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Prespecified-time bipartite synchronization of coupled reaction-diffusion memristive neural networks with competitive interactions


  • In this paper, we investigate the prespecified-time bipartite synchronization (PTBS) of coupled reaction-diffusion memristive neural networks (CRDMNNs) with both competitive and cooperative interactions. Two types of bipartite synchronization are considered: leaderless PTBS and leader-following PTBS. With the help of a structural balance condition, the criteria for PTBS for CRDMNNs are derived by designing suitable Lyapunov functionals and novel control protocols. Different from the traditional finite-time or fixed-time synchronization, the settling time obtained in this paper is independent of control gains and initial values, which can be pre-set according to the task requirements. Lastly, numerical simulations are given to verify the obtained results.

    Citation: Ruoyu Wei, Jinde Cao. Prespecified-time bipartite synchronization of coupled reaction-diffusion memristive neural networks with competitive interactions[J]. Mathematical Biosciences and Engineering, 2022, 19(12): 12814-12832. doi: 10.3934/mbe.2022598

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  • In this paper, we investigate the prespecified-time bipartite synchronization (PTBS) of coupled reaction-diffusion memristive neural networks (CRDMNNs) with both competitive and cooperative interactions. Two types of bipartite synchronization are considered: leaderless PTBS and leader-following PTBS. With the help of a structural balance condition, the criteria for PTBS for CRDMNNs are derived by designing suitable Lyapunov functionals and novel control protocols. Different from the traditional finite-time or fixed-time synchronization, the settling time obtained in this paper is independent of control gains and initial values, which can be pre-set according to the task requirements. Lastly, numerical simulations are given to verify the obtained results.



    The coronavirus family comprises a diverse range of viruses that can be found in different animal species, including cats, camels, bats, and cattle. In rare cases, animal coronaviruses can infect humans and spread among them, as has been seen with SARS, MERS, and the current COVID-19 pandemic [1,2]. Since it first emerged in Saudi Arabia in 2012, the Middle East respiratory syndrome (MERS-CoV) has claimed the lives of 1791 individuals, according to various sources [3,4]. Meanwhile, the 2003 outbreak of severe acute respiratory syndrome (SARS) resulted in the deaths of 774 individuals [5].

    Camels have been identified as the primary carriers of the MERS-CoV virus according to scientific research. Human-to-human transmission is the leading cause of MERS-CoV cases, responsible for 75 to 88 percent of all cases, while the remaining cases are caused by transmission from camels to humans. It is important to note that the virus can spread through respiratory discharge from infected individuals, such as coughing. In addition, close contact, including caring for or living with an infected person, can also result in the transmission of the virus. Since the discovery of MERS-CoV in April 2012, there have been a total of 536 reported cases, with 145 resulting in death. This gives a case fatality rate of 27 percent. The majority of cases have been recorded in the Middle East, specifically in countries such as Saudi Arabia, Jordan, and Qatar, as noted in [6]. It is crucial to maintain awareness of this disease and take appropriate precautions, particularly in areas where the virus has been reported, in order to prevent its spread.

    The transmission of MERS-CoV between camels and humans is influenced by various environmental factors. The Hajj and Umrah pilgrimages are significant contributors to the spread of the virus, as these events attract more than 10 million individuals from different parts of the world to Saudi Arabia. Mathematical modeling has proven to be a valuable tool for understanding the outbreak, developing effective control strategies, and exploring the immune response to MERS-CoV. Several modeling studies have been conducted to investigate the MERS-CoV outbreak, as highlighted in [7,8,9]. One of the most extensive MERS-CoV epidemics was documented by Assire et al. in [10], who provided evidence suggesting that the virus can be transmitted from person to person. The Kingdom of Saudi Arabia (KSA) has reported the highest number of cases, with most of the cases being recorded there. It is imperative to take appropriate measures to mitigate the spread of the virus, especially in areas that have reported cases, in order to prevent further outbreaks. The consumption of unpasteurized camel milk, which is a common practice in KSA, is a potential cause of camel-to-human transmission of MERS-CoV, as suggested by [11]. Furthermore, Poletto et al. have proposed that the movement and mingling of individuals during the Hajj and Umrah events may play a significant role in the spread of MERS-CoV, as noted in [12]. Other activities, such as camel racing and the opening and closing of camel markets, have also been identified as potential contributors to the transmission of MERS-CoV. Several researchers have constructed mathematical models to study various diseases and real-world problems, including MERS-CoV, as mentioned in [13,14,15,16]. These models have proven to be useful in predicting the spread of the virus, designing effective control strategies, and exploring the immune response to MERS-CoV. It is important to continue this research in order to better understand the disease and limit its impact on public health.

    This study utilizes the next-generation matrix (NGM) approach to model the transmission and spread of MERS-CoV between humans and camels. The researchers calculate the fundamental reproductive number and determine the local stability of the model using the Routh-Hurwitz (RH) criterion. Furthermore, the global stability of the model is assessed through the Castillo-Chavez and Lyapunov type function methods, and the stability conditions are determined in terms of R0. The parameters that impact the transmission of the disease are analyzed through sensitivity analysis of the fundamental reproductive numbers. On the other hand, there have been numerous effective studies have been conducted related to the modelling of infectious diseases [17,18,19], their stability analyses [20,21,22], bifurcation and chaos properties [23,24,25,26,27,28,29,30].

