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Enhancing the trustworthiness of chaos and synchronization of chaotic satellite model: a practice of discrete fractional-order approaches.

Rashid, S ; Hamidi, SZ ; et al.
In: Scientific reports, Jg. 14 (2024-05-09), Heft 1, S. 10674
Online academicJournal

Theoretical and mathematical codynamics of nonlinear tuberculosis and COVID-19 model pertaining to fractional calculus and probabilistic approach 

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel virus known as coronavirus 2 (SARS-CoV-2) that affects the pulmonary structure and results in the coronavirus illness 2019 (COVID-19). Tuberculosis (TB) and COVID-19 codynamics have been documented in numerous nations. Understanding the complexities of codynamics is now critically necessary as a consequence. The aim of this research is to construct a co-infection model of TB and COVID-19 in the context of fractional calculus operators, white noise and probability density functions, employing a rigorous biological investigation. By exhibiting that the system possesses non-negative and bounded global outcomes, it is shown that the approach is both mathematically and biologically practicable. The required conditions are derived, guaranteeing the eradication of the infection. Sensitivity analysis and bifurcation of the submodel are also investigated with system parameters. Furthermore, existence and uniqueness results are established, and the configuration is tested for the existence of an ergodic stationary distribution. For discovering the system's long-term behavior, a deterministic-probabilistic technique for modeling is designed and operated in MATLAB. By employing an extensive review, we hope that the previously mentioned approach improves and leads to mitigating the two diseases and their co-infections by examining a variety of behavioral trends, such as transitions to unpredictable procedures. In addition, the piecewise differential strategies are being outlined as having promising potential for scholars in a range of contexts because they empower them to include particular characteristics across multiple time frame phases. Such formulas can be strengthened via classical technique, power-law, exponential decay, generalized Mittag–Leffler kernels, probability density functions and random procedures. Furthermore, we get an accurate description of the probability density function encircling a quasi-equilibrium point if the effect of TB and COVID-19 minimizes the propagation of the codynamics. Consequently, scholars can obtain better outcomes when analyzing facts using random perturbations by implementing these strategies for challenging issues. Random perturbations in TB and COVID-19 co-infection are crucial in controlling the spread of an epidemic whenever the suggested circulation is steady and the amount of infection eliminated is closely correlated with the random perturbation level.

Keywords: Co-infection TB and COVID-19 model; Deterministic and probabilistic model; Fractional calculus; Global positive solution; Ergodic stationary distribution; Probability density function; Quasi-equilibrium

Introduction

The COVID-19 outbreak has posed novel obstacles to worldwide medical systems, resulting in enormous impacts on nations around the globe. Undoubtedly, the battle against COVID-19 has taken up much of the attention, but it is important to remember that TB has existed as a problem for quite a while. Mankind has been plagued by this extremely contagious sickness for ages. Ultimately, 2020 will likely go down in history as the year that the coronavirus ailments, or COVID-19, took center stage. The outbreak's causative agent, the SARS-CoV-2, first appeared in China in the second half of 2019[1],[2]. Even though COVID-19 continues to be a topic widely discussed in academic journals and news reports, it's crucial to remember about other infectious illnesses, such as TB[3],[4].

The COVID-19 outbreak has had a major effect on the TB treatment mechanism, resulting in a reduction in both detection and transmission. This is explained by the repercussions of TB care and limitations on accessibility for patients, which have led to an increase in TB-related mortality[5],[6]. In order to successfully combat both of these transmissible illnesses, this viewpoint assessment seeks to point out the overlap between COVID-19 and TB, emphasizing their combined menace and suggesting common approaches.

Furthermore, there are some notable clinical commonalities between the COVID-19 epidemic and TB. Since pulmonary secretions are an important way that these ailments are communicated, proximity and congested surroundings are favorable. Furthermore, COVID-19 and TB are especially dangerous for disadvantaged and underprivileged groups, such as the elderly, people with preexisting medical disorders, and people with compromised immunological capabilities. The COVID-19 epidemic has had a complex effect on TB. The increased challenge has caused a diversion to medical supplies, which has disrupted attempts to diagnose, address and regulate TB. Security measures, prohibitions on traveling and restricted availability of healthcare resources have made it more difficult to identify cases of TB and diagnose patients on time. The combination of these two contagious illnesses has produced a complicated scenario that needs prompt monitoring and all-encompassing approaches. Both COVID-19 and TB have a number of similarities, most notably the way in which their respective causal agents-mycobacterium TB and SARS-CoV-2-are transmitted[7]. Pulmonary system emissions are the route of transmission for both infections[8],[9]. Both COVID-19 and TB can spread via aerosols and droppings, with the respiratory tract being their usual site of infection. It is crucial to remember, though, that such illnesses may impact a variety of organs[10]. In addition, finding and evaluating interactions as well as safeguarding medical personnel and individuals at risk are essential elements of healthcare safety for these illnesses. To create comprehensive and inexpensive prevention and treatment strategies, it is essential to comprehend the channels and components impacting propagation. Numerous decades of therapeutic and laboratory research on TB have yielded a plethora of data that can be used to identify, prioritize and evaluate exposures[8]. It should come as no surprise that more research is needed to better understand how SARS-CoV-2 spreads, and there is ongoing debate regarding the distinct functions played by airborne particles, microbes and big pulmonary secretions[11]. In particular, excessive growth occurrences have been linked to the propagation of these two diseases[12],[13]. Figure 1 listed below shows a graphic that illustrates several of the prevalent therapeutic manifestations and multi-organ dysfunction.

Graph: Figure 1 Identical indications and multi-organ connection to TB and COVID-19.

Whereas the implantation time for TB can range from 2 weeks to many decades until the TB infection advances, that of COVID-19 is less lengthy, ranging from 1 to 14 days. The manifestations of COVID-19 include anemia, wheezing, throat irritation, diminished or absent perception, flavor loss, vomiting, muscular soreness, and exhaustion. Usually, these indications start off suddenly. On the other hand, TB causes a high temperature, perspiration at night, a persistently persistent cough, bleeding in the cough, decreased hunger, heartburn, and exhaustion. On the other hand, TB manifestations appear gradually and with a subtle beginning. When it comes to COVID-19, those with coexisting illnesses, including HIV, insulin resistance, being overweight, persistent lung disease, persistent cardiac problems, and impaired immune systems, are more likely to have extreme symptoms. These inherent medical issues may exacerbate the advancement of the sickness. Conversely, concomitant conditions, including type II diabetes, sickle cell syndrome, severe obstructive pulmonary ailments, HIV, and a weakened immune system, are recognized to escalate the likelihood and intensity of TB transmission. Combating and curing serious forms of both COVID-19 and TB require an understanding of and commitment to controlling these coexisting conditions[14],[15]. Figure 2 lists some of the prevalent danger indicators for both TB and COVID-19.

Graph: Figure 2 Basic danger signs for TB and COVID-19.

Meanwhile, the testing process facilities have been disrupted by COVID-19, resulting in decreased personnel objectives, longer evaluation processing times, and the unavailability of forensic equipment. The timely delivery of TB screening tests as well as their accessibility have been greatly impacted by these delays. Screening findings may take longer to reach people, which could postpone therapeutic beginnings and raise the danger of tuberculosis spreading throughout populations[16]. Screening TB infections and locating regions with widespread dissemination require efficient acquisition and inspection methods. The distribution of resources and focused treatments can be guided by observational reports. Effective use of statistical analysis and health monitoring networks can help with preventive choices and offer real-time information[17].

During the years, a great deal of mathematical concepts have been developed to help us understand the world in which we live. In order to regulate presentations involving considerable obstacles, powerful artificial intelligence algorithms have been constructed, and the concept of space and time modeling has been put into practice. Some of the algorithmic techniques that are particularly commonly applied in modeling and prediction involve the idea of differentiation. Differential equations (DEs) are scientific techniques that have been created using this concept. In the beginning endeavor, researchers suggested a number of algorithms via multifaceted associations. The variation in the compositions could include local (exchange rate, conformable derivative, and fractal derivative)[18]–[20]; nonlocal/singular kernel (Riemann–Liouville, Liouville–Caputo, and multiple expressions)[21]; local/non-singular kernel (Caputo–Fabrizio operators)[22]; and finally non-local/non-singular (Atangana–Baleanu–Caputo operators)[23]. For a variety of interpretations of differential derivatives or the individuals who structured the foundations, a number of academics suggest numerous novel approaches. Fractional-order (FO) calculus has a connection to realistic endeavors and finds extensive application in multiple domains such as atomic physics, optics, image encryption, nanotechnology, and infectious disease[18]–[20],[24].

