are given by

    {F1(t,Sh(t))=Λh(ϕh+c1)Sh(t)+ηVh(t),F2(t,Eh(t))=ϕhSh(t)c2Eh(t),F3(t,Ih(t))=a1Eh(t)c3Ih(t),F4(t,Ch(t))=a2Ih(t)c4Ch(t),F5(t,Rh(t))=νCh(t)+ωIh(t)μhRh(t),F6(t,Vh(t))=λSh(t)c5Vh(t),F7(t,Sr(t))=ΛrϕrSr(t)μrSr(t),F8(t,Er(t))=ϕrSr(t)c6Er(t),F9(t,Ir(t))=a3Er(t)μrIr(t), (3.3)

    with ϕh=(b1Ih(t)+b2Ir(t))/Nh(t), ϕr=b3Ir(t)/Nr(t), c1=μh+λ, c2=μh+a1, c3=ω+a2+μh+δ1, c4=ν+μh+δ2, c5=μh+η, and c6=a3+μr with Sh00, Eh00, Ih00, Ch00, Rh00, Vh00, Sr00, Er00, and Ir00. The suggested model (3.2) is said to be the CPC-MPOX model.

    Since the variables in real-world phenomena have positive values, particularly the epidemic model based on the human population, all variables and parameters are considered to be positive. Moreover, the invariant region is essential in mathematical modeling as it guarantees that solutions remain biologically feasible and mathematically meaningful. In this part, we investigate the factors that guarantee the solutions of the CPC-MPOX model (3.2) are positive, and we locate the invariant area, ensuring that the solution is bounded. To achieve this purpose, we define

    R9+={FR9:F0andF(t)=(Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t))T}.

    Theorem 4.1. All solutions of the CPC-MPOX model (3.2) under the initial conditions are bounded in R9+.

    Proof. From the CPC-MPOX model (3.2), we obtain

    {CPCDα0,tSh(t)=Λh+ηVh(t)0,CPCDα0,tEh(t)=ϕhSh(t)0,CPCDα0,tIh(t)=a1Eh(t)0,CPCDα0,tCh(t)=a2Ih(t)0,CPCDα0,tRh(t)=νCh(t)+ωIh(t)0,CPCDα0,tVh(t)=λSh(t)0,CPCDα0,tSr(t)=Λr0,CPCDα0,tEr(t)=ϕrSr(t)0,CPCDα0,tIr(t)=a3Er(t)0. (4.1)

    If a set of the conditions (Sh0,Eh0,Ih0,Ch0,Rh0,Vh0,Sr0,Er0,Ir0)R9+, then according to the above system (4.1), the solution F cannot avoid from the hyper-planes: (Sh, Eh, Ih, Ch, Rh, Vh, Sr, Er, Ir) = (0,0,0,0,0,0,0,0,0). Additionally, the vector field points into R9+ on each hyperplane that is surrounded by the nonnegative constants. This means that R9+ is the positively invariant region.

    Theorem 4.2. Let a positive set of solutions (Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t)) under the initial conditions. Then, there exists a domain Ω=Ωh×ΩrR6+×R3+, that is positively invariant so that

    Ωh={(Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t))R6+andNhΛh/μh}, (4.2)
    Ωr={(Sr(t),Er(t),Ir(t))R3+andNhΛr/μr}. (4.3)

    Proof. Since Nh(t)=Sh(t)+Eh(t)+Ih(t)+Ch(t)+Rh(t)+Vh(t), then from the proposed model (3.2), we have

    CPCDα0,tNh(t)=CPCDα0,tSh(t)+CPCDα0,tEh(t)+CPCDα0,tIh(t)+CPCDα0,tCh(t)+CPCDα0,tRh(t)+CPCDα0,tVh(t)=ΛhμhNh(t)δ1Ih(t)δ2Ch(t).

    In the case of no disease, we get CPCDα0,tNh(t)=ΛhμhNh(t). It implies that

    CPCDα0,tNh(t)0ifNh(t)Λhμh,for allt[0,T].

    By a particular comparison principle, we obtain

    Nh(t)Nh(0)eμht+Λhμh(1eμht).

    Then, we get

    Nh(t)ΛhμhifNh(0)Λhμh.

    Thus, the feasible region of human groups (4.2) is completed.

    Similarly, since Nr(t)=Sr(t)+Er(t)+Ir(t), then

    CPCDα0,tNr(t)=CPCDα0,tSr(t)+CPCDα0,tEr(t)+CPCDα0,tIr(t)=ΛrμrNr(t).

    It implies that

    CPCDα0,tNr(t)0ifNr(t)Λrμr,for allt[0,T].

    By a particular comparison principle, we have

    Nr(t)Nr(0)eμrt+Λrμr(1eμrt).

    Then, we have

    Nr(t)ΛrμrifNr(0)Λrμr.

    Thus, the feasible region of rodent groups (4.3) is obtained. This shows the boundedness of the solutions for the CPC-MPOX model (3.2). Hence, the region Ω=Ωh×Ωr, defined as (4.2) and (4.3), is positively invariant. We therefore conclude that the proposed model is epidemiologically feasible and well-posed in Ω. The proof is complete.

    The equilibrium points of the the CPC-MPOX model (3.2) can be calculated by setting the right-hand side equal to zero. This gives two possible positive equilibria, which are

    ● The MPOX free equilibrium (E0MFE); this point is defined when there is no disease in the population:

    E0MFE=(S0h,E0h,I0h,C0h,R0h,V0h,S0r,E0r,I0r)=(c5Λhc1c5λη,0,0,0,0,λΛhc1c5λη,Λrμr,0,0).

    Note that: c1c5λη=μh(μh+η+λ)>0, N0h=S0h+E0h+I0h+C0h+R0h+V0h, and N0r=S0r+E0r+I0r.