    In addition, the study employs an optimal control analysis to minimize the number of infected individuals and increase the number of cured individuals in the community. By identifying the factors that contribute to the spread of MERS-CoV, this research can inform effective control strategies and minimize the impact of the disease on public health.

    In this section, we introduce a transmission model for MERS-CoV that accounts for transmission between people-camel and human-human. The model is formulated using a set of differential equations that describe the dynamics of six distinct population groups. These groups include the susceptible population (S(t)), the exposed population (E(t)), the symptomatic and infectious population (I(t)), the asymptomatic but infectious population (A(t)), the hospitalized population (H(t)), and the recovered population (R(t)). To simplify the modeling process, we make the following four assumptions.

    a. All the parameters and variables are non-negative.

    b. Four transmission routes are considered for the disease transmission, which is from individuals symptomatic to asymptomatic, from which to hospitalize, and then reservoir, which are camels for MERS-CoV.

    c. The rate of death because of MERS-CoV is considered in the compartment that contains the infection.

    d. We suppose two types of recoveries, the first one is natural and the second one is with treatment.

    Utilizing the above-considered assumptions, we obtain the non-linear system of ODEs as,

    ˙S(t)=ϕη1I(t)S(t)η2ϕA(t)S(t)η3qH(t)S(t)η4C(t)S(t)ϖ0S(t),˙E(t)=η1I(t)S(t)+η2ϕA(t)S(t)+η3qH(t)S(t)+η4C(t)S(t)(ξ+ϖ0)E(t),˙I(t)=ξρE(σ1+σ2)II(t)(ϖ0+ϖ1),˙A(t)=(1ρ)ξE(t)(ν+ϖ0)A(t),˙H(t)=σ1I(t)+νA(t)(σ3+ϖ0)H(t),˙R(t)=σ2I(t)+σ3H(t)ϖ0R(t),˙C(t)=ψ1I(t)+ψ2A(t)θC(t), (2.1)

    with the initial conditions

    Ics={S(0),I(0),E(0),H(0),A(0),C(0),R(0)}0. (2.2)
    Table 1.  The description of control parameters in the considered model (2.1).
    Parameter Description
    ϕ New born ratio
    η1,η2,η3,η4 Transmission rates
    ξ Progression towards Infected I(t)
    σ1 Hospitalization rate (symtomatic)
    σ2 Recovery rate (without hospitalization)
    σ3 Recovery rate (hospitalized)
    θ Lifetime (Camels)
    ψ1 Virus transmission rate from C(t) (by symptomatic)
    ψ2 Virus transmission rate from C(t) (by asymptomatic)
    ν The rate at which asymptomatic individuals become hospitalized
    ϖ0 The natural death rate
    ϖ1 The death rate due to MERS-CoV
    ρ The rate at which exposed individuals become infected

     | Show Table
    DownLoad: CSV

    Consider, Np(t) which represents the total population of humans in such a manner that Np(t)=E(t)+A(t)+S(t)+I(t)+R(t)+H(t), then Np(t) is bounded with lower bound to be 0 and the upper-bound ϕϖ0, i.e., 0Np(t)ϕϖ0.

    Using this fact, we present the following theorem:

    Theorem 1. If Np(t) represents the number of human and 0Np(t)ϕϖ0 and Np(t)ϕϖ0, then suggested model (2.1) is well defined in the region as follows:

    ψh={(S,I,E,H,A,R,CR7+,whereNp(t)ϕϖ0,C(ψ1+ψ2)ϕϖ0}.

    Let us adopt B as Banach space, and positive u=t+, so

    B=ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u), (3.1)

    where the norm on the space B is supposed to be as Π=7i=1Πj=(Π1,Π2,Π3,Π4,Π5,Π6,Π7)B.

    Further, B+ represents cone(+ive) of ϖ1(0,u), so from Eq (3.1), B+ is given as

    B=ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u)×ϖ1(0,u).

    Hence the state space of system (2.1) yields:

    Δ={S,I,E,H,A,C,RB+0Np(t)ϕϖ0,0<S(t)+H(t)+A(t)+R(t)+I(t)ϕϖ0,C(ψ1+ψ2)ϕϖ0}.

    We suppose an operator which is linear as L and vector ψ=(S,I,A,E,H,C,R), implies that Lψ=(Li)T, here i=1,2,,7 where

    L1=(dSdtϖ0S,0,0,0,0,0,0),L2=(0,dEdt(ξ+ϖ0),0,0,0,0,0),L3=(0,ξρ,dIdt(σ1+σ2+ϖ0+ϖ1),0,0,0,0),L4=(0,ξ(1ρ),dAdt(ν+ϖ0)A,0,0,0,0),L5=(0,0,σ1,ν,dHdt(σ3+ϖ0)H,0,0),L6=(0,0,σ2,0,σ3,dRdtϖ0R,0),L7=(0,0,ψ1,ψ2,0,0,dCdtθ),

    and domain D(L) is

    D(L)={ϕB:ψLC[0,u), ϕ(0)=Ics}. Here, LC[0,u) represent the set containing continuous functions which is defined on the [0,u). Consider O is the nonlinear operator, that is O:BB defined as,

    O(ψ)=(ϕη1ISη2ϕASη3qHSη4CSη1IS+η2ϕAS+η3qHS+η4CS00000). (3.2)

    Suppose V(t)=(S(t),I(t),H(t),E(t),A(t),R(t),C(t)) then the suggested system can be written as

    dvdt=L(V(t))+O(V(t)),V(0)B,

    where V0=(Ics)T. Utilizing the results in [31,32], we present the existence of the system's (3.2) solution, so we define following theorem:

    Theorem 2. For each V0B+, there arises an interval (maximal) [0,t0), and unique continuous solution V(t,V0), in such a way that,

    V(t)=V(0)eLt+eL(tr)O(V(σ)).