Recently, a subfield of mathematical physics and comprehension known as fractional calculus uses FO derivatives to study how inventions and documentation operate. FO modeling, as opposed to integer-order settings, can employ reminiscence memory of the power, exponential decay, or generalized Mittag–Leffler (GML) formation kernel to capture non-local spatial–temporal interactions. The conceivable benefits of using the fractional approach by Atangana–Baleanu involve all non-localities that are inherent within the explanation, just like in all previous variations. However, the most significant characteristic is that it has a nonsingular and non-local kernel, represented by the GML functionality, which, from an empirical viewpoint, includes the clarification and advancement of competencies delineated by a series of privileges. Kumar et al.[25] contemplated a new investigation on fractional HBV models through Caputo and Atangana–Baleanu–Caputo derivatives. Mekkaoui et al.[26] presented the predictor–corrector for non-linear DEs and integral equations with fractional operators. Atangana and Araz[27] described a successive midpoint method for nonlinear DEs with integer and Caputo–Fabrizio derivatives. On the other hand, it has been shown that the previously mentioned approach precisely conveys the complex compositions of many practical representations[23],[27]. The piecewise derivative, which has recently gained prominence[28], was presented by Atangana and Araz[29] and distinguishes from every derivative by the fact that it may reprise the interconnected paths that comprise these fractional algorithms in a differentiation technique. Every aspect that happens demonstrates that while the prevalence of the codynamics of COVID-19 and TB is probabilistic instead of deterministic in nature, knowledgeable research is based on an empirical methodology. A number of academics investigated the real-world growth of viruses and bacteria using the fundamental concept of probabilistic modeling, as reported in Refs.[30],[31].

Certain probabilistic COVID-19 individuals via TB concurrent infection outbreak frameworks using theropetic representatives hydroxychloroquine, azithromycin, lopinavir/ritonavir, and darunavir/cobicistat conjunction systems have been successfully defined to examine the influence of probabilistic white noise and offer several efficient initiatives for governing infection interactions. These frameworks are founded on the randomly generated linear disruptive methodology, which assumes the biological nature of ambient white noise correlates to the dimension of every compartment. Moreover, it has been demonstrated experimentally that a probabilistic COVID-19 and TB system that includes immunological dysfunction affected by inherent and adapted resistance can prevent an epidemic of co-infection. Motivated by these findings[32],[33], we also presume that the random perturbation is closely connected to specific populations of evolution of TB and COVID-19 diagnostics. In order to illustrate the significant influence of a probabilistic framework condition mentioned in Ref.[34], we performed to create this paper. Additionally, we create a probabilistic mathematical structure utilizing piecewise fractional derivative expressions to analyze the co-infection process incorporating the positive immunomodulation against COVID-19, likely because of trained innate immunity and crossed heterologous immunity within predetermined time intervals. In order to achieve this, we separate the population into two groups: the incidence and occurrence of exacerbated immune dysregulation and decreased lymphocyte function, along with erroneous variations. The probability that the most recent COVID-19-infected TB will be engaged is represented by the proportion ψ(0,1) , whereas the unexplained component 1-ψ will not be implicated. In addition, we established the global positive solutions of the co-infection model with a unique ergodic and stationary distribution (ESD) technique to illustrate the biological properties and statistical viability of this structure. We also provide the precise definition of the probabilistic density function (P.D.F) at a quasi-equilibrium point that represents the probabilistic COVID-19 approach, which reflects significant spontaneous features in probabilistic relevance. The ESD and P.D.F surrounding the quasi-equilibrium point of the randomized multidimensional codynamics framework will be better understood as a result of this investigation. The intention of the investigation is to acquire an improved comprehension of how the infection persists over time in the probabilistic codynamics system. In general, fractional operators examine simulations conducted numerically of the proposed system that include crossover structures and white noise.

Codynamics model and preliminaries

The general population is divided into eight indistinguishable groups in this category, which are designated as susceptible people, (S) , latent TB patients who do not exhibit TB-associated indications and are not pathogenic LT , influential TB-infected people IT , COVID-19-infested humans who do not exhibit indications but are transmissible EC , COVID-19-diagnosed people who exhibit scientific backing indications and are pathogenic IC , both inactive TB and COVID-19-contaminated people LTC , current TB and COVID-19-contaminated humans ITC , and retrieved people R consisting of both TB and COVID-19. The underlying computational framework for the codynamics of TB and COVID-19 is developed in this portion. Considering such, all people at moment τ , represented by N(τ) , are provided by

1 N(τ)=S(τ)+LT(τ)+IT(τ)+EC(τ)+IC(τ)+LTC(τ)+ITC(τ)+R(τ).

Graph

We hypothesized that acquisition increases the vulnerable community at an intensity of . Every person in every compartment experiences an inevitable mortality rate of β . Equivalent to formula (1), vulnerable individuals contract TB via interaction with current TB individuals via agent transmission ψT . The acceptable interaction rate for TB transmission is indicated by α1 within this manifestation. It is believed that people with persistent TB are undiagnosed and cannot pass on the illness[35]. Likewise, those at risk contract COVID-19 at an intensity of transmission ψC , which is determined as in formula (1), after effectively coming into proximity to COVID-19-infected people. The efficient interaction probability for COVID-19 infection is represented by α2 in this case. Furthermore, we hypothesized that people in the hidden TB segment LT depart at an incidence of μ to segment IT , at an incidence of transmission of λψC to the persistent TB as well as COVID-19 contaminated group, whilst certain of them recuperate at an intervention incidence of ϖ . Additionally, those in the TB-infected category IT recuperate due to the illness at an incidence of δ , with the surviving percentage either transferring to the transmission category ITC at a pace of ς3 or dying at a speed of ζT via TB-induced mortality.

The overall community in cohort LTC potentially dies at COVID-19-induced mortality pace ζC or advances at an intensity of ρ to become contaminated category ITC . As seen in Fig. 3, it is believed that the other people will be moved to the other cohort at a consistent multiplicity of η . In other words, the general population classified as LTC migrates at an intensity of ς2η to category IT , then at a pace of ς1η to compartment IC group, and finally recovers at a pace of (1-(ς1+ς2))η . Additionally, we hypothesized that, although the codynamics-induced mortality prevalence is represented by ζTC , people in compartment ITC depart for compartments IT,IC or R , correspondingly, at an intensity of θ2ξ,θ1ξ or (1-(θ1+θ2))ξ. Furthermore, at an intensity of ϵψT,ϕ or φ2, the COVID-19 exposure people EC can choose to depart to compartment LTC,IC or R , respectively. Comparably, the number of individuals in compartment IC is either moved to the codynamics cohort at an intensity of ν or restored at a steady pace of φ3 . ζC represents the disease-induced fatality rate within this category. Figure 3 displays the suggested system's process layout.

Graph: Figure 3 Flow diagram for depicting the codynamics process of TB-COVID-19 model (2).

It leads to frameworks for the subsequent nonlinear DEs determined by the procedure illustration:

2 S˙=-(ψT+ψC+β)S,LT˙=ψTS-(β+μ+λψC+ϖ)LT,IT˙=μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT,EC˙=ψCS-(β+ϵψT+φ1+φ2)EC,0τ1,IC˙=φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC,LTC˙=λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC,ITC˙=ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC,R˙=ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC-βR,

Graph

where ψT=α1N(τ)(IT(τ)+ITC(τ)) and ψC=α2N(τ)(EC(τ)+IC(τ)+LTC(τ)+ITC(τ)), containing positive initial conditions (ICs) S(0)0,LT0,IT0,EC0,IC0,LTC0,ITC0,R0.

Table 1 Description of model's parameters.

Symbols

Description

β

People' spontaneous mortality rate

ρ

Rate of transmission of COVID-19 andTB exposure within the contaminated group

φ1

Transmission rate of infection among those inoculated to COVID-19

φ3

Probability of recuperation for a COVID-19 influenced person

ϵ

Percentage of TB exposure in people subjected to COVID-19

ϖ

Recuperation percentage of inactive TB infections

ν

Percentage of COVID-19 afflicted people who have TB disease

ς3

COVID-19 contamination incidence among TB patients

φ2

Probability of recuperation for those subjected to COVID-19

η

Probability at which people exit the LTC group

ς1

TB healing rate for LTC of long-term care residents

ς2

Percentage of LTC patients recuperating with COVID-19

ξ

Proportion at which people quit the affected group ITC

θ1

ITC patients' rate of TB recurrence

θ2

COVID-19 recuperation percentage among ITC participants

λ

Percentage of people suffering from TB who also get COVID-19

δ

Recoverability percentage of TB patients

ζT

Mortality rate from TB

ζC

Mortality rate from COVID-19 infection

ζTC

Mortality incidence as a result of both infections co-occurring

Recruiting rate for those who are vulnerable

α1

Prevalence of TB infection propagation

α2

Rate of COVID-19 propagation

μ

Percentage of people confronted with TB who get the disease

ψT

Intensity transmission for TB (the likelihood of contracting a virus from a TB sick person)

ψC

COVID-19 intensity of illness: the likelihood of contracting the virus from a person who has COVID-19 illness

Table 1 provides a description of the system's characteristics.