    ● The MPOX endemic equilibrium (EMEE); this point is defined when there is disease transmission in the population:

    EMEE=(Sh,Eh,Ih,Ch,Rh,Vh,Sr,Er,Ir),

    where

    Sh=c5Λhc5(ϕh+c1)ηλ,Eh=c5Λhϕhc2[c5(ϕh+c1)ηλ],Ih=c5Λha1ϕhc2c3[c5(ϕh+c1)ηλ],Ch=c5Λha1a2ϕhc2c3c4[c5(ϕh+c1)ηλ],Rh=νc5Λha1a2ϕhμhc2c3c4[c5(ϕh+c1)ηλ]+ωc5Λha1ϕhμhc2c3[c5(ϕh+c1)ηλ],Vh=c5Λhλc5[c5(ϕh+c1)ηλ],Sr=Λrϕr+μr,Er=ϕrΛrc6(ϕr+μr),Ir=a3ϕrΛrc6μr(ϕr+μr).

    Next, the basic reproduction number is conducted as an epidemic indicator. It is an essential fundamental epidemiological parameter used to assess the long-term dynamics of the epidemic, which is denoted by R0. It is also defined as the expected number of secondary infections generated by a single infected individual throughout their infectious period. The basic reproduction number can be used as a disease control measure because it indicates the spread of a disease in terms of transmission within a population. It helps determine whether an outbreak or epidemic will occur or the infection will eventually disappear. Here, we will calculate it by using the next-generation technique as in [53]. For the proposed model, the disease-free state variables are Sh,Rh,Sr while the infected state variables are Eh,Ih,Ch,Vh,Er,Ir. Therefore,

    F=(0b1S0hN0h000b2S0hN0h00000000000000000000000b3000000)andV=(c200000a1c300000a2c4000000c5000000c600000a3μr),

    where F and V denote the transmission and transitions matrices, respectively. Then, the next-generation matrix is provided as below:

    FV1=(a1b1S0hc2c3N0hb1S0hc3N0h00a3b2S0hc6μrN0hb2S0hμrN0h0000000000000000000000a3b3c6μrb3μr000000).

    This implies the spectral radius of (4.2) (R0)

    R0=max{Rh0,Rr0}=max{a1b1S0hc2c3N0h,a3b3c6μr}.

    Remark 4.3. We can notice that:

    If R0h>1 and R0r>1, then R0>1.

    If R0h<1 and R0r>1, then R0=R0r>1.

    If R0h>1 and R0r<1, then R0=R0h>1.

    If R0h<1 and R0r<1, then R0<1.

    For the following two theorems, the stability of the equilibrium points will be analyzed. To do this, the Jacobian matrix (J) of the system is given by

    J=(b1Ih+b2IrNhc10b1ShNh00η00b2ShNhb1Ih+b2IrNhc2b1ShNh00000b2ShNh0a1c300000000a2c40000000ωνμh0000λ0000c5000000000b3IrNrμr0b3SrNr000000b3IrNrc6b3SrNr0000000a3μr). (4.4)

    Theorem 4.4. If R0<1, then the MPOX free equilibrium of the CPC-MPOX model (3.2) is locally asymptotically stable with the necessary and sufficient criteria:

    |arg(θi)|>απ2,i=1,2,...,9. (4.5)

    Proof. From the asumption R0<1, it implies that Rh0<1 and Rr0<1. By applying matrix (4.4) at the point E0MFE, we have

    J(E0MFE)=(c10b1S0hN0h00η00b2S0hN0h0c2b1S0hN0h00000b2S0hN0h0a1c300000000a2c40000000ωνμh0000λ0000c5000000000μr0b30000000c6b30000000a3μr).

    Then, the characteristic equation is computed by |J(E0MFE)θˆI|=0, and ˆI is a identity matrix. This yields the eigenvalues as the following:

    θ1=c4,θ2=μr,θ3=μh,θ4,5=12((c1+c5)±(c1+c5)24(μh(μh+η+λ))),θ6,7=12((c2+c3)±(c2+c3)24(c2c3a1b1S0hN0h)),θ8,9=12((μr+c6)±(μr+c6)24(μrc6a3b3)).

    Obviously, the eigenvalues θ1,θ2,θ3, and θ4,5 have negative real parts. Since Rh0<1 and Rr0<1, then the eigenvalues θ6,7 and θ8,9 also have negative real parts, respectively. This assures the assumption (4.5) with 0<α1. Therefore, the point E0MFE is locally asymptotically stable.

    For the following theorem, we will utilize the Routh-Hurwitz criterion to investigate the local stability of endemic equilibria. Here, we will determine the conditions under which the endemic equilibrium point is locally asymptotically stable. The Jacobian matrix (4.4) yields the following matrix for EMEE:

    J1(EMEE)=(b1Ih+b2IrNhc10b1ShNh00η00b2ShNhb1Ih+b2IrNhc2b1ShNh00000b2ShNh0a1c300000000a2c40000000ωνμh0000λ0000c5000000000b3IrNrμr0b3SrNr000000b3IrNrc6b3SrNr0000000a3μr).

    We can easily see two negative eigenvalues; one is ω1=μh, and another one is ω2=c4. For the rest of the equilibrium points, we consider the reduced matrix

    J2(EMEE)=(b1Ih+b2IrNhc10b1ShNhη00b2ShNhb1Ih+b2IrNhc2b1ShNh000b2ShNh0a1c30000λ00c50000000b3IrNrμr0b3SrNr0000b3IrNrc6b3SrNr00000a3μr).

    This yields the associated characteristic equation as follows:

    ω7+ϵ1ω6+ϵ2ω5+ϵ3ω4+ϵ4ω3+ϵ5ω2+ϵ6ω+ϵ7=0, (4.6)

    with ϵk denoting the coefficients of ω7k,k=1,2,3,,7 after resetting the polynomial equation in the formula form. Since the proof of the local asymptotic stable needs the negative real parts of all roots of (4.6), we use the Routh-Hurwitz criteria to obtain the conditions for the stability of EMEE. We define the following notation, h1=(ϵ1ϵ2ϵ3)/ϵ1, h2=(ϵ1ϵ4ϵ5)/ϵ1, h3=(ϵ1ϵ6ϵ7)/ϵ1, g1=(ϵ3h1ϵ1h2)/h1, g2=(ϵ5h1ϵ1h3)/h1, g3=ϵ7, d1=(h2g1h1g2)/g1, d2=(h3g1h1g3)/g1, e1=(g2d1g1d2)/d1, e2=g3, and f1=(d2e1d1e2)/e1.