    Theorem 3. The suggested system (2.1) is invariant (positively) subjected to the non-negative R7+.

    Proof. Consider ψ and h1=(ξ+ϖ0), h2=(σ1+σ2+ϖ0+ϖ1), h3=(ν+ϖ0), h4=(σ1+ν), h5=(θϖ0),

    dϕdt=Lϕ+D.L=[ϖ0000000h100000ξρh20000ξ(1ρ)0h30000σ2νh4000ψ1ψ20h5], D=[ϕ00000]. (3.3)

    It could be noted from Eq (3.3), matrix D is positive, while the off-diagonal of L are non-negative, so the properties of Metzler type matrix holds. Thus the suggested system is invariant in R7.

    Theorem 4. We assume a positive initial population value for the problem specified in Eq (2.2) and, if the solutions to the model in Eq (2.1) exist, they will be positive for all u.

    Proof. Let us consider the first equation

    dSdt=ϕη1I(t)S(t)η2ϕA(t)S(t)η3qH(t)S(t)η4C(t)S(t)ϖ0S(t). (3.4)

    By constant formula of alternation, we obtain the solution (3.4),

    S(t)=S(0)exp[dt(η1I(t)S(t)η2ϕA(t)S(t)η3qH(t)S(t)η4C(t)S(t))]dx+ϕexp[dt(η1I(t)S(t)η2ϕA(t)S(t)η3qH(t)S(t)η4C(t)S(t))]dx×[dt+(η1I(t)S(t)+η2ϕA(t)S(t)+η3qH(t)S(t)+η4C(t)S(t))]dx.

    S(t)>0, in the same pattern one can present that, the remaining equations in (2.1) are positive.

    The main focus of our study is to examine the mathematical and biological plausibility of the system described in Eq (2.1). To achieve this, we carry out a qualitative analysis of the system dynamics. Initially, we compute the threshold parameter R0, which is commonly referred to as the basic reproduction number. This metric allows us to evaluate the inherent capacity of the disease to spread, and determine whether or not an epidemic will persist or eventually fade out. Additionally, we investigate the equilibria of the system and discuss the factors that lead to system stability.

    In this study, we have performed a qualitative analysis of the suggested system in order to identify the conditions under which it remains stable. To achieve this, we have calculated the equilibria of the mathematical model described in Eq (2.1).

    One of the most important equilibrium points for this system is the disease-free equilibrium (DFE), which represents the state of the system when no disease is present. In order to determine the DFE point for the system, we equate the right-hand side of the equations to zero, with the exception of the susceptible class S, which we set to its initial value S0. By doing so, we are able to obtain the DFE point, which we denote as D0. This point represents an important baseline for the system, against which we can compare the behavior of the system in the presence of disease.

    Overall, our qualitative analysis of the suggested system has allowed us to gain a deeper understanding of its behavior under various conditions, including the DFE point which is a key reference point for the system.

    D0=(ϕϖ0,0).

    We utilize linear stability to study the dynamics of the DFE point and calculate the condition if the equilibrium point turns towards stability and the model becomes under control.

    The endemic equilibrium (EE) point is expressed by D1=(S,E,I,A,H,R,C), and it occurs in the presence of disease

    S=ϕ(ν+ϖ0)ξρ+(σ3+ϖ0)Q((η1+ν(1ρ)(σ1+σ2+ϖ0))ϖ2),E=(σ1+σ2+ϖ0)(Q1)(ξρ)(σ3+ϖ0)QI,I=ξ(1ρ)(σ1+σ2+ϖ0)(R01)(ν+ϖ0)νρ,A=η2ϕξ(1ρ)(σ1+σ2+ϖ0)(ν+ϖ0)ξρQ2I,H=σ1(ν+ϖ0)(1ρ)(R01)(σ3+ϖ0)(ξ+ϖ0)νI,R=σ2(σ3+ϖ0)(ν+ϖ0)ξ+σ1QI(σ3+ϖ0)(ν+ϖ0),C=ψ1(ν+ϖ0)ξρI+ψ2ξ(1ρ)(R01)(ν+ϖ0)ξρ.

    The above equations present that, EE of the model (2.1) exists only, if R0 is greater than one. Thus we state the following theorem.

    Theorem 5. The EE point D1=(S,E,I,A,H,R,C) exists only in case R0 is greater than one.

    The definition of (R0) can be described as the number of individuals who become infected after being in contact with an infected individual in a population that is initially fully susceptible and without any prior infections. If R0>1, it means that an epidemic is likely to occur, while if R0<1, an outbreak is unlikely. The value of R0 is crucial in determining the strength of control measures that need to be implemented to contain the epidemic. In order to calculate R0 for the suggested model (2.1), we use the method described in [33], we have

    F=[0η1S0η2ϕS0η3qS0η4S000000000000000000000],
    V=[b10000ξρb2000b30b4000σ1νb500ψ1ψ20ϖ2],

    where b1=(ξ+ϖ0), b2=(σ1+σ2+ϖ0+ϖ1), b3=ξ(1ρ), b4=(ν+ϖ0) b5=(σ3+ϖ0). R0 represents spectral-radius of NGM ˉH=FV1.