To help readers that are acquainted with fractional calculus, we provide the related summary herein (see[21]–[23] comprehensive discussion on fractional calculus).

0cDτωG(τ)=1Γ(1-ω)0τG(q)(τ-q)ωdq,ω(0,1].

Graph

The index kernel is involved in the Caputo fractional derivative (CFD). Whenever experimenting with a particular integral transform, such as the Laplace transform[36],[37], the CFD accommodates regular ICs.

0CFDτωG(τ)=M¯(ω)1-ω0τG(q)exp[-ω1-ω(τ-q)]dq,ω(0,1],

Graph

where M¯(ω) indicates the normalization function M¯(0)=M¯(1)=1.

The non-singular kernel of the Caputo-Fabrizio fractional derivative (CFFD) operator has drawn the attention of numerous researchers. Furthermore, representing an assortment of prevalent issues that obey the exponential decay memory is best suited to utilize the CFFD operator[38]. With the passage of time, developing a mathematical model using the CFFD became a remarkable field of research. In recent times, several mathematicians have been busy with the development and simulation of CFFD DEs[39].

The ABC fractional derivative operator is described as follows:

0ABCDτωG(τ)=ABC(ω)1-ω0τG(q)Eω[-ω1-ω(τ-q)ω]dq,ω(0,1],

Graph

where ABC(ω)=1-ω+ωΓ(ω) represents the normalization function.

The memory utilized in Atangana–Baleanu–Caputo fractional derivative (ABCFD) can be found intuitively within the index-law analogous for an extended period as well as exponential decay in a number of scientific concerns[40],[41]. The broad scope of the connection and the non-power-law nature of the underlying tendency are the driving forces behind the selection of this version. The impact of the kernel, considered crucial in the dynamic Baggs–Freedman framework, was fully produced by the GML function[42].

To far better perceive the propagation of TB and COVID-19, we indicate a dynamic mechanism (2) that includes the co-infection within the context of CFD, CFFD and ABCFD, respectively. This is because FO algorithms possess inherited properties that characterize the local/non-local and singular/non-singular dynamics of natural phenomena, presented as follows:

3 cDτωS=-(ψT+ψC+β)S,cDτωLT=ψTS-(β+μ+λψC+ϖ)LT,cDτωIT=μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT,cDτωEC=ψCS-(β+ϵψT+φ1+φ2)EC,1τ2,cDτωIC=φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC,cDτωLTC=λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC,cDτωITC=ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC,cDτωR=ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC-βR,

Graph

4 CFDτωS=-(ψT+ψC+β)S,CFDτωLT=ψTS-(β+μ+λψC+ϖ)LT,CFDτωIT=μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT,CFDτωEC=ψCS-(β+ϵψT+φ1+φ2)EC,1τ2,CFDτωIC=φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC,CFDτωLTC=λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC,CFDτωITC=ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC,CFDτωR=ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC-βR,

Graph

5 ABCDτωS=-(ψT+ψC+β)S,ABCDτωLT=ψTS-(β+μ+λψC+ϖ)LT,ABCDτωIT=μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT,ABCDτωEC=ψCS-(β+ϵψT+φ1+φ2)EC,1τ2,ABCDτωIC=φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC,ABCDτωLTC=λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC,ABCDτωITC=ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC,ABCDτωR=ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC-βR.

Graph

The arrangement of this article is as follows: In "Codynamics model and preliminaries" section, explanations for fractional calculus, along with several key notions and model (2) details, are provided. Moreover, a detailed analysis of the FO co-infection system's (3) equilibrium stability is presented in "Codynamics model and preliminaries" section. In "Stochastic configuration of codynamics of TB-COVID-19 model" section, a probabilistic form of the TB and COVID-19 models' (28) codynamics is proposed and a detailed description of the unique global positive solution for each positive initial requirement is presented. The dynamical characteristics of the mechanism's appropriate conditions for the presence of the distinctive stationary distribution are provided. The P.D.F enclosing a quasi-stable equilibrium of the probabilistic COVID-19 framework is presented in "Stochastic COVID-19 model without TB infection" section. Numerous numerical simulations in view of piecewise fractional derivative operators are presented in "Numerical solutions of co-dynamics model using random perturbations" section to validate the diagnostic findings we obtained in "Stochastic configuration of codynamics of TB-COVID-19 model" and "Stochastic COVID-19 model without TB infection" sections. In conclusion, we conceal our findings to conclude this study.

Positivity and boundedness

Since we interact with living communities, each approach ought to be constructive and centred on a workable area. We utilized the subsequent hypothesis that guarantees these.

Theorem 1

Assume that the set Ξ~:=(S,LT,IT,EC,IC,LTC,ITC,R) is a positive invariant set for the suggested FO model (3).

Proof

In order to demonstrate whether the solution to a set of equations (3) is positive, then (3) yields

6 0cDτωS|S=0=0,0cDτωLT|LT=ψTS0,0cDτωIT|IT=0=μLT0,0cDτωEC|EC=0=ψCS0,0cDτωIC|IC=0=φ1EC0,0cDτωLTC|LTC=0=λψCLT+ϵψTEC0,0cDτωITC|ITC=0=ρLTC+ς3IT+νIC0,0cDτωR|R=0=ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC0.

Graph

Therefore, the outcomes related to the FO model (3) are positive. Finally, the variation in the entire community is described by

0cDτωΞ~+ζTIT-ζC(IC+LTC)-ζTCITC-βN-βN.

Graph

Addressing the variant previously mentioned, we get

Ξ~(τ)(Ξ~(0)-β)Eω(-βτω)+β.

Graph

Consequently, we derive the GML function's asymptotic operation[43] as

Ξ~(τ)β.

Graph

Adopting the same procedure for other systems of equations in the model (3), which indicates that the closed set Ξ~ is a positive invariant domain for the FO system (3).

  • Assuming that every requirement is non-negative throughout time τ , we exhibit that the outcomes remain non-negative and bounded in the proposed region, Π . We'll look at the co-infection model (3) Ξ~:=(S,LT,IT,EC,IC,LTC,ITC,R) spreads in the domain, which is described as Π:={Ξ~+8:0Nβ}.
  • According to the afflicted categories in co-infection model (3), disease-free equilibrium (DFE) and endemic equilibrium (EE) are the biologically significant steady states of FO model (3). We establish the fractional derivative to get the immune-to-infection steady state as 0cDτωS,0cDτωLT,0cDτωIT,0cDτωEC,0cDτωIC,0cDτωLTC,0cDτωITC,0cDτωR, to zero of the FO model (3) have no infection, and get
  • E0=(β,0,0,0,0,0,0,0).

Graph

  • The dominating eigenvalue of the matrix FG-1 correlates with the basic reproductive quantity R0CT of structure (3), in accordance with the next generation matrix approach[44]. Thus, we find
  • F=ψTS0ψCS000,Φ=(β+μ+λψC+ϖ)LT-θ2ξITC-ς2ηLTC-μLT+(β+ς3+ζT+δ)IT(β+ϵψT+φ1+φ2)EC-φ1EC-ς1ηLTC-θ1ξITC+(β+ν+ζC+φ3)IC-λψCLT-ϵψTEC+(β+ζC+ρ+η)LTC-ρLTC-ς3IT-νIC+(β+ζTC+ξ).

Graph

The next generation matrix at DEF can then be obtained by using the Jacobian of F and G examined at E0 as

FG-1=μK1(β+μ+ϖ)K7K1K7φ1K3(β+ω+φ2)K7K3K7K5(β+ζC+ρ+η)K7-α1(β+ν+ζC+φ3)(β+ς3+ζTδ+θ2ξ)K7000000μK2(β+μ+ϖ)K7K2K7φ1K4(β+ω+φ2)K7-α2(β+ς3+ζT+δ)(β+ξ+ζTC+ν)-θ2ς3ξK7K6(β+φ1+φ2)K7-α2(β+ς3+ζT+δ)(β+ζC+ρ+η)K7000000000000000000,

Graph

where

Kκ=-α1((β+ν+ζC+φ3)(β+ξ+ζTC)+(β+ν+ζC+φ3)ς3-θ1νξ),κ=1,-α2ς3(θ1ξ+β+ν+ζC+φ3),κ=2,-α1ν(θ2ξ+β+ς3+ζT+δ),κ=3,-α2(β+ς3+ζT+δ)((β+ν+φ3+ζC)(β+ξ+ζTC)+φ1(β+ξ+ζTC)+νφ1-θ1νξ)-θ2ς3ξ(φ1+β+ν+ζC+φ3),κ=4,νρξ(θ2ς1-θ1ς2)+(β+ν+ζC+φ3)(-α1ρ(νξ+β+ς3+ζT+δ)+ης2(β+ξ+ς3+ζTC))+ς1νη(β+ς3+ζT+δ),κ=5,-α2((β+ς3+ζT+δ)(β+ν+ζC1+φ3)(β+ξ+ζTC+ρ)+θ1ξ(ρ-ν)(β+ς3+ζT+δ)+(β+ς3+ζT+δ)ης1(β+ξ+ζTC+ν)+ς2ης3(β+ν+ζC+φ3+θ1ξ)-θ2ς3ξ(ς1η+β+ν+ζC+φ3)),κ=6,θ1νξ(β+ς3+ζT+δ)+(β+ζC+ρ+η)(θ2ς3ξ-(β+ς3+ζT+δ)(β=ξ+ζTC)),κ=7.