    Thus, the Hurwitz assumptions concerning (4.6), which ensure that all roots have negative real parts, are as follows: (H1).(i)ϵ1>0; (ii)ϵ7>0; (iii)ϵ1ϵ2>ϵ3; (iv)ϵ1ϵ2ϵ3+ϵ1ϵ5>ϵ21ϵ4+ϵ23; (v)h2g1>h1g2; (vi)g2d1>g1d2; and (vii)d2e1>d1e2. Therefore, we can conclude this part by the following theorem:

    Theorem 4.5. Suppose that the necessary and sufficient assumption (H1) of Hurwitz criteria is satisfied, then the MPOX endemic equilibrium of the CPC-MPOX model (3.2) is locally asymptotically stable.

    In this part, an analysis of the CPC-MPOX model (3.2) will be investigated applying Banach's contraction mapping principle [54]. First, the Banach space on [0,T] for all continuous real-valued functions is given by X=C(I×R9,R) under the norm Y=(Sh,Eh,Ih,Ch,Rh,Vh,Sr,Er,Ir)=Sh+Eh+Ih+Ch+Rh+Vh+Sr+Er+Ir, where Sh, Eh, Ih, Ch, Rh, Vh, Sr, Er, IrX and Sh=supt[0,T]|Sh(t)|=Bh1, Eh=supt[0,T]|Eh(t)|=Bh2, Ih=supt[0,T]|Ih(t)|=Bh3, Ch=supt[0,T]|Ch(t)|=Bh4, Rh=supt[0,T]|Rh(t)|=Bh5, Vh=supt[0,T]|Vh(t)|=Bh6, Sr=supt[0,T]|Sr(t)|=Br1, Er=supt[0,T]|Er(t)|=Br2, and Ir=supt[0,T]|Ir(t)|=Br3. Next, assume FX and YC([0,T],R), and the CPC-MPOX model (3.2) can be presented as

    {CPCDα0,tY(t)=F(t,Y(t)),t[0,T],α(0,1],[0.1cm]Y(0)=Y0, (5.1)

    where

    Y(t)=(Sh(t)Eh(t)Ih(t)Ch(t)Rh(t)Vh(t)Sr(t)Er(t)Ir(t)),Y(0)=(Sh(0)Eh(0)Ih(0)Ch(0)Rh(0)Vh(0)Sr(0)Er(0)Ir(0))=(Sh0Eh0Ih0Ch0Rh0Vh0Sr0Er0Ir0),F(t,Y(t))=(F1(t,Sh)F2(t,Eh)F3(t,Ih)F4(t,Ch)F5(t,Rh)F6(t,Vh)F7(t,Sr)F8(t,Er)F9(t,Ir)),

    when Gi,i=1,2,,9 are given by (3.3). Then, the problem (5.1) can be written applying Definition 2.4 as below

    Y(t)e(K1(α)K0(α)t)Y(0)=1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,Y(s))ds. (5.2)

    From the problem (5.1), the Eq (5.2) can be presented in the integral form:

    Sh(t)=e(K1(α)K0(α)t)Sh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F1(s,Sh(s))ds, (5.3)
    Eh(t)=e(K1(α)K0(α)t)Eh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F2(s,Eh(s))ds, (5.4)
    Ih(t)=e(K1(α)K0(α)t)Ih0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F3(s,Ih(s))ds, (5.5)
    Ch(t)=e(K1(α)K0(α)t)Ch0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F4(s,Ch(s))ds, (5.6)
    Rh(t)=e(K1(α)K0(α)t)Rh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F5(s,Rh(s))ds, (5.7)
    Vh(t)=e(K1(α)K0(α)t)Vh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F6(s,Vh(s))ds, (5.8)
    Sr(t)=e(K1(α)K0(α)t)Sr0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F7(s,Sr(s))ds, (5.9)
    Er(t)=e(K1(α)K0(α)t)Er0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F8(s,Er(s))ds, (5.10)
    Ir(t)=e(K1(α)K0(α)t)Ir0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F9(s,Ir(s))ds. (5.11)

    Define an operator F:XX where F=(F1,F2,F3,F4,F5,F6,F7,F8,F9). In consideration of (5.3) to (5.11), we obtain

    (F1Sh)(t)=e(K1(α)K0(α)t)Sh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F1(s,Sh(s))ds,(F2Eh)(t)=e(K1(α)K0(α)t)Eh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F2(s,Eh(s))ds,(F3Ih)(t)=e(K1(α)K0(α)t)Ih0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F3(s,Ih(s))ds,(F4Ch)(t)=e(K1(α)K0(α)t)Ch0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F4(s,Ch(s))ds,(F5Rh)(t)=e(K1(α)K0(α)t)Rh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F5(s,Rh(s))ds,(F6Vh)(t)=e(K1(α)K0(α)t)Vh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F6(s,Vh(s))ds,(F7Sr)(t)=e(K1(α)K0(α)t)Sr0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F7(s,Sr(s))ds,(F8Er)(t)=e(K1(α)K0(α)t)Er0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F8(s,Er(s))ds,(F9Ir)(t)=e(K1(α)K0(α)t)Ir0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F9(s,Ir(s))ds.

    Next, the transformation of the CPC-MPOX model (3.2) to Y=FY that is a fixed point problem, will be later applied with a fixed point theory to prove that the CPC-MPOX model (3.2) has a solution.

    Theorem 5.1. Suppose that FX corresponding with the assumption (A1) is as follows:

    (A1) There is a constant Nmax=max{N1,N2,N3,N4,N5,N6,N7,N8,N9}>0, such that

    {|Fi(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t),Ir(t))Fi(t,Sh(t),Eh(t),Ih(t),Ch(t),Rh(t),Vh(t),Sr(t),Er(t)),Ir(t))|Ni(|Sh(t)Sh(t)|+|Eh(t)Eh(t)|+|Ih(t)Ih(t)|+|Ch(t)Ch(t)|+|Rh(t)Rh(t)|+|Vh(t)Vh(t)|+|Sr(t)Sr(t)|+|Er(t)Er(t)|+|Ir(t)Ir(t)|),

    where i=1,2,3,,9 and Sh, Eh, Ih, Ch, Rh, Vh, Sr, Er, IrX, and t[0,T].