    So R0 for model (2.1) is

    R0=η1ξρS0Q+η2ϕS0(1ρ)(ν+ϖ0)(ξ+ϖ0)+η3qS0Q1(ν+ϖ0)(σ3+ϖ0)Q+η4S0Q2ϖ2(ν+ϖ0)Q, (4.1)

    where

    Q=(ξ+ϖ0)(σ1+σ2+ϖ0+ϖ1),Q1=ξϖ20ψ2ξσ21ϖ2ξσ1σ2ϖ2ξσ1ϖ0ϖ2ξσ1ϖ1ϖ2+ξσ1σ3ψ2+ξσ2σ3ψ2+ξσ1ϖ0ψ2+ξσ2ϖ0ψ2+ξσ3ϖ0ψ2+ξσ3ϖ1ψ2+ξϖ0ϖ1ψ2+ρξσ21ϖ2+ξρϖ20ψ2+νρξσ3ψ1+νρξϖ0+ξρσ1σ2ϖ2+ξρσ1ϖ1ϖ2ξρσ1σ3ψ2ξρσ2σ3ψ2ξρσ1ϖ0ψ2+ξρσ3ϖ0ψ1ξρσ3ϖ0ψ2ξρσ3ϖ1ψ2ξρϖ0ϖ1ψ2,Q2=η4S0(ξψ2σ2+ξψ2σ1+ξψ2ϖ0+νξρψ1ξρψ2σ2ξρψ2σ1+ξρψ1ϖ0ξρψ2ϖ0).

    The R0 of this model is composed of four components: transmission from individuals who are symptomatic to those who are asymptomatic, transmission from asymptomatic individuals to those who require hospitalization, transmission from hospitalization to the reservoir (camels for MERS-CoV), and transmission from the reservoir to susceptible individuals. These four modes of transmission collectively determine the risk of disease spread during this epidemic.

    We study the dynamics of the proposed system (2.1) at DFE with aid of Theorem 6 as follows:

    Theorem 6. The DFE point D0=(S0,I0,E0,H0,A0,C0,R0), is asymptotically stable (locally) if R01.

    Proof. The Jacobian-matrix of the model at DFE point (D0,0,0,0,0,0), is:

    J0=(ϖ00η1Sη2ϕSη3qSη4S0(ξ+ϖ0)η1Sη2ϕSη3qSη4S0ξρ(σ1+σ2+ϖ0+ϖ1)0000ξ(1ρ)0(ν+ϖ0)0000σ1ν(σ3+ϖ0)000ψ1ψ20ϖ2). (4.2)

    Characteristic equation of Jacobian matrix (4.2) is:

    (ζ+ϖ0)(δ+ζ)(a1ζ3+ζ4+a2ζ2+a4+a3ζ)=0, (4.3)

    where

    a1=σ1+σ2+νϖ0+σ3ϖ0ν,a2=σ2+ϖ0+ξϖ0σ1(1R0),a3=2ϖ20+σ1+σ2+σ3+ϖ0+νσ1+σ3+σ1ϖ0+σ1ξ+ξ(1ρ)+ξν,a4=η3qSξ(1ρ)+ξνσ1+ϖ0ξ(1ρ)σ1η3Sqϖ0νρ.

    a1a3a2>a22a4+a22 if R0<1. By RH criteria the real parts of all the roots for characteristic polynomial P(ζ) are negative, which shows that D0 is asymptotically local stable [34,35].

    The upcoming proof presents the global stability at DFE point D0. To analyze the global stability analysis at F0 we introduce the Lyapunov function as follows.

    Theorem 7. When the reproductive number R0 is less than 1, the disease-free equilibrium of the system is globally and asymptotically stable.

    Proof. Consider the Lyapunov function as

    U(t)=12[(SS0)+E(t)+I(t)+A(t)+H(t)+(CC0)]2+[d1S(t)+d2E(t)+d3A(t)+d4H(t)+d5C(t)]. (4.4)

    Here di for i=1,2,3,4,5 are arbitrary constants, to be considered after differentiating Eq (4.4), and using (2.1), so we obtain

    U(t)=[(SS0)+E+A+I+H+(CC0)][ϕϖ0Np(t)+ψ1I+ψ2Aϖ2C+QQ1(ϕ(1R0)ϖ0E(t))].

    By considering the +ive parameter d1=d2=d3=QQ1, d4=1Q2, d5=ϖ0 and after the interpretation we obtain

    U(t)=[(SS0)+E+I+A+H+(CC0)][ϖ0(ϕNp(t))ψ1Iψ2Aϖ2WQQ1(ϕ(1R0)ϖ0E(t))],

    where

    F0=bNϖ0.

    U(t) is negative when S>S0 and R0<1 and U(t)=0 in case if S=S0 by the LaSalle's invariance principle [36,37], and E=A=I=H=C=0. Thus the DFE is globally asymptotic stable in F0.

    Theorem 8. If the threshold value is greater than 1, then the model (2.1) around EE point D1 is locally as well as globally asymptotically stable.

    Proof. The linearization of model (2.1) around EE point D1 is,

    J0=(A0η1Sη2ϕSη3qSη4SA1(ξ+ϖ0)η1Sη2ϕSη3qSη4S0ξρA10000ξ(1ρ)0(ν+ϖ0)0000σ1νA2000ψ1ψ20ϖ2),

    where

    A=η1I+η2ϕA+η3qH+η4S,A1=(σ1+σ2+ϖ0),A2=(σ3+ϖ0).