Graph

The fundamental reproducing quantity of the pairing system is shown by the highest spectral radius of the subsequent generation's matrix. It is evident that the matrix FG-1 has four eigenvalues that are equivalent to zero. The truncated matrix yields the additional eigenvalues as

μK1(β+μ+ϖ)Kφ1K3(β+φ1+φ2)KμK2(β+μ+ϖ)KK4(β+φ1+φ2)K.

Graph

Consequently, by calculating the eigenvalues of FG-1 , it is possible to simply determine that

δ1~=(β+μ+ϖ)Q4+μ(β+φ1+φ2)Q1-122(β+μ+ϖ)(β+φ1+φ2)(θ1νξ(β+ς3+ζT+δ)+(β+ζC+ρ+η)(θ2ς3ξ-(β+ς3+ζT+δ)(β+ξ+ζTC))),δ2~=(β+μ+ϖ)Q4+μ(β+φ1+φ2)Q1+122(β+μ+ϖ)(β+φ1+φ2)(θ1νξ(β+ς3+ζT+δ)+(β+ζC+ρ+η)(θ2ς3ξ-(β+ς3+ζT+δ)(β+ξ+ζTC))),

Graph

where

1=μ2K12(β+φ1+φ2)2-2μ(β+μ+ϖ)(β+φ1+φ2)Q1Q2+4φ1μ(β+μ+ϖ)(β+φ1+φ2)K22+(β+μ+ϖ)2K42.

Graph

Therefore, the co-dynamics structure's (3) fundamental reproductive quantity R0 is provided by R0CT=max{R0C,R0T}.

Here, we shall then demonstrate how transmission persists in the FO mechanism. It explains how widespread the virus is within the framework. From the viewpoint of biology, the virus continues in the bloodstream if the infectious proportion is elevated for a sufficiently long time τ .

However, the linearization technique is used to examine the local stabilization of the codynamics algorithm's DFE state. At the DFE state E0, the Jacobean matrix of system (3) is displayed as

7 JE0=-β0-α1-α2-α2-α2-(α1+α2)00-(β+μ+ϖ)α1000α100μ-(β+ς3+ζT+δ)00ς2ηθ2ξ0000α2-β-φ1-φ2α2α2α20000φ1-β-ν-ζC-φ3ς1ηθ1ξ000000-(β+ζC+ρ+η)0000ς30νρ-(β+ξ+ζTC)00ϖδφ2φ3(1-(ς1+ς2))η(1-(θ1+θ2))η-β.

Graph

The analysis of E0 's localized temporal equilibrium relies upon the eigenvalues' interpretation. Here, δ1,2~=-β and δ3~=-(β+ρ+η+ζC) are obtained by broadening the following polynomial |JE0-δI|=0 . Moreover, we get the additional δ 's based on the simplified matrix's |JE0-δI|=0 described as

J-δI5=μ-(β+ς3+δ+ζT+δ~)00θ2ξ0ς30ν-(δ~+β+ξ+ζC)00φ1-(δ~+β+ν+φ3+ζC)θ1ξ000α2φ1+(δ~+β+ν+φ3+ζC)(α2-δ~-β-ξ-φ1)/φ1100002,

Graph

where 1=α2φ1+(δ~+β+ν+φ3+ζC)(α2-δ~-β-ξ-φ1)/φ1,2=α1(ς3+(δ~+β+ξ+ζC))/ς3+(β+ς3+ζT+δ+δ~/μ)(θ2ξς3-(β+ς3+ζT+δ+δ~)(β+ξ+ζTC+δ~)/ς3)). After simple computations, the characteristic polynomial of the above matrix is presented as

8 U(δ~)=-μς3φ1α2φ1+(δ~+β+ν+φ3+ζC)(α2-δ~-β-ξ-φ1)φ1{α1(ς3+(δ~+β+ξ+ζC))ς3+(β+ς3+ζT+δ+δ~μθ2ξς3-(β+ς3+ζT+δ+δ~)(β+ξ+ζTC+δ~)ς3}.

Graph

In other words, the outcomes to the U(δ~) are the eigenvalues:

9 U(δ~)=δ~5+d1δ~4+d2δ~3+d3δ~2+d4δ~+d5=0,

Graph

where

10 d1=α2-β-φ1-φ2,d2=α2φ1+(β+ν+ζC+φ3)(α2-β-φ1-φ2)-(α2-2β-φ1-φ2-ν-ζC-φ3)×(β+ς3+ζT+δ+ξ+ζTC-μ-ϖ)+(μα1+θ2ξς3-(β+ς3+ζT+δ)(β+ξ+ζTC)-(β+ς3+ζT+δ)(β+μ+ϖ)-(β+μ+ϖ)(β+ξ+ζTC)),d3=μα1(ς3+β+ξ+ζTC)+(β+μ+ϖ)(θ2ξς3-(β+ς3+ζT+δ)(β+ξ+ζTC))-(α2φ1+(β+ν+φ3+ζC)(α2-β-φ1-φ2))(β+ς3+ζT+δ+φ1+φ2-ξ-ζTC)-(α2-2β-φ1-φ2-ν-ζC-φ3)(μα1+θ2ξς3-(β+ς3+ζT+δ)(β+ξ+ζTC)-(β+μ+ϖ)(2β+ς3+ζT+δ+ξ+ζTC)),d4=-(α2φ1+(β+ν+ζC+φ3)(α2-β-φ1-φ2))(μα1+θ2ξς3-(β+μ+ϖ)(2β+ς3+ζT+δ+ξ+ζTC))-(α2-2β-φ1-φ2-ν-ζC-φ3)(μα1(ς3+β+ξ+ζTC)+(β+μ+ϖ)×(θ2ξς3-(βς3+ζT+δ)(β+ξ+ζTC))),d5=(α2φ1+(β+ν+φ3+ζC)(α2-β-φ1-φ2))(μα1(ς3+β+ξ+ζTC)+(β+μ+ϖ)(θ2ξς3-(β+ς3+ζT+δ)(β+ξ+ζTC))).

Graph

Therefore, if the subsequent requirements apply, the roots of expression (10) exhibit negative real portions according to the Routh–Hurwitz stability specifications as

11 dȷ>0,ȷ=1,...,5,d1d2d3>d32+d12d4,(d1d4-d5)(d1d2d3-d32-d12d4)>d5(d1d2-d3)2+d1d52.

Graph

Graph: Figure 4 Evolution of the basic reproduction number R0CT with the aid of R0C and R0T.

Figure 4 is illustrated by depicting in 3D evolution of the threshold parameter R0CT of model (3) as a function of R0C and R0T.

The forthcoming result is established thanks to Theorem 2 in[44].

Theorem 2

The DFE point of the FO codynamics model (3) is locally asymptotically stable if the prerequisite specified in formula (12) is satisfied.

Existence and uniqueness of solutions

This section shows that there is only one solution for the system (3). Now, we demonstrate that the framework's solution is distinctive. Initially, we construct framework (3) in the form of:

12 cDτωS=Q1(τ,S(τ)),cDτωLT=Q2(τ,LT(τ)),cDτωIT=Q3(τ,IT(τ)),cDτωEC=Q4(τ,EC(τ)),cDτωIC=Q5(τ,IC(τ)),cDτωLTC=Q6(τ,LTC(τ)),cDτωITC=Q7(τ,ITC(τ)),cDτωR=Q8(τ,R(τ)),

Graph

where

13 Q1(τ,S(τ))=-(ψT+ψC+β)S,Q2(τ,LT(τ))=ψTS-(β+μ+λψC+ϖ)LT,Q3(τ,IT(τ))=μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT,Q4(τ,EC(τ))=ψCS-(β+ϵψT+φ1+φ2)EC,Q5(τ,IC(τ))=φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC,Q6(τ,LTC(τ))=λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC,Q7(τ,ITC(τ))=ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC,Q8(τ,R(τ))=ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC-βR.