    If

    K1(α)[K20(α)]1Nmax<1, (5.12)

    then the CPC-MPOX model (3.2) has a unique solution.

    Proof. Define a bounded, closed, and convex subset Dra:={(Sh,Eh,Ih,Ch,Rh,Vh,Sr,Er,Ir)X:(Sh,Eh,Ih,Ch,Rh,Vh,Sr,Er,Ir)ra} with a radius ra defined as

    raKmax+K1(α)K20(α)Fmax[1K1(α)K20(α)Nmax]1,

    where Kmax=max{Sh0, Eh0, Ih0, Ch0, Rh0, Vh0, Sr0, Er0, Ir0} and Fmax=max{F1, F2, F3, F4, F5, F6, F7, F8, F9}. Let supt[0,T]|Fi(s,0)|=Fi<+, i=1, 2, 3, , 9. The process is divided into two parts.

    Step I. We prove that FDraDra.

    For any (Sh(t), Eh(t), Ih(t), Ch(t), Rh(t), Vh(t), Sr(t), Er(t), Ir(t))Dra, t[0,T], we have

    |(F1Sh)(t)||e(K1(α)K0(α)t)Sh0|+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))×[|F1(s,Sh(s))F1(s,0)|+|F1(s,0)|]dsSh0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))[N1[|Sh(t)|+|Eh(t)|+|Ih(t)|+|Ch(t)|+|Rh(t)|+|Vh(t)+|Sr(t)|+|Er(t)|+|Ir(t)|]+F1]dsSh0+K1(α)K20(α)[N1(|Sh(t)|+|Eh(t)+|Ih(t)|+|Ch(t)||+|Rh(t)|+|Vh(t)+|Sr(t)|+|Er(t)|+|Ir(t)|)+F1]Sh0+K1(α)K20(α)[N1ra+F1].

    In the same process, we also have

    |(F2Eh)(t)|Eh0+K1(α)K20(α)[N2ra+F2],|(F3Ih)(t)|Ih0+K1(α)K20(α)[N3ra+F3],|(F4Ch)(t)|Ch0+K1(α)K20(α)[N4ra+F4],|(F5Rh)(t)|Rh0+K1(α)K20(α)[N5ra+F5],|(F6Vh)(t)|Vh0+K1(α)K20(α)[N6ra+F6],|(F7Sr)(t)|Sr0+K1(α)K20(α)[N7ra+F7],|(F8Er)(t)|Er0+K1(α)K20(α)[N8ra+F8],|(F9Ir)(t)|Ir0+K1(α)K20(α)[B9ra+F9].

    This yields that

    (FY)(t)Kmax+K1(α)K20(α)[Nmaxra+Fmax].

    Therefore, FDraDra.

    Step II. We prove that F is a contraction.

    Let (Sh, Eh, Ih, Ch, Rh, Vh, Sr, Er, Ir)Dra and (Sh, Eh, Ih, Ch, Rh, Vh, Sr, Er, Ir)Dra, for t[0,T]. We obtain that

    |(F1Sh)(t)(F1Sh)(t)|1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))|F1(s,Sh(s))F1(s,Sh(s))|ds1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))ds×N1{|Sh(t)Sh(t)|+|Eh(t)Eh(t)|+|Ih(t)Ih(t)|+|Ch(t)Ch(t)|+|Rh(t)Rh(t)|+|Vh(t)Vh(t)|+|Sr(t)Sr(t)|+|Er(t)Er(t)|+|Ir(t)Ir(t)|}.

    This yields that,

    |(F1Sh)(t)(F1Sh)(t)|K1(α)K20(α)N1Y(t)ˉY(t).

    Likewise, we obtain

    |(F2Eh)(t)(F2Eh)(t)|K1(α)K20(α)N2Y(t)ˉY(t),|(F3Ih)(t)(F3Ih)(t)|K1(α)K20(α)N3Y(t)ˉY(t),|(F4Ch)(t)(F4Ch)(t)|K1(α)K20(α)N4Y(t)ˉY(t),|(F5Rh)(t)(F5Rh)(t)|K1(α)K20(α)N5Y(t)ˉY(t),|(F6Vh)(t)(F6Vh)(t)|K1(α)K20(α)N6Y(t)ˉY(t),|(F7Sr)(t)(F7Sr)(t)|K1(α)K20(α)N7Y(t)ˉY(t),|(F8Er)(t)(F8Er)(t)|K1(α)K20(α)N8Y(t)ˉY(t),|(F9Ir)(t)(F9Ir)(t)|K1(α)K20(α)N9Y(t)ˉY(t).

    Since F=(F1,F2,F3,F4,F5,F6,F7,F8,F9) and Nmax>0, then

    F(Sh,Eh,Ih,Qh,Rh,Sr,Er,Ir)F(Sh,Eh,Ih,Qh,Rh,Sr,Er,Ir)K1(α)K20(α)NmaxY(t)ˉY(t).

    Under the assumption (5.12), we can conclude that F is a contraction. Then, we get F has a unique fixed point. Therefore, the CPC-MPOX model (3.2) has a unique solution.

    Next, we investigate some sufficient criteria of the Ulam's stability for the CPC-MPOX model (3.2). The definitions of these types and some necessary remarks are provided below.

    Assume that κFY>0 is a constant and PFYC([0,T],R+). The inequalities are given:

    |CPCDα0,tY(t)F(t,Y(t))|κFY, (5.13)
    |CPCDα0,tY(t)F(t,Y(t))|κFYPFY(t), (5.14)
    |CPCDα0,tY(t)F(t,Y(t))|PFY(t), (5.15)

    where t[0,T] and κFY=max(κFYj)T, for j=1,2,,9.