    Using row transformation, we obtain:

    J0=(A0η1Sη2ϕSη3qSη4S0Bη1Sη2ϕSη3qSη4S00B1η2ϕSη3qSη4S000B2η3qSη4S0000B3000000B4), (4.5)

    where B=(ξ+ϖ0)(η1I+η2ϕA+η3qH+η4S), B1=(σ1+σ2+ϖ0+ϖ1)(ξ+ϖ0)A,B2(ν+ϖ0)(ξ+ϖ0)(R01)A, B3(σ1+σ2+ϖ0+ϖ1)(σ3+ϖ0), B4=ϖ2ξρ(σ1+σ2+ϖ0+ϖ1).

    Ξ1=A<0,Ξ2=B<0,Ξ3=B1<0,Ξ4=B2<0,Ξ5=B3<0,Ξ6=B4<0.

    When R0>1 the real parts of eigenvalues are negative, hence the model (2.1) is asymptotically locally stable at D1 [38].

    Theorem 9. If R0 is greater than 1, then EE point D1 is globally asymptotically stable and is not stable if less than 1.

    Proof. In order to show the asymptotic global stability of the considered model (2.1) at EE point D1, we utilize the Castillo-Chavez technique [39,40]. Now let us take the sub-system of (2.1),

    dS(t)dt=ϕη1ISη2ϕASη3qHSη4CSϖ0S,dE(t)dt=η1IS+η2ϕAS+η3qHS+η4CS(ξ+ϖ0)E,dI(t)dt=ξρE(σ1+σ2)I(ϖ0+ϖ1)I. (4.6)

    Consider P and P2 be the linearized matrix and second-additive of the model which contains the first three equations of system (2.1), which becomes

    P=(δ110δ13δ21δ22δ2300δ33),P2=((δ11+δ22)δ23δ13δ32(δ11+δ33)δ12δ31δ21(δ22+δ33)). (4.7)

    Let Q(χ)=Q(S(t),E(t),I(t))=diag{SE,SE,SE}, then Q1(χ)=diag{ES,ES,ES}, the derivative of Qf(χ) w.r.t time, implies that

    Qf(χ)=diag{˙SE˙ESE2,˙SE˙ESE2,˙SES˙EE2}. (4.8)

    Now QfQ1=diag{K1,K1,K1} and QP22Q1=P22, where K1=˙SS˙EE A=QfQ1+QP22Q1, and

    A=(A11A12A21A22),A11=˙SS˙EEη1Iη2ϕAη3qH(ν+ϖ0),A12=[η1Sη2S],A21=[ξρ0],A22=[u110u21u22].u11=˙SS˙EEη1Iη2ϕAη3qHϖ0,u21=η1Iη2ϕAη3qHη4C,u22=˙SS˙EEξ2ϖ0. (4.9)

    Let (n1,n2,n3) be vector in R3 and . of (n1,n2,n3) presented by,

    n1,n2,n3=max{n1,n2+n3}. (4.10)

    Here we consider the Lozinski-measure introduced in [41], δ(A)sup{ϱ1,ϱ2}=sup{δ(A11)+A12,δ(A22)+A21}, where hi=δ(Aii)+Aij for i=1,2 and ij,

    ϱ1=δ(A11)+A12,ϱ2=δ(A22)+A21, (4.11)

    where δ(A11)=˙SS˙EEη1Iη2ϕAη3qH(ξ+ϖ0), δ(A22)=max{˙SS˙EEη1Iη2ϕAη3qHϖ0,η1Iη2ϕAη3qHη4C}=˙SS˙EEη1Iη2ϕAη3qHη4C}, A12=η1S and A21=max{ξρ,0}=ξρ. Therefore ϱ1 and ϱ2 become, i.e, ϱ1˙SS2ϖ0ξρ and ϱ2˙SS2ϖ0ξmin{σ1,νρ}, which presents δ(A){˙SS+σ1min{ξ,σ1}2ϖ0}. Hence δ(B)˙SS2ϖ0. Integrating δ(A) in [0,t] and also considering limt, we have

    limtsupsup1tt0δ(A)dt<2ϖ0,ˉk=limtsupsup1tt0δ(A)dt<0. (4.12)

    So that the system of the first three compartments of model (2.1) is globally asymptotically stable.

    To find the relation of parameters to R0 in the disease transmission we use the formula ΔR0h=R0khR0 where h is the parameter, introduced by [34,35]. This makes it easy to identify the variables that have a substantial impact on reproduction number, using the above formula we have

    ΔR0η1=R0η1η1R0=0.60143>0,ΔR0η2=R0η2η2R0=0.0020302>0,ΔR0η3=R0η3η3R0=0.083624>0,ΔR0η4=R0η4η4R0=0.90820>0,ΔR0ξ=R0ξξR0=0.130434>0,ΔR0ϖ2=R0ϖ2ϖ2R0=1.002654<0,ΔR0ϖ0=R0ϖ0ϖ0R0=1.33673<0,ΔR0ϖ1=R0tϖ1ϖ1R0=0.0043>0,ΔR0ψ1=R0ψ1ψ1R0=0.006549>0,ΔR0ϕ=R0ϕϕR0=.9999999997>0,ΔR0ψ2=R0ψ2ψ2R0=0.996194>0,ΔR0ν=R0ννR0=0.843190<0,ΔR0σ1=R0σ1σ1R0=0.012374<0,ΔR0σ2=R0σ2σ2R0=0.00773<0.
    Figure 1.  The graphs show the affect of various parameters on R0 and the variations in them.