Graph

Integral transform applied to both sides of equations (14) yields

14 S(τ)-S(0)=1Γ(ω)0τ(τ-p)ω-1Q1(p,S)dp,LT(τ)-LT(0)=1Γ(ω)0τ(τ-p)ω-1Q2(p,LT)dp,IT(τ)-IT(0)=1Γ(ω)0τ(τ-p)ω-1Q3(p,IT)dp,EC(τ)-EC(0)=1Γ(ω)0τ(τ-p)ω-1Q4(p,EC)dp,IC(τ)-IC(0)=1Γ(ω)0τ(τ-p)ω-1Q5(p,EC)dp,LTC(τ)-LTC(0)=1Γ(ω)0τ(τ-p)ω-1Q6(p,LTC)dp,ITC(τ)-ITC(0)=1Γ(ω)0τ(τ-p)ω-1Q7(p,ITC)dp,R(τ)-R(0)=1Γ(ω)0τ(τ-p)ω-1Q8(p,R)dp.

Graph

The kernels Qι,(ι=1,...,8) satisfies the Lipschitz condition and contraction, as demonstrated.

Theorem 3

Q1 satisfies the Lipschitz condition and contraction if the following condition holds: 0α1(σ3+σ7)+α2(σ4+σ5+σ2+σ5)+β<1.

Proof

For S and S1, we have

Q1(τ,S)-Q1(τ,S1)=(α1(IT+ITC)+α2(EC+IC+ITC+LT)+β)(S(τ)-S1(τ))(α1(IT+ITC))+α2(EC+IC+ITC+LT)+β)S(τ)-S1(τ).

Graph

Suppose V1=α1(σ3+σ7)+α2(σ4+σ5+σ2+σ5)+β , where ITσ3,ITCσ7,ECσ4ICσ5,ITCσ7,LTσ2 are a bounded functions. So, we have

15 Q1(τ,S)-Q1(τ,S1)V1S(τ)-S1(τ).

Graph

After obtaining the Lipschitz criterion for Q1 , hence, Q1 is a contraction if 0α1(σ3+σ7)+α2(σ4+σ5+σ2+σ5)+β<1 .

In the same manner, Qȷ(ȷ=2,..,7) satisfy the Lipschitz condition as follows:

Q2(τ,LT)-Q2(τ,LT1)V2LT(τ)-LT1(τ),Q3(τ,IT)-Q3(τ,IT1)V3IT(τ)-IT1(τ),Q4(τ,EC)-Q4(τ,EC1)V4EC(τ)-EC1(τ),Q5(τ,IC)-Q5(τ,IC1)V5LT(τ)-IC1(τ),Q6(τ,LTC)-Q6(τ,LTC1)V6S(τ)-LTC1(τ),Q7(τ,ITC)-QT(τ,ITC1)V7S(τ)-S1(τ),Q8(τ,r)-Q8(τ,R1)V8R(τ)-R1(τ),

Graph

where V2=ψTσ1-(β+μ+λψC+ϖ),V3=μσ2+ς2ησ6+θ2ξσ7-(β+ς3+ζT+δ),V4=ψCσ1-(β+ϵψT+φ1+φ2),V5=φ1σ4+ρησ6+θ1ξσ7-(β+ζC+ν+φ3),V6=λψCσ2+ϵψTσ4-(β+ζC+ρ+ξ),V7=ρσ6+ς3σ3+νσ5-(β+ζTC+ξ),V8=ϖσ2+φ2σ4+δσ3+φ3σ5+(1-(ς1+ς2))ησ6+(1-(θ1+θ2))ξσ7-β.

For ȷ=2,...,8, we find 0Vȷ<1, then Vȷ are contractions. Assume the following recursive pattern, as suggested by system (15):

Θ1n(τ)=Sn(τ)-Sn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q1(p,Sn-1)-Q1(p,Sn-2))dp,Θ2n(τ)=LTn(τ)-LTn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q2(p,LTn-1)-Q2(p,LTn-2))dp,Θ3n(τ)=ITn(τ)-ITn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q3(p,ITn-1)-Q3(p,ITn-2))dp,Θ4n(τ)=ECn(τ)-ECn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q4(p,ECn-1)-Q4(p,ECn-2))dp,Θ5n(τ)=ICn(τ)-ICn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q5(p,ICn-1)-Q5(p,ICn-2))dp,Θ6n(τ)=LTCn(τ)-LTCn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q6(p,LTCn-1)-Q6(p,LTCn-2))dp,Θ7n(τ)=ITCn(τ)-ITCn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q7(p,ITCn-1)-Q7(p,ITCn-2))dp,Θ8n(τ)=Rn(τ)-Rn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q8(p,Rn-1)-Q8(p,Rn-2))dp,

Graph

with S(0)0,LT(0)0,IT(0)0,EC(0)0,IC(0)0,LTC(0)0,ITC(0)0,R(0)0.

Throughout the above system, we compute the norm of its first equation and then

Θ1n(τ)=Sn(τ)-Sn-1(τ)=1Γ(ω)0τ(τ-p)ω-1(Q1(p,Sn-1)-Q1(p,Sn-2))dp1Γ(ω)0τ(τ-p)ω-1(Q1(p,Sn-1)-Q1(p,Sn-2))dp.

Graph

Therefore, (16) possesses Lipschitz's condition, then we have

Θ1n(τ)V1Γ(ω)0τΘ1(n-1)(p)dp.

Graph

Analogously, we find

16 Θ2n(τ)V2Γ(ω)0τΘ2(n-1)(p)dp,Θ3n(τ)V3Γ(ω)0τΘ3(n-1)(p)dp,Θ4n(τ)V4Γ(ω)0τΘ4(n-1)(p)dp,Θ5n(τ)V5Γ(ω)0τΘ5(n-1)(p)dp,Θ6n(τ)V6Γ(ω)0τΘ6(n-1)(p)dp,Θ7n(τ)V7Γ(ω)0τΘ7(n-1)(p)dp,Θ8n(τ)V8Γ(ω)0τΘ8(n-1)(p)dp.

Graph

As a consequence, we can write

Sn(τ)=ι=1Θ1ι(τ),LTn(τ)=ι=1Θ2ι(τ),ITn(τ)=ι=1Θ3ι(τ),ECn(τ)=ι=1Θ4ι(τ),ICn(τ)=ι=1Θ5ι(τ),LTCn(τ)=ι=1Θ6ι(τ),LTCn(τ)=ι=1Θ7ι(τ),Rn(τ)=ι=1Θ8ι(τ).

Graph

Theorem 4

A system of solutions described by the codynamics model (3) exists if there exists τ1 such that (τ1VȷΓ(ω))<1,(ȷ=1,...,8).

Proof

By means of (16) and (17), we have

Θ1n(τ)Sn(0)(V1τΓ(ω))n,Θ2n(τ)LTn(0)(V2τΓ(ω))n,Θ3n(τ)ITn(0)(V3τΓ(ω))n,Θ4n(τ)ECn(0)(V4τΓ(ω))n,Θ5n(τ)ICn(0)(V5τΓ(ω))n,Θ6n(τ)LTCn(0)(V6τΓ(ω))n,Θ7n(τ)ITCn(0)(V7τΓ(ω))n,Θ8n(τ)Rn(0)(V8τΓ(ω))n.

Graph

Thus, the system is continuous and has a solution. Now we shall explain how the functions listed above may be used to construct a model solution (15). We make the assumption that

S(τ)-S(0)=Sn(τ)-Θ~1n(τ),LT(τ)-LT(0)=LTn(τ)-Θ~2n(τ),IT(τ)-IT(0)=ITn(τ)-Θ~3n(τ),EC(τ)-EC(0)=ECn(τ)-Θ~4n(τ),IC(τ)-IC(0)=ICn(τ)-Θ~5n(τ),LTC(τ)-LTC(0)=LTCn(τ)-Θ~6n(τ),ITC(τ)-ITC(0)=ITCn(τ)-Θ~7n(τ),R(τ)-R(0)=Rn(τ)-Θ~6n(τ).

Graph

Therefore, we have

Θ~1n(τ)=1Γ(ω)0τ(Q1(p,S)-Q1(p,Sn-1))dp1Γ(ω)0τQ1(p,S)-Q1(p,Sn-1)dpτV1Γ(ω)S-Sn-1.

Graph

After recursive procedure, we have the following:

Θ~1n(τ)(τV1Γ(ω)).

Graph

Thus, Θ~1n(τ)0asn.

Similarly, we may establish that Θ~ȷn(τ)0,(ȷ=2,...,8)asn.

To examine the uniqueness of the solution, we assume that there is another solution of the system, such as S1(τ),LT1(τ),IT1(τ),EC1(τ),IC1(τ),LTC1(τ),ITC1(τ)andR1(τ). Then

S(τ)-S1(τ)=1Γ(ω)0τ(Q1(p,S)-Q1(p,Sn-1))dp.

Graph

After taking norm, we get

S(τ)-S1(τ)1Γ(ω)0τQ1(p,S)-Q1(p,Sn-1)dp.

Graph

Utilizing the Lipschitz condition, we have

S(τ)-S1(τ)τV1Γ(ω)S-Sn-1.

Graph

Consequently, we have

17 S(τ)-S1(τ)(1-τV1Γ(ω))0.

Graph

Theorem 5

The codynamics model (3) has a unique solution, provided that (1-τV1Γ(ω))>0.