    Definition 5.2. The CPC-MPOX model (3.2) is called UH stable if there exists a constant ΦFY>0 such that for every κFY>0 and each solution ZYX of (5.13), there exist a solution YX of (3.2) with

    |ZY(t)Y(t)|ΦFYκFY, (5.16)

    where t[0,T] and ΦFY=max(ΦFYi)T, i=1,2,,9.

    Definition 5.3. The CPC-MPOX model (3.2) is called generalized UH stable if there exists a function PFYC([0,T],R+), with PFY(0)=0 so that for κFY>0 and for each solution ZYX of (5.14), there exist a solution YX of (3.2) with

    |ZY(t)Y(t)|PFY(κFY), (5.17)

    where t[0,T], and PFY=max(PFY)T,i=1,2,,9.

    Definition 5.4. The CPC-MPOX model (3.2) is called UHR stable with respect to PFYC([0,T],R+) if there exists a number ΩFY>0 so that for every κFY>0 and for each solution ZYX of (5.15), there exists a solution YX of (3.2) with

    |ZY(t)Y(t)|ΩFYκFYPFY(t), (5.18)

    where t[0,T],ΩFY=max(ΩFYi)T, and PFY=max(PFYi)T,i=1,2,,9.

    Definition 5.5. The CPC-MPOX model (3.2) is called generalized UHR stable with respect to PFYC([0,T],R+) if there exists a number ΩFY>0 so that for each solution ZYX of (5.15), there exists a solution YX of (3.2) with

    |ZY(t)Y(t)|ΩFYPFY(t), (5.19)

    where t[0,T],ΩFY=max(ΩFYi)T, and PFY=max(PFYi)T, i=1,2,,9.

    Remark 5.6. ZYX is the solution of (5.13), if and only if, there is χY(0)=0 satisfied |χY(t)|κGY, χY=max(χYi)T,i=1,2,,9,κFY>0, and CPCDα0,tY(t)=F(t,Y(t))+χY(t).

    Remark 5.7. ZYX is the solution of (5.14), if and only if, there is ψYX satisfied |ψY(t)|κFYPFY(t),ψY=max(ψYi)T,PFY=max(PFYi)T, i=1,2,,9, and CPCDα0,tY(t)=F(t,Y(t))+ψY(t).

    Lemma 5.8. Assume that ZYX is a solution of (5.13), then

    |ZY(t)ZY01K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds|κFYK1(α)(K0(α))2. (5.20)

    Proof. Let ZY be the solution of (5.13). From Remark (5.6), we have

    {CPCDα0,tZ(t)=F(t,Z(t))+χY(t),ZY(0)=ZY00. (5.21)

    Thus, the solution to (5.21) is provided below:

    ZY(t)=ZY0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))χY(s)ds.

    Therefore,

    |ZY(t)ZY01K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds|1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))χY(s)dsK1(α)(K0(α))2κFY.

    The proof is completed.

    Theorem 5.9. Assume the conditions in Theorem 5.1 and Lemma 5.8 are satisfied, then the CPC-MPOX model (3.2) is UH stable.

    Proof. Assume that κFYR+ and ZY is a solution of (5.13). Let YX be a unique solution of (3.2), then

    |ZY(t)Y(t)||ZY(t)ZY01K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds|+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))|F(s,ZY(s))F(s,Y(t))|dsK1(α)(K0(α))2(κFY+Nmax|ZY(t)Y(t)|).

    Setting

    ΦFY:=K1(α)(K0(α))2(1K1(α)(K0(α))2Nmax)1,

    this yields that |ZY(t)Y(t)|ΦFYκFY. Hence, by Definition 5.2, the CPC-MPOX model (3.2) is UH stable.

    Corollary 5.10. Setting PFY(κFY)=ΦFYκFY with PFY(0)=0 in Theorem 5.9, by Definition 5.3, the CPC-MPOX model (3.2) is UH stable.

    The following conditions are necessary to prove the UHR and generalized UHR stability.

    (D1) There is an increasing function PFYC([0,T],R+) and a number λFY>0, so that

    CPCIα0PFY(t)λFYPFY(t).

    Lemma 5.11. Let ZYX be the solution of (5.15), then

    |ZY(t)ZY01K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds|κFYλFYPFY(t). (5.22)

    Proof. Let ZYX be a solution of (5.15). Applying Remark 5.7, we obtain

    {CPCDα0,tZ(t)=F(t,Z(t))+ψY(t),ZY(0)=ZY00. (5.23)

    Hence, a solution of (5.23) is provided below:

    ZY(t)=ZY0+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))ψY(s)ds.

    Since,

    |ZY(t)ZY01K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds|1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))|ψY(s)|dsκFYλFYPFY(t),

    then, the inequality (5.22) is achieved.

    Theorem 5.12. Assume the conditions in Theorem 5.1 and Lemma 5.11 are satisfied, then the CPC-MPOX model (3.2) is UHR stable.

    Proof. Let κFYR+ and ZY be the solution of (5.15). Suppose that YX is a unique solution of the CPC-MPOX model (3.2), then

    |ZY(t)Y(t)||ZY(t)ZY01K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))F(s,ZY(s))ds|+1K0(α)t0(ts)α1E1,α(K1(α)K0(α)(ts))|F(s,ZY(s))F(s,Y(t))|dsκFYλFYPFY(t)+K1(α)(K0(α))2Nmax|ZY(t)Y(t)|.

    Setting

    ΦGY:=λGY(1K1(α)(K0(α))2Mmax)1,

    this yields that |ZY(t)Y(t)|ΦFYκFYPFY(t). Hence, by Definition 5.4, the CPC-MPOX model (3.2) is UHR stable.

    Corollary 5.13. Setting κGY=1 in Theorem 5.12, by Definition 5.5, the CPC-MPOX model (3.2) is UHR stable.

    This section derives the numerical schemes for solving the approximated solution of the CPC-MPOX model (3.2) by utilizing the decomposition technique for the CPC derivative operator. Next, we create an approximation design for the CPC derivative operator via α(0,1] of a function f(t). We will make a sequence of N+1 equations under N+1 conditions for the fractional Cauchy problem in the context of CPC derivative operator [47]. A sequence (fN) of the solutions to such systems eventually leads to the solution of the obtained problem.