    These demonstrate the relevance of many factors in disease transmission. It also measures the change in R0 as a function of a parameter modification. The sensitivity indices show that there is indeed a direct relationship between R0 and a set of variables S1=[η1,η2,η3,η4,ϕ,ψ1,ψ2], while has an inverse relation with S2=[ϖ0,ϖ2,σ1,σ2,ν]. This demonstrates that higher the value of parameters S1 increases the value of threshold quantity greatly, but increasing the value for parameters S2 decreases the value of threshold value.

    Figure 2.  The graphs show the affect of various parameters on R0 and the variations in them.

    In this part, we validate our analytical conclusion. We employ the Runge-Kutta technique of fourth order [42]. Some factors are chosen for demonstration purposes, while others are derived from publicly available data. The parameters are chosen in a way that is more biologically realistic. For the simulation, we use the following parameters. ϕ=0.00004;η1=0.007;ϖ0=0.0003;η2=0.003; ψ2=0.00008;ϖ1=0.0001;η3=0.005;ξ=0.002; η4=0.0001;σ2=0.000001;ϕ=0.016;q=0.00007;ϖ2=0.00003;σ1=0.001;σ3=0.0007; ψ1=0.0006;ν=0.000002. Figures 3 and 4 depict the performance of the proposed model based on the aforementioned parameters, which validate the theorem's analytical discovery (4.2). According to the theoretical understanding of these findings, whenever R0<1, each curve of solution of the sensitive population takes 150–300 days to achieve equilibrium. Likewise, the exposed community takes 250 to 150 days, the infected populace takes 200 to 100 days, and the asymptomatic populace, hospitalized, and recovered requires 100 to 50 days. Camel dynamics initially grow and then achieve an equilibrium state, as seen in illustration 0.

    Figure 3.  The demonstration of dynamics of S,I,E,A compartments population in case R0<1.
    Figure 4.  The demonstration of dynamics of various compartments populations (Hospitalized individuals, Recovered population, and Reservoir (MERS CoV), such that camel's in case R0<1).

    Next, we consider the parameters η1=0.007; σ1=0.001; ϖ1=0.0001; ψ1=0.0006; η2=0.003; ϖ2=0.00003; ϕ=0.00004; σ2=0.000001; η3=0.005; ϖ0=0.0003; η4=0.0001; ξ=0.002; ϕ=0.016; σ3=0.0007; q=0.00007; ν=0.000002. ψ2=0.00008; and find R0=9.89887 which is greater than 1. We investigate the dynamics of the given model in the vicinity of the EE point. The numerical simulations based on the aforementioned settings are displayed in Figures (5) and (6), which validate the finding presented in Theorem (8).

    Figure 5.  The demonstration of dynamics of S,I,E,A compartments populations in case R0>1.
    Figure 6.  The demonstration of dynamics of various compartments population (Hospitalized individuals, Recovered populace, and (MERS CoV) reservoir, such that camel's in case R0>1).

    We develop control techniques based on sensitivity as well as model dynamics (2.1). The maximal sensitivity indices parameter is (η1,η2,η3,η4), and increasing this value by 10 percent, raises the threshold value. To limit the progress of the illness, we must minimize these parameters by using the control variables E1(t),E2(t),E3(t),E4(t) to represent (awareness about the mask, isolation people (infected), oxygen therapies, ventilation and self-care from the camels.)

    Our main goals are the reduction of MERS-CoV in the populace with increasing R(t) and decreasing I(t), A(t) and H(t), reservoir C(t) with applying control parameters (time-dependent) E1(t),E2(t),E3(t),E4(t).

    i. E1(t) represents the control parameter (time-dependent) represents the awareness concerning surgical masks and hand washing.

    ii. E2(t) represents the control parameter (time-dependent) represents quarantining of infected persons.

    iii. E3(t) represents the control parameter (time-dependent) represents mechanical ventilation (oxygen therapy).

    iv. E4(t) represents the control parameter (time-dependent) self-care that is keeping distance from camels, avoiding raw milk, or eating improperly cooked meat.

    By the use of these control parameters in our suggested optimal control problem which we obtain by modifying model (2.1):

    dS(t)dt=ϕη1IS(1E1(t))η2ϕAS(1E1(t))η3qHS(1E1(t))η4CS(1E1(t))ϖ0S,dE(t)dt=η1IS(1E1(t))+η2ϕAS(1E1(t))+η3qHS(1E1(t))+η4CS(1E1(t))(ξ+ϖ0+E1(t))E,dI(t)dt=ξρE(σ1+σ2)I(ϖ0+ϖ1)IE2(t)I,dA(t)dt=ξE(1ρ)(ν+ϖ0)AE2(t)A,dH(t)dt=σ1I+νA(σ3+ϖ0)HE3(t)H,dR(t)dt=σ1IE2(t)+σ3HE3(t)ϖ0R,dC(t)dt=ψ1I+ψ2Aϖ2C(t)E4(t)C(t), (6.1)

    with the initial conditions

    Ics={S(0),I(0),E(0),H(0),A(0),C(0),R(0)}0

    The purpose here is to demonstrate that it is feasible to apply time-dependent control mechanisms while reducing the expense of doing so. We assume that the expenses of control schemes are nonlinear and take a quadratic shape, [43], which are cost variables that balance the size and importance of the sections of the optimization problem. As a result, we select the observable (cost) function as,

    J(E1,E2,E3,E4)=T0[ζ1I+ζ2A+ζ3H+ζ4C+12(ζ5E21(t)+ζ6E22(t)+ζ7E23(t)+ζ8E24(t)]dt. (6.2)

    In Eq (6.2) ζ1, ζ2, ζ3, ζ4, ζ5, ζ6, ζ7, ζ8, stand for weight constants. ζ1, ζ2, ζ3, ζ4 express relative costs of infected (I), asymptomatic (A), hospitalized (H) and reservoir (C), while ζ5, ζ6, ζ7, ζ8 show associated-cost of control parameters. 12ζ5E21, 12ζ8E24, 12ζ6E22, 12ζ7E23, describe self care, treatment and isolation.