Proof

Assuming that condition (18) is vaild,

S(τ)-S1(τ)(1-τV1Γ(ω))0.

Graph

Then S(τ)-S1(τ)=0. Hence, we have S(τ)=S1(τ). Similarly, we can prove that LT(τ)=LT1(τ),IT(τ)=IT1(τ),EC(τ)=EC1(τ),IC(τ)=IC1(τ),LTC(τ)=LTC1(τ),ITC(τ)=ITC1(τ),R(τ)=R1(τ).

Influence of TB on COVID-19

We started by describing the basic reproductive quantity, R0C , by means of R0T (and vice versa), in order to examine the effect of TB illness on COVID-19 (and vice versa)[45]. By interpreting the value of β as a component of R0T using the formula (2), we get

18 R0T=μα1(β+μ+ϖ)(β+ζT+δ).

Graph

Now, we have

19 R0C=α2R0T(R0T(ζC+φ1+φ3)-K8/2+R0T(R0TK82+4μα1)/2)(R0T(R0TK82+4μα1)/2+(φ1+φ3)R0T-K8R0T/2)(R0T(R0TK82+4μα1)/2+(ζC+φ3)R0T-K8R0T/2),

Graph

where K8=(μ+ϖ+ζT+δ). Furthermore, the R0CR0T>0, it also indicates that the COVID-19 outbreak is made worse by the spread of TB viruses.

Remark 1

The population's TB proliferation possesses no noticeable influence with the propagation of COVID-19 provided R0CR0T=0 . On the other hand, the transmission of COVID-19 will be significantly adversely affected by the outbreak of TB if R0CR0T<0 .

Furthermore, by quantifying R0T in the context of R0C and determining the meaning of the partial derivative of R0C with regard to R0T , the effect of COVID-19 of TB infections is able to be rectified.

Analysis of COVID-19

When the infection of TB is disregarded, the deterministic model (2) becomes the subsequent system:

20 S˙=-α2N1(EC+IC)-βS=Φ^1,EC˙=α2N1(EC+IC)-(β+φ1+φ2)EC=Φ^2,IC˙=φ1EC-(β+ζC+φ3)IC=Φ^3,R˙=φ2EC+φ3IC-βR=Φ^4.

Graph

The basic reproduction number R0C of the model (21) is presented as

21 R0C=α2(β+ζC+φ3+φ1)(β+φ1+φ2)(β+ζC+φ3).

Graph

Sensitivity analysis

The sensitivity analysis of the model parameters for the COVID-19 submodel, as stated in (21), is carried out in this subsection. The sensitivity of a parameter, ε contemplate, is expressed as[46] and indicates how the framework behaves in response to a slight variation in a parameter value as

Sε=R0CεεR0C.

Graph

In our case, the sensitivity analysis of each parameters for (21) becomes:

22 Sα2=R0Cα2α2R0C=1,Sβ=R0CββR0C=-β(ζC(ζC+2β+3φ3+φ1)+β(β+4φ3+2φ1)+φ3(2φ3+2φ2+φ1)+φ1(φ1+φ2))(ζC+β+φ3)(β+φ2+φ1)(ζC+β+2φ3+φ1),SζC=R0CζCζCR0C=-ζCφ1(ζC+β+φ3)(ζC+β+φ3+φ1),Sφ3=-R0Cφ3φ3R0C=-φ3φ1(ζC+β+φ3)(ζC+β+φ3+φ1),Sφ1=-R0Cφ1φ1R0C=-φ1(ζC+φ3-φ2)(φ2+β+φ3)(ζC+β+φ3+φ1),Sφ2=-R0Cφ2φ2R0C=-φ2(φ2+β+φ3).

Graph

Here, we notice that the dissemination of COVID-19 is boosted by the contact rate α1 . Additionally, the transmission rate φ1 from the unprotected group to the afflicted group has a positive effect on the dissemination of the virus if ζC+φ3-φ2<0. In other words, the prevalence will rise as the values of these factors rise. The additional parameters β,φ3,ζC and φ2 have adverse effects; therefore, raising their values will result in a drop in the frequency of COVID-19 infections. Nonetheless, the sensitivity analysis investigation does not take into account the immoral increase in the individual fatality rate as a means of controlling the spread of illness.

Bifurcation analysis

In what follows, we investigate the solution behavior of (21) by taking α2 as the bifurcation parameter. Calculating the value of α2 from R0C , i.e, α2(β+φ1+φ2)(β+ζC+φ3+φ1)((β+ζC+φ1+φ2)(β+ζC+φ3))=1, we have α2=(β+φ1+φ2)(β+ζC+φ3)β+ζC+φ3+φ1. By replacing α2 , we can determine the eigenvalues of the Jacobin matrix at the DFE point, as per the outcome provided in Ref.[44]. Thus, substituting α2=α2 in (7), it gives zero eigenvalue. This means that the Jacobean matrix JE0 in (7) at α2=α2 has a left eigenvector (associated with the zero eigenvalue) which is calculated from oTJE0 . Here, o=[o1,o2,o3,o4] , for which o1=0,o2=ζC+β+φ1+φ3β+φ2+φ1,o3=1 and o4=0.

Likewise, eTJE0=0 can be used to determine the right eigenvector linked to the zero eigenvalue when e=[e1,e2,e3,e4], for which e1=β(ζC+φ2+β)+(φ2+φ1)(ζC+β+φ3)φ2(ζC+β+φ3)+φ1φ3,e2=β(ζC+φ2+β)φ2(ζC+β+φ3)+φ1φ3,e3=βφ2φ2(ζC+β+φ3)+φ1φ3 and e4=1.

Now, suppose that Φ^ represents the right-hand side of the th equation in the COVID-19 submodel (21) and let ϰ denote the corresponding state variable for =1,...,4 .

Introduce

23 y1=,ι,ȷnoωιωȷ2Φ^ϰιϰȷ(0,0)andy2=,ιnoωι2Φ^ϰιϰ1(0,0).

Graph

The local dynamics of (21) near the bifurcation point α2=α are then calculated by the signs of two associated constants y1 and y2 with ϰ1=α2-α . Note that, in Φ^(0,0) , the first zero corresponds to the DFE, E0C , for (21). In other words, Φ^(0,ϰ1), for =1,...,4 if and only if the right-hand sides of (21) are equal to zero at E0C.

Moreover, from ϰ1=α2-α , we have ϰ1=0 when α2=α , which is the second zero component in Φ^(0,0) . For the (21), the associated nonzero partial derivatives at the E0C are

24 2Φ^1EC2=-2α2β,2Φ^1ECIC=-2α2β,2Φ^1ECR=2α2β,2Φ^1IC2=-2α2β,2Φ^1ECIC=-2α2β,2Φ^1ICR=2α2β,2Φ^2EC2=2α2β,2Φ^2ECIC=2α2β,2Φ^2ICR=-2α2β,2Φ^2IC2=2α2β,2Φ^2ICEC=2α2β,2Φ^2ICR=-2α2β.

Graph

Next, with the aforementioned expressions for y1 , it is evident that

25 y1=β2(β+φ3+ζC)(β+φ3+ζC+φ1+φ3)(φ3φ1+φ1(β+φ3+ζC)){2β(β+φ3+φ1+ζC)φ2(β+φ3+ζC)+φ1φ3-1}.

Graph

It can be demonstrated that the corresponding non-vanishing partial derivatives for the corresponding sign of y2 are

26 2Φ~1ECα2=-1,2Φ~1ICα2=-1,2Φ~2ECα2=1,2Φ~2ECα2=1.

Graph

It is evident from the aforementioned statements as well that y2=β(ζC+β+φ3+φ1)2(β+φ2+φ1)(φ2(β+φ3+ζC)+Φ1φ3).

From the bifurcation coefficient y1 's sign varies on the minimal value of recurrence that generates bistability () , and we find that y2 is always positive from the estimates of y1 and y2 . Therefore, a subsequent proposition is established by applying the result of Ref.[44].

Proposition 1

The system (21) has a forward bifurcation if the minimal value =2β(ζC+β+φ1+φ3)/φ2(β+φ3+ζC+φ1φ3) of the virus infection that causes bistability is smaller than unity.

We then conclude with the following theorem

Theorem 6

If R0C=1, then

  • (i)The model (21) undergoes a backward bifurcation whenever
  • y2>0

• .

  • (ii)The model (21) undergoes a forward bifurcation whenever
  • y2<0

• .

The bifurcation phenomenon is illustrated in Fig. 5a,b, where we have carried out a numerical simulation of the infection model (21). The system parameter values are presented in Table 2, the calculation gives y2=0.4321>0 and y1=0.0032>0 , the backward bifurcation condition is then satisfied and we obtain Fig. 5a. Also, the forward bifurcation Fig. 5b is obtained for ϰ1=α2-α. Here, the parameters we have used may not all be epidemiologically realistic (see[47]).