    Theorem 6.1. Assume that N is a positive number and fAC2([0,T],R). Let

    AN=Ni=0Γ(i+α1)i!Γ(2α)Γ(α1),BN,i=Γ(i+α1)(i1)!Γ(2α)Γ(α1), (6.1)

    Vi:[0,T]R be functions defined by

    Vi(t)=t0si1[Qα(1α)f(s)+αQ1αC2αf(s)]ds. (6.2)

    Then,

    CPCDα0,tf(t)=ANtα1[Qα(1α)f(t)+αQ1αC2αf(t)]Ni=1t1αiBN,iVi(t)+Etr(t), (6.3)

    where limNEtr(t)=0 for t[0,T].

    Proof. Using Definition 2.3 and K1(α)=Qα(1α), K0(α)=αQ1αC2α, α(0,1], we have

    CPCDα0,tf(t)=1Γ(1α)t0[Qα(1α)f(s)+αQ1αC2αf(s)](ts)αds.

    Let u=Qα(1α)f(s)+αQ1αC2αf(s) and dv=(ts)αds. Using the integrating by part technique, yields that

    CPCDα0,tf(t)=t1αΓ(2α)[Qα(1α)f(0)+αQ1αC2αf(0)]+1Γ(2α)t0(ts)α+1dds[Qα(1α)f(s)+αQ1αC2αf(s)]ds. (6.4)

    Applying the generalized binomial theorem, it follows that

    (ts)1α=(ta)1α(1sata)1α=(ta)1αi=0Γ(i+α1)Γ(α1)i!(sata)i. (6.5)

    Plugging (6.5) into (6.4), it follows that

    CPCDα0,tf(t)=Etr(t)+t1αΓ(2α)[Qα(1α)f(0)+αQ1αC2αf(0)]+1Γ(2α)t0t1αNi=0Γ(i+α1)Γ(α1)i!(st)idds[Qα(1α)f(s)+αQ1αC2αf(s)]ds,

    where

    Etr(t)=1Γ(2α)t0t1αRN(s)dds[Qα(1α)f(s)+αQ1αC2αf(s)]ds,RN(s)=i=N+1Γ(i+α1)i!Γ(α1)(st)i. (6.6)

    Hence, by direct calculation, we get

    CPCDα0,tf(t)=Etr(t)+t1αΓ(2α)[Qα(1α)f(0)+αQ1αC2αf(0)]+t1αΓ(2α)Ni=0Γ(i+α1)Γ(α1)i!tit0sidds[Qα(1α)f(s)+αQ1αC2αf(s)]ds=Etr(t)+t1αΓ(2α)[Qα(1α)f(0)+αQ1αC2αf(0)]+t1αΓ(2α)t0dds[Qα(1α)f(s)+αQ1αC2αf(s)]ds+t1αΓ(2α)Ni=1Γ(i+α1)Γ(α1)i!tit0sidds[Qα(1α)f(s)+αQ1αC2αf(s)]ds=Etr(t)+t1αΓ(2α)[Qα(1α)f(t)+αQ1αC2αf(t)]+t1αΓ(2α)Ni=1Γ(i+α1)Γ(α1)i!tit0sidds[Qα(1α)f(s)+αQ1αC2αf(s)]ds.

    Let u=si and dv=dds[Qα(1α)f(s)+αQ1αC2αf(s)]ds. Using the integrating by part technique, it follows that

    CPCDα0,tf(t)=Etr(t)+t1αΓ(2α)[Qα(1α)f(t)+αQ1αC2αf(t)]+t1αΓ(2α)Ni=1Γ(i+α1)tiΓ(α1)i!ti[Qα(1α)f(t)+αQ1αC2αf(t)]t1αΓ(2α)Ni=1Γ(i+α1)Γ(α1)i!tit0isi1[Qα(1α)f(s)+αQ1αC2αf(s)]ds=Etr(t)+t1αΓ(2α)Ni=0Γ(i+α1)Γ(α1)i![Qα(1α)f(t)+αQ1αC2αf(t)]t1αΓ(2α)Ni=1Γ(i+α1)Γ(α1)i!tit0isi1[Qα(1α)f(s)+αQ1αC2αf(s)]ds.

    Now, we show that Etr(t)0 as N for t[0,T], and to show this, we give an upper bound for the error term. Since Γ(x+α)Γ(x)xα and s/t<1,

    |RN(s)|=i=N+1Γ(i+α1)i!(st)ii=N+1Γ(i+α1)i!i=N+1iα2Nsα2ds.

    Then,

    |RN(s)|1N1α(1α). (6.7)

    Substituting (6.7) into (6.6) with M(t)=maxs[0,T]|dds[Qα(1α)f(s)+αQ1αC2αf(s)]| implies the following upper bound:

    |Etr(t)|t2αM(t)N1α(1α)Γ(2α). (6.8)

    The righthand side of (6.8) tends to zero for all t(0,T) as N.

    To obtain the numerical approximation of the CPC-MPOX model (3.2), we apply Theorem 6.1. Then,

    CPCDα0,tSh(t)=ANtα1[Qα(1α)Sh(t)+αQ1αC2αSh(t)]Ni=1t1αiBN,iVShi(t),CPCDα0,tEh(t)=ANtα1[Qα(1α)Eh(t)+αQ1αC2αEh(t)]Ni=1t1αiBN,iVEhi(t),CPCDα0,tIh(t)=ANtα1[Qα(1α)Ih(t)+αQ1αC2αIh(t)]Ni=1t1αiBN,iVIhi(t),CPCDα0,tCh(t)=ANtα1[Qα(1α)Ch(t)+αQ1αC2αCh(t)]Ni=1t1αiBN,iVChi(t),CPCDα0,tRh(t)=ANtα1[Qα(1α)Rh(t)+αQ1αC2αRh(t)]Ni=1t1αiBN,iVRhi(t),CPCDα0,tVh(t)=ANtα1[Qα(1α)Vh(t)+αQ1αC2αVh(t)]Ni=1t1αiBN,iVVhi(t),CPCDα0,tSr(t)=ANtα1[Qα(1α)Sr(t)+αQ1αC2αSr(t)]Ni=1t1αiBN,iVSri(t),CPCDα0,tEr(t)=ANtα1[Qα(1α)Er(t)+αQ1αC2αEr(t)]Ni=1t1αiBN,iVEri(t),CPCDα0,tIr(t)=ANtα1[Qα(1α)Ir(t)+αQ1αC2αIr(t)]Ni=1t1αiBN,iVIri(t),