    Our objective is to obtain OC pair E1, E2, E3, E4, i.e.,

    J(E1,E2,E3,E4)=min{J(E1,E2,E3,E4),E1,E2,E3,E4U}, (6.3)

    dependent on model (6.1), we consider, the control-set of parameters as:

    U={(E1,E2,E3,E4)/uI(t)is Lebesgue-measurable on the[0,1],0uI(t)1,i=1,2,3,4}. (6.4)

    We obey the result [44], stating that the solution of the system exists in the case when control parameters are bounded as well as Lebesgue measurable. So, we consider that the suggested control system can be presented as:

    dΩdt=AΩ+BΩ.

    In above system Ω=(S,I,E,H,A,C), A(Ω) and B(Ω) represent linear and nonlinear bounded coefficient, respectively, so that

    A=[ϖ0000000y100000νρy20000ν(ρ+1)0y30000σ1ϵ(σ2+ϖ0+E3)000ψ1ψ20(θ+E4)], (6.5)

    where y1=(ν+ϖ0+E1), y2=(σ1+σ2+ϖ0+ϖ1+E2), y3=(ϵ+ϖ0+ϖ2+E2).

    B(Ω)=(ϕη1IS(1E1(t))ηθAϕS(1E1(t))η3qHS(1E1(t))η4CS(1E1(t))η1IS(1E1(t))+η2ϕAS(1E1(t))+η3qHS(1E1(t))+η4CS(1E1(t))0000).

    Considering L(Ω)=FΩ+AΩ,

    |F(Ω1)F(Ω2|p1|S1S2|+p2|E1E2|+p3|I1I2|+p4|A1A2|+p5|H1H2|+p6|C1C2|P|S1S2|+|E1E2|+|C1C2|+|I1I2|+|H1H2|+|A1A2|.

    Here P=max(p1,p2,p3,p4,p5,p6,p7,p8) does not depend on the suggested model state-classes. We can also express

    |L(Ω1)L(Ω2)||W(Ω1)W(Ω2)|,

    where W=(P,A) is less than , L is continuous in the Lipschitz sense, and from the description the system classes are non-negative, it obviously shows that the solution of model (6.1) exists. For the existence of the solution let us consider, and prove the following theorem:

    Theorem 10. There exist an OC E=(E1,E2,E3,E4)E, to control-system presented in Eqs (6.1) and (6.2).

    Proof. As it is obvious that the control and system variables are not negative. It is also worth noting that U (set of variables) is closed and convex by expression. Furthermore, the control problem is bounded, indicating the problem's compactness. The expression ζ1I+ζ2A+ζ3H+ζ4C+12(ζ5E21(t)+ζ6E22(t)+ζ7E23(t)+ζ8E24(t) is convex as well, w.r.t the set U. It guarantees the existence of OC for OC variables (E1,E2,E3,E4).

    Here, we determine the best solution to control problems (6.1) and (6.2). For this, we employ the Lagrangian, and Hamiltonian equations, as shown below:

    L(I,C,A,H,E1,E2,E3,E4)=ζ1I+ζ2A+ζ3H+ζ4C+12(ζ5E21(t)+ζ6E22(t)+ζ7E23(t)+ζ8E24(t).

    To define the Hamiltonian (H) associated with the model, we use the notion Θ = (Θ1,Θ2,Θ3,Θ4,Θ5,Θ6,Θ7) and Υ=(Υ1,Υ2,Υ3,Υ4,Υ5,Υ6,Υ7) then,

    H(x,u,Θ)=L(x,u)+ΘΥ(x,u),

    where

    Υ1(x,u)=ϕη1IS(1E1(t))η2ϕAS(1E1(t))η3qHS(1E1(t))η4CS(1E2(t))ϖ0S,Υ2(x,u)=η1IS(1E1(t))+η2ϕAS(1E1(t))+η3qHS(1E1(t))+η4CS(1E2(t))(ξ+ϖ0+E1)E,Υ3(x,u)=ξρE(σ1+σ2)I(ϖ0+ϖ1)IE2(t)I(t),Υ4(x,u)=ξ(1ρ)E(ν+ϖ0)AE2(t)A,Υ5(x,u)=σ1I+νA(σ3+ϖ0)HE3(t)H,Υ6(x,u)=σ1IE2(t)+σ3HE3(t)ϖ0R,Υ7(x,u)=ψ1I+ψ2Aϖ2CE4(t)C(t), (6.6)

    and Z(x,u)=Υ1(x,u),Υ2(x,u),Υ3(x,u),Υ4(x,u),Υ5(x,u),Υ6(x,u),Υ7(x,u).