Graph: Figure 5 Simulation of the codynamics model (3) to illustrate the occurrence of (a) forward (b) backward bifurcation.

Stochastic configuration of codynamics of TB-COVID-19 model

We examine how random interference affects the distinctiveness and presence of a stable dispersion, as well as the gradual disappearance of diseases, in the system (2). The formula that follows is a representation of the stochastic adaptation relating to the model (2) is

27 dS=[-(ψT+ψC+β)S]dτ+1SdB1(τ),dLT=[ψTS-(β+μ+λψC+ϖ)LT]dτ+2LTdB2(τ),dIT=[μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT]dτ+3ITdB3(τ),dEC=[ψCS-(β+ϵψT+φ1+φ2)EC]dτ+4ECdB4(τ),2τ,dIC=[φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC]dτ+5ICdB5(τ),dLTC=[λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC]dτ+6LTCdB6(τ),dITC=[ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC]dτ+7ITCdB7(τ),dR=[ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηLTC+(1-(θ1+θ2))ξITC-βR]dτ+8RdB8(τ),

Graph

in which ȷ indicate the variability in noise and Bȷ(τ),(ȷ=1,...,8) are conventional one-dimensional autonomous Brownian movements. The additional parameters have the same relevance as they do in system (2).

In the sequel, let (Υ,F,{Fτ}τ0,P) be a complete probability space and its filtration {Fτ}τ0 needs to fulfill the standard requirements (that is., it must be right continuous and comprise all P -null sets), whilst Bȷ(τ),(ȷ=1,...,8) are stated on the complete probability space. In addition, take R+={Λ0},R+8={Λ=(Λ1,...,Λ8)R8:Λȷ>0,ȷ=1,...,8}. For any matrix M, its transpose is indicated by MT¯.

Utilizing Λ(τ)=(S(τ),LT(τ),IT(τ),EC(τ),IC(τ),LTC(τ),ITC(τ),R(τ))T¯ as the solution of model (28) supplemented by ICs Λ(0)=(S(0),LT(0),IT(0),EC(0),IC(0),LTC(0),ITC(0),R(0))T¯. Furthermore, we utilize z1..zκ to represent max{z1...zκ} and z...zκ to show min{z1...zκ}.

Firstly, we assert an outcome about the existence–uniqueness of a global non-negative solution for system (28).

Theorem 7

Assume that there is a unique solution Λ(τ)R+8 of structure (28) on [0,) for any starting value Λ(0)R+8. It stays in R+8 having probability 1 (a.s).

Proof

Here, we overlook the initial portion of the explanation just to display the essential Lyapunov function because it is comparable to Theorem 2.1 in[34].

Introducing a C2 -functional Φ0 on R+8R+ by

28 Φ0(Λ)=[(S--lnS)+(LT-1-lnLT)+(IT-1-lnIT)+(EC-1-lnEC)+(IC-1-lnIC)+(LTC-1-lnLTC)+(ITC-1-lnITC)+(R-1-lnR)],

Graph

where the value of the non-negative constant will be obtained hereafter. When we implement Itô's algorithm[48] to Φ0 , we obtain

29 dΦ0(Λ)=LΦ0(Λ)dτ+1(S-)dB1(τ)+2(LT-1)dB2(τ)+3(IT-1)dB3(τ)+4(EC-1)dB4(τ)+5(IC-1)dB5(τ)+6(LTC-1)dB6(τ)+7(ITC-1)dB7(τ)+8(R-1)dB8(τ),

Graph

where LΦ0:R+8R is determined by

30 LΦ0(Λ)=(1-S)[-(ψT+ψC+β)S]+212+(1-1LT)[ψTS-(β+μ+λψC+ϖ)LT]+1222+(1-1IT)[μLT+ς2ηLTC+θ2ξITC-(β+ς3+ζT+δ)IT]+1232+(1-1EC)[ψCS-(β+ϵψT+φ1+φ2)EC]+1242+(1-1IC)[φ1EC+ρηLTC+θ1ξITC-(β+ζC+ν+φ3)IC]+1252+(1-1LTC)[λψCLT+ϵψTEC-(β+ζC+ρ+η)LTC]+1262+(1-1ITC)[ρLTC+ς3IT+νIC-(β+ζTC+ξ)ITC]+1272+(1-1R)[ϖLT+φ2EC+δIT+φ3IC+(1-(ς1+ς2))ηITC+(1-(θ1+θ2))ξLTC-βR]+1282(-(ψT+ψC+β))+(β+μ+λψC+ϖ)+(β+ς3+ζT+δ)+(β+ϵψT+φ1+φ2)+(β+ζC+ν+φ3)+(β+ζC+ρ+η)+(β+ζTC+ξ)+β+12(12+22+32+42+52+62+72+82).

Graph

Letting =/ψT+ψC+β. As a result, we have

31 LΦ0(Λ)(β+μ+λψC+ϖ)+(β+ς3+ζT+δ)+(β+ϵψT+φ1+φ2)+(β+ζC+ν+φ3)+(β+ζC+ρ+η)+(β+ζTC+ξ)+β+12(ψT+ψC+β12+22+32+42+52+62+72+82):=K,

Graph

where the constant K is non-negative. According to Ref.[34], we similarly exclude the remaining portion of the explanation. The documentation is now complete.

Stationary distribution

Our primary concern with the stochastic outbreak framework is the virus's permanence. In this portion, we employ a novel method to demonstrate that structure (28) has a unique ESD, depending on the hypothesis of Khasminskii[49].

By developing appropriate Lyapunov functions, we will show adequate conditions for the development of a unique ESD. A key component of our major result's explanation is the lemma that follows.

Assume that Y(τ) is an ordinary time-homogeneous Markov phenomenon with RS . Its stochastic DE is as follows:

32 dY(τ)=b(y)(τ)+w=1sηw(Y)dBw(τ),

Graph

and the diffusion matrix is A1(ϰ)=(aȷκ(ϰ))ȷ1,sκ,aȷκ(ϰ)=w=1lηwȷ(ϰ)ηwκ(ϰ). Consider the differential operator L connected to (36) as follows:

33 L=ȷ=1sbȷ(ϰ)ϰȷ+12ȷ,κ=1sQȷκ(ϰ)2ϰȷϰκ.

Graph

Lemma 1

([49]) Let us suppose the subsequent characteristics of a bounded open region DϵRS with a regular boundary:

( H1 ): In the region DϵRS and some neighborhood therefore, the least significant eigenvalue of the diffusion matrix Q(ϰ) is bounded away from zero.

( H2 ): a positive C2 -function Φ so that LΦ is negative for all RS\Dϵ.

Then the Markov procedure Y(τ) has a stationary distribution π(.). Also, consider F(ϰ) be a mapping which is positive in regard to the measure π,ϰRS, ones obtain

34 P{limT1T0TF(Y(τ))dτ=RSF(ϰ)φ2(dϰ)}=1.

Graph

To begin with, we establish a few concepts for ease of use in later explanations. By resolving the subsequent (36) as

35 =(ψT+ψC+β+122)S~,ψTS~=(β+μ+λψC+ϖ+222)LT~,λψCLT~=(β+ζC+ρ+η+622)LTC~,ϖLT~+(1-(ς1+ς2))ηLTC~=(β+822)R,

Graph

we find

36 S~=ψT+ψC+β+122,LT~=ψT(ψT+ψC+β+122)(β+μ+λψC+ϖ+222),LTC~=λψC(ψT+ψC+β+122)(β+μ+λψC+ϖ+222)(β+ζC+ρ+η+622),R~=ϖψT(β+ζC+ρ+η+622)+(1-(ς1+ς2)η)λψC(ψT+ψC+β+122)(β+μ+λψC+ϖ+222)(β+ζC+ρ+η+622)(β+822).

Graph

Afterwards, by addressing the subsequent formula's:

37 θ2ξITC~=(β+ς3+ζT+δ+322)IT~,EC~=1,φ1EC~+θ1ξITC~=(β+ζC+ν+φ3+522)IC~,ς3IT~+νIC~=(β+ζTC+ξ+722),

Graph

which lead us

38 IT~=θ2(φ1(G1G3(G1G2-θ22ξ2ς3)-(G1G3-θ1θ2ξ2ν)(G1G2-θ22ξ2ς3)+θ1θ23ξ4ν))θ1G2F1,EC~=1,IC~=φ1G1(G1G2-n2ξ2ς3)F1,ITC~=φ1(G1G3(G1G2-θ22ξ2ς3)-(G1G3-θ1θ2ξ2ν)(G1G2-θ22ξ2ς3)+θ1θ23ξ4ν)θ1ξF1,

Graph

where G1=β+ζTC+ξ+722, G2=β+ς3+ζT+δ+ρ322, G3=β+ζC+ν+φ3+522, with

F1=(G1G3-θ1θ2ξ2ν)(G1G2-θ22ξ2ς3)-θ1θ23ξ4ν.

Graph

Introduce

39 R0S=ψCS~(β+ϵψT+φ1+φ2)+422.

Graph

Theorem 8

If we suppose that R0S>1 , then structure (28) permits a unique ESD, π(.).

Proof

It is necessary to validate assumptions (H1) and (H2) in Lemma 1 for the purpose of establishing Theorem 8.

To begin with, we create an appropriate Lyapunov function Φ and identify a closed set DϵR+8 that ensures supϰR+8\DϵLΦ(ϰ) is negative in order to ensure the efficacy of (H2) in Lemma 1.

For this, let us suppose

S~=SS¯,LT~=LTLT¯,LTC~=LTCLTC¯,R~=RR¯.

Graph

Implementing Itô's technique to -lnS, we find

40 L(-lnS)-S+(α1(IT+ITC)+α2(EC+IC+LTC+ITC)+β)+122=-S~S¯+(α1(IT+ITC)+α2(EC+IC+LTC+ITC)+β)+122=-S¯+α1(IT+ITC)+α2(EC+IC+LTC+ITC)-S¯(1S~-1).

Graph

Applying the variant lnϰϰ-1(ϰ>0), we have ln1S~1-S~S~.

Again, considering (36), we have

41 L(-lnS)-S~ln1S~+α1(IT+ITC)+α2(EC+IC+LTC+ITC)=S~lnS~+α1(IT+ITC)+α2(EC+IC+LTC+ITC).

Graph

Adopting the similar technique to -lnLT,-lnLTC, and -lnR, respectively, we have

42 L(-lnLT)ψTS~IT~lnIT-λα2L~TCL~TlnL~TC+λψCL~TlnR~,L(-lnLTC)λψCIT~LTC~lnIT~+(β+ζC+ρ+η)L~TClnL~TC-λα2βlnR~R~,L(-lnR)-ϖLT~R~lnLT~-(1-(ς1+ς2))ηLTC~R~lnLTC~-βlnR~R~.

Graph

Now, introducing a C2 -mapping Φ1 as

Φ1(Λ)=-lnS-a1lnLT-a2lnLTC-a3lnR,

Graph

so that

43 a1ψTS~LT~-a2λψCLT~LTC~-a3ϖLT~R~=0,a1λα2L~TCL~T+a2(β+ζC+ρ+η)L~TC-a3(1-(ς1+ς2))ηLTC~R~=0,-a2λα2β-a3βR~+λψCL~T=0,

Graph

where

a1=λψC2L~Tβα2ψTS~L~TC-L~T(R~L~TψC-ϖα2L~TR~L~TC)α2ψTS~R~2L~TC(λ2βψTL~TS~+L~CR~(β+ζC+ρ+η)L~TCL~TR~α2β/F2),a2=ψCL~Tα2β-λ2α2L~TCR~+R~L~C(β+ζC+ρ+η)λα2L~TL~TCβ2S~ψTR~F2,a3=λ2βψTL~TS~+L~CR~(β+ζC+ρ+η)L~TCL~TR~α2β/F2,

Graph

where F2=L~TC(1-(ς1+ς2))ηR~+λα2L~TC(L~TR~ψC-ϖα2R~L~TL~TC)ψTS~+L~T(β+ζC+ρ+η)βλα2T~TCR~.

Implementing the Itô's technique to Φ1 and considering (42)–(44), we have

44 LΦ1S~lnS~+(a1ψTS~LT~-a2λψCLT~LTC~-a3ϖLT~R~)lnLT~+(a1λα2L~TCL~T+a2(β+ζC+ρ+η)L~TC-a3(1-(ς1+ς2))ηLTC~R~)lnLTC~-(a2λα2β+a3βR~-λψCL~T)lnR~+α1(IT+ITC)+α2(EC+IC+LTC+ITC)=S~lnS~+α1(IT+ITC)+α2(IC+ITC).

Graph

Then, we describe a C2 -function Φ2 as

45 Φ2(Λ)=-lnLT-b1lnS-b2lnLTC-b3lnR,

Graph

which leads to

46 b1S~-λψCLT~LTC~=0,b2(β+ζC+ρ+η)LTC~-b3(1-(ς1+ς2))ηLTC~R~=0,b2λα2βR~-b3βR~+λψCL~T=0,

Graph

where

b1=λψCS~LT~LTC~,

Graph

b2=λψC(1-(ς1+ς2))ηL~TC2R~β(β+ζC+ρ+η)LT~R~-λα2β,b3=λψC(β+ζC+ρ+η)R~β(β+ζC+ρ+η)LT~R~-λα2β.

Graph

Implementing the Itô's technique to Φ2 and considering (45)–(47), we have

47 LΦ2(Λ)((β+ζC+ρ+η)L~TC-b3(1-(ς1+ς2))ηL~TCR~)lnLTC~+b1α1IT+α2(IC+ITC).

Graph

Furthermore, we indicate

EC~=ECEC¯,IT~=ITIT¯,IC~=ICIC¯,ITC~=ITCITC¯.

Graph

Implementing Itô's technique to -lnEC, one obtains

48 L(-lnEC)-ψCSEC+(β+ϵψT+φ1+φ2)+422-ψCSEC+(β+ϵψT+φ1+φ2)+422-ψCS~EC~(S~EC~-1)-(R0S-1)((β+ϵψT+φ1+φ2)+422)+ψCS~EC~lnEC~-ψCS~EC~lnS~,

Graph

where

R0S=ψCS~(β+ϵψT+φ1+φ2)+422.

Graph

Analogously, implementing Itô's technique to -lnIT,-lnIC and -lnITC, we find

49 L(-lnIT)μLT~I~TlnLT~-ς2ηLTC~I~TlnLTC~-θ2ξITC~I~TlnITC~+(β+ς3+ζT+δ)1I~TI~T,L(-lnIC)φ1EC~I~ClnEC~-ρηLTC~I~ClnLTC~-θ1ξITC~I~ClnITC~+(β+ζC+ν+φ3)1I~ClnI~C,L(-lnITC)ρLTC~I~TClnLTC~-ς3IT~I~TClnIT~-νIC~I~TClnIC~+(β+ζTC+ξ)1I~TClnI~TC.

Graph

Introducing

50 Φ3(Λ)=-lnEC-c1lnIT-c2lnIC-c3ITC,

Graph

which leads to

51 c1(β+ς3+ζT+δ)I~T-c3ς3I~TC-ψCS~E~C=0,c2β+ζC+ν+φ3IC~-c3νIC~I~TC=0,-c1θ2ξITC~IT~-c2θ1ξITC~IC~+c3(β+ζTC+ξ)=0,

Graph

where

c1=ψTCIT~ITC~((β+ζTC+ξ)(β+ζC+ν+φ3)-θ1ξνIC~)F3,

Graph

c2=ν(β+ς3+ζτ+δ)IC~2ς3(β+ζC+ν+ξ)IT~(ψTCIT~ITC~((β+ζTC+ξ)(β+ζC+ν+φ3)-θ1ξνIC~)F3)-νψC1S~IC2~ς3(β+ζC+ν+φ3)EC~,

Graph

c3=(β+ς3+ζT+δ)ITC~ς3IT~(ψTCIT~ITC~((β+ζTC+ξ)(β+ζC+ν+φ3)-θ1ξνIC~)F3)-ψCS~ITC~ς3.

Graph

As F3=ς3ψCS~(β+ζC+ν+φ3)-θ1ξν(β+ς3+ζT+δ)IC~ITC~EC~+(β+ζTC+ξ)(β+ς3+ζT+δ)(β+ζC+ν+φ3)EC~ITC~.

Now, considering (49)–(52), we have

52 LΦ3(Λ)=-(R0S-1)(β+ϵψT+φ1+φ2+422)+ψCS~EC~lnEC~-ψCS~EC~lnS~.

Graph

Furthermore, we describe

53 Φ4(Λ)=Φ3(Λ)+d1Φ1(Λ)+d2Φ2(Λ).

Graph

Thus, we conclude that d1=α1ψCS~2ITCL~T~(L~T+a1S~)EC~ and d2=c1α2ψCS~LTC2I~C~(λψCL~TC+b1I~TC)EC~.

In view of (45), (48) and (53), we have

54 LΦ4(Λ)-(R0S-1)(β+ϵψT+φ1+φ2+422)+α1(d1+b1d2)IT+α2(a2d1+d2)IC.

Graph

Introducing

55 Φ5(Λ)=Φ4(Λ)-α2(a2d1+d2)θ2ξIT.

Graph

Again, implementing the Itô's technique to Φ5, we have

56 LΦ5(Λ)-(R0S-1)(β+ϵψT+φ1+φ2+422)+[α1(d1+b1d2)+α2(a2d1+d2)(β+ς3+ζT+δ)θ2ξ]IT.

Graph

Introducing

57 Φ6(Λ)=-lnS-lnLT