    and

    VShi(t)=t0si1[Qα(1α)Sh(s)+αQ1αC2αSh(s)]ds,VEhi(t)=t0si1[Qα(1α)Eh(s)+αQ1αC2αEh(s)]ds,VIhi(t)=t0si1[Qα(1α)Ih(s)+αQ1αC2αIh(s)]ds,VChi(t)=t0si1[Qα(1α)Ch(s)+αQ1αC2αCh(s)]ds,VRhi(t)=t0si1[Qα(1α)Rh(s)+αQ1αC2αRh(s)]ds,VVhi(t)=t0si1[Qα(1α)Vh(s)+αQ1αC2αVh(s)]ds,VSri(t)=t0si1[Qα(1α)Sr(s)+αQ1αC2αSr(s)]ds,VEri(t)=t0si1[Qα(1α)Er(s)+αQ1αC2αEr(s)]ds,VIri(t)=t0si1[Qα(1α)Ir(s)+αQ1αC2αIr(s)]ds,

    where AN and BN,i are given by (6.1) under the conditions

    VShi(t)=ti1[Qα(1α)Sh(t)+αQ1αC2αSh(t)],VShi(0)=0,i=1,,N,VEhi(t)=ti1[Qα(1α)Eh(t)+αQ1αC2αEh(t)],VEhi(0)=0,i=1,,N,VIhi(t)=ti1[Qα(1α)Ih(t)+αQ1αC2αIh(t)],VIhi(0)=0,i=1,,N,VChi(t)=ti1[Qα(1α)Ch(t)+αQ1αC2αCh(t)],VChi(0)=0,i=1,,N,VRhi(t)=ti1[Qα(1α)Rh(t)+αQ1αC2αRh(t)],VRhi(0)=0,i=1,,N,VVhi(t)=ti1[Qα(1α)Vh(t)+αQ1αC2αVh(t)],VVhi(0)=0,i=1,,N,VSri(t)=ti1[Qα(1α)Sr(t)+αQ1αC2αSr(t)],VSri(0)=0,i=1,,N,VEri(t)=ti1[Qα(1α)Er(t)+αQ1αC2αEr(t)],VEri(0)=0,i=1,,N,VIri(t)=ti1[Qα(1α)Ir(t)+αQ1αC2αIr(t)],VIri(0)=0,i=1,,N.

    This section uses the numerical algorithm from the previous section to obtain the numerical solutions of the CPC-MPOX model (3.2). The values of the basic parameters are listed as in Table 2 with the initial condition: Sh(0)=3.4×108, Eh(0)=1000, Ih(0)=100, Ch(0)=100, Rh(0)=1×106, Vh(0)=1×106, Sr(0)=9×104, Er(0)=100, and Ir(0)=100. From the given data, we obtain R0=1.5379×104>1,ϵ1=1.42043,ϵ2=0.69421,ϵ3=0.13750,ϵ4=0.01003,ϵ5=0.00018,ϵ6=9.32369×109,ϵ7=1.03004×1013,h1=0.59741,h2=0.00990,h3=9.32362×109,g1=0.11395,g2=0.00018,g3=1.03004×1013,d1=0.00896,d2=9.32308×109,e1=0.00018,e2=1.03004×1013,f1=9.31797×109. Consequently, these calculated values satisfy the conditions (i)–(vii) in Theorem 4.5. Thus, the endemic equilibrium point is locally asymptotically stable.

    Table 2.  The values of parameter used for the simulations of the CPC-MPOX model (3.2).
    Parameter Value in days Source Parameter Value in days Source
    Λh 11731.91 [55] ω 0.4670 [40]
    Λr 0.016 [9] ν 0.0843 [40]
    b1 0.5701 [40] μh 1/(79×365) [55]
    b2 0.2508 [40] μr 0.000016 [9]
    b3 0.2461 [40] λ 0.2393 [40]
    a1 0.0486 [40] η 0.201 [40]
    a2 0.1119 [40] δ1 0.0011 [40]
    a3 0.1053 [40] δ2 0.00010091 [40]

     | Show Table
    DownLoad: CSV

    Here, Figure 2 shows the numerical solutions for the classical MPOX model (3.1) of each group of human and rodent populations, while Figure 3 expresses the numerical solutions utilizing the CPC fractional operator for the CPC-MPOX model (3.2) with varies α=0.995, 0.985, 0.975, 0.965, 0.955. As shown in both of the mentioned figures, the findings demonstrate that the fractional order model follows the same trend as the traditional model but is more flexible and has a higher degree of freedom. At larger fractional orders, increasing and decreasing behavior converges to the classical model more quickly than small fractional orders. Furthermore, from Figure 3 observation, a slight adjustment in the fractional order α was found to cause only a minor change in the behavior. This indicates that variations in the fractional order have a negligible impact on the stability of the disease dynamics across different groups within the proposed model. In addition, the simulation takes place over a 500-day period. Under certain conditions, solution trajectories in all population groups reach the steady-state for all various values of α as time passes. Figure 2a and Figure 3a indicate the behavior of the susceptible humans. It is observed that the amount of them decreases rapidly in a short time in the beginning and tends to a steady-state as time tends to infinity. Figure 2b, Figure 3b, Figure 2c, Figure 3c, Figure 2d, Figure 3d, Figure 2i, and Figure 3i indicate the behavior of the exposed, infectious, clinically ill humans, and the infected rodents, respectively. We can see that the populations of each group are quite similar in order to gradually increase before reaching a steady state as time passes. Figure 2e and Figure 3e indicate the behavior of the recovered humans, and we extended the period to 5000 days for trend clearly observation. We found that the behavior of this group is increasing and tends to the steady state in the end. The behavior of the vaccinated humans is shown in Figure 2f and Figure 3f, demonstrating rapid population growth in a very short time and then reaching the equilibrium point. The behavior of the susceptible rodents drops initially before tending to a steady state, as seen in Figure 2g and Figure 3g. While Figure 2h and Figure 3h indicate the behavior of the exposed rodents, the population climbs to a peak and then falls until reaching a stable state.