    Here we utilize, the principle [45,46] to Hamiltonian, in order to obtain an optimality solution, which is stated that if the solution expressed with (x,u) is optimal, then a function Θ, such that

    ˙x=HΘ,0=Hu,ΘA(t)=Hx.H(t,x,u,Θ)x=maxE1,E2,E3,E4[0,1]H(x(t),E1,E2,E3,E4,ΘA(t)); (6.7)

    and the condition of transversality

    Θ(tf)=0. (6.8)

    Thus to obtain the adjoint variables and OC variables, we use the principles Eq (6.7). So we get

    Theorem 11. Suppose that optimal and control-parameters are expressed by S, E, A, I, H, C, R be the optimal-state (E1,E2,E3,E4) for system (6.1)-(6.2). Then ΘA(t) (adjoint variables set) satisfies:

    Θ1(t)=(Θ1Θ2)(η1I+η2ϕA+η3qH+η4C)(1E1)(t)+Θ1ϖ0,Θ2(t)=(Θ2Θ4)ξ+(Θ4Θ3)ξρ+Θ2ϖ0+Θ2E1(t),Θ3(t)=ζ1+(Θ1Θ2)η1S(1E1(t))+(Θ3Θ5)σ1Θ6ξ1E2(t)Θ7Θ4(t)=ζ2+(Θ1Θ2)η2ϕS(1E1(t))+(Θ4Θ5)ν+Θ4(ϖ0+E2(t))Θ7ψ2,Θ5(t)=ζ3(Θ1Θ2)η3qS(1E1(t))+(σ3+u0+E3(t))Θ5Θ6σ3E3(t),Θ6(t)=ϖ0Θ6,Θ7(t)=ζ4+(Θ1Θ2)η4S(1E1(t))+Θ7(ϖ2+E4(t)), (6.9)

    having terminal condition

    ΘA(t)=0. (6.10)

    The OC variables E1(t), E2(t), E3(t), E4(t) are

    E1(t)=max[min[(Θ2Θ1)η1IS+η2ϕA+η3qH+η4CS+Θ2Eζ5,1],0],E2(t)=max[min[(Θ3I+Θ6σ1R+Θ4A+Θ5H)ζ6,1],0],E3(t)=max[min[(Θ5HΘ6σR)ζ7,1],0],E4(t)=max[min[(Θ7C)ζ8,1],0]. (6.11)

    Proof: The adjoint-model (6.9) is obtained by applying the principle (6.7) and the transversality conditions from the outcomes of ΘA(t)=0. For optimal functions set E1,E2,E3 and E4, we utilized Hu. In the next part, we evaluate the optimality problem numerically. Since it will be easier for such readers to understand as compared to analytical data. The optimization problem system is defined by its control-system (6.1), adjoint-system (6.9), boundary conditions, and OC functions.

    Using the RK technique of order four, we calculate the optimal control model (6.1) to observe the influence of masks, treatment, isolations, and self-care from camels. We employ the forward RK technique to get the solution of system (2.1) with starting conditions in the time interval [0, 50]. To obtain a solution to the adjoint-system (6.9), we apply the backward RK technique in the same domain with the assistance of the transversality constraint. For simulation purposes, we consider the parameters as: ν=0.0071; ϖ1=0.014567125; η1=0.00041; η3=0.0000123; η4=0.0000123; θ=0.98; σ1=0.0000404720925; σ3=0.00135; q=0.017816; ψ1=0.05; ϖ0=0.00997; η2=0.0000123; ϕ=0.003907997; σ2=0.000431; ρ=0.00007; ϖ2=0.014567125 ψ2=0.06;. These parameters are considered in such a manner that more feasible biologically. Weight constants, here are taken as ζ1=0.6610000; ζ2=0.54450; ζ3=0.0090030; ζ4=0.44440; ζ6=0.3550; ζ7=0.67676; ζ8=0.999. So we get the upcoming behaviours shown in Figures 7a, 7b, 7c, 7d, 8a, 8b, 8c.

    Figure 7.  The graphs depict the dynamic of the classes with control and without controls.
    Figure 8.  The graphs depict the dynamic of the classes with control and without controls.

    These figures reflect the dynamics of susceptibles, exposed, infected people, asymptomatic persons, hospitalized, recovered, and MERS reservoirs, i.e., camels with and also without control. Our major goal in using the OC tool is to reduce the number of persons who are infected while increasing the number of those who are not infected, as demonstrated by numerical findings.

    In this study, we developed a mathematical model to analyze the transmission of MERS-CoV between people and its reservoir (camels), with the goal of assessing the transmission risk of MERS-CoV. We calculated the model's fundamental reproductive number, R0, and employed stability theory to examine the local and global behavior of the model and determine the conditions that lead to stability. We also evaluated the sensitivity of R0 to understand the impact of each epidemiological parameter on disease transmission. To minimize the number of infected individuals and intervention costs, we incorporated optimal control into the model, which included time-dependent control variables such as supportive care, surgical masks, treatment, and public awareness campaigns about the use of masks. Furthermore, our biological interpretation of the results indicates that if the basic reproduction number is less than one, the susceptible population decreases for up to 60 days, and then becomes stable, indicating that the population will remain stable. Our numerical simulations validated the effectiveness of our control strategies in reducing the number of infected individuals, asymptomatic cases, hospitalizations, and MERS-CoV reservoir, while increasing the susceptible and recovered populations. These simulations support our analytical work.

    This study is supported via funding from Prince Sattam bin Abdulaziz University project number PSAU/2023/R/1444.



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