    Figure 2.  Simulations of Sh(t), Eh(t), Ih(t), Ch(t), Rh(t), Vh(t), Sr(t), Er(t), and Ir(t) of the CPC-MPOX model (3.2).
    Figure 3.  Simulations of Sh(t), Eh(t), Ih(t), Ch(t), Rh(t), Vh(t), Sr(t), Er(t), and Ir(t) of the CPC-MPX model (3.2) when α{0.995,0.985,0.975,0.965,0.955}.

    Additionally, we place greater emphasis on examining the influence of the immunity-induced recovery rate ω on the dynamics of three human compartments regarding the MPOX infection, which are exposed, infectious, and clinically ill individuals. The parameter representing the recovery rate is varied with the following values: 0.4670 (baseline from Table 2), 0.5137 (10% increase), 0.5604 (20% increase), 0.6538 (40% increase), and 0.8406 (80% increase) under vary α=1, 0.9 and 0.8 as seen in Figures 46, respectively. These graphs present two significant observations. First, an increase in ω levels corresponds to a clear reduction in the amount of infected individuals across all groups. Second, lower α values lead to a slightly faster decline in the amount of infected humans.

    Figure 4.  Impact of recovery rate ω when α=1.00.
    Figure 5.  Effect of recovery rate ω when α=0.90.
    Figure 6.  Effect of recovery rate ω when α=0.80.

    Similarly, investigating the impact of the contact rates between infected individuals or infected rodents on exposed, infected, and clinically ill humans is also highly significant. In this context, the parameter value for the contact rate of infected individuals with the susceptible population is utilized as follows: 0.5701 (baseline from Table 2), 0.62711 (10% increase), 0.68412 (20% increase), 0.79814 (40% increase), and 0.91216 (60% increase). The contact rate of infected rodents with the susceptible population is utilized as follows: 0.2508 (baseline from Table 2), 0.27588 (10% increase), 0.30096 (20% increase), 0.35112 (40% increase), and 0.40128 (60% increase). Figures 79 demonstrate the impact of varying contact rate parameters b1 and b2 under different values of α: 1, 0.9, and 0.8, respectively. The graphs indicate that the contact rate substantially influences the population sizes of the respective groups. An increase in the contact rate leads to a corresponding increase in the amount of individuals in the groups mentioned. Besides, a reduction in the value of α leads to a slightly faster decline in the population sizes of all groups.

    Figure 7.  Effect of infected contact rates b1 and b2 when α=1.00.
    Figure 8.  Effect of infected contact rates b1 and b2 when α=0.9.
    Figure 9.  Effect of infected contact rates b1 and b2 when α=0.8.

    Therefore, based on all of the simulations above in various scenarios, we found a key finding that the fractional order or the memory index, the immunity-induced recovery rate, and the contact rates between infected individuals or infected rodents are factors that play an important role in determining whether monkeypox infection levels increase or decrease in the human population. These parameters can serve as control measures for monkeypox transmission.

    This study presented a CPC fractional derivative model for the spread of the monkeypox virus, accounting for interactions between humans and rodents. The model was developed to analyze system behavior and identify parameters that can help control the disease. For the theoretical part, we proved the positiveness and boundedness of solutions and examined the equilibrium points and the basic reproduction number. We investigated the local asymptotically stable steady state. We verified the qualitative results of the suggested model, including the existence and uniqueness results, using the Banach contraction mapping principle. Various Ulam's stability was demonstrated to ensure the existing solutions. The exactness of the theoretical guarantee is confirmed via the numerical simulations in all diagrams utilizing a decomposition formula for a constant proportional Caputo derivative. For the numerical and graphical parts, the graphical results highlight the key advantage of our proposed CPC-MPOX model. It proves to be more realistic and practical than the traditional model, and its flexibility enhances precision, enabling us to achieve superior outcomes compared to the classical approach. Using the value of the parameters in Table 2, it was shown by numeric calculation that R0>1 and all conditions of Routh-Hurwitz criteria are satisfied. Hence, we concluded that the endemic equilibrium point is locally asymptotically stable, which supports Theorem 4.5. Furthermore, the suggested model is shown by rising the value parameters of the recovery rate due to immunity and the contact rates of susceptible humans with infected humans and infected rodents at various levels and different fractional orders to analyze the effect in population dynamics influenced by the spread of MPOX via graphical simulation. The study demonstrated that the factors in our case can be incorporated into the control mechanisms of monkeypox transmission. These findings may offer valuable insights into the prevention and control of MPOX outbreaks in the future.

    For future work, applying the CPC derivatives operator to study and analyze other epidemic models in real-world situations can be a proper alternative technique. On the other hand, other fractional operators, such as piece-wise and stochastic operators, can be considered for MPOX virus transmission to investigate real-world situations more realistically.

    Jutarat Kongson: Conceptualization, Methodology, Writing-original draft, Writing-review & editing, Formal analysis, Funding acquisition; Chatthai Thaiprayoon: Conceptualization, Methodology, Writing–original draft, Writing–review & editing, Software, Supervision; Weerawat Sudsutad: Conceptualization, Methodology, Writing-original draft, Writing-review & editing, Formal analysis. All authors have read and agreed to the published version of the manuscript.

    The authors declare they have not used Artificial Intelligence (AI) tools in creating this article.

    J. Kongson (jutarat_@go.buu.ac.th) and C. Thaiprayoon (chatthai@go.buu.ac.th) would like to thank Burapha University for providing bench space and support.

    This work was financially supported by (i) Burapha University (BUU), (ii) Thailand Science Research and Innovation (TSRI), and (iii) National Science Research and Innovation Fund (NSRF) (Fundamental Fund: Grant no. 75/2567).

    The authors declare no conflict of interest.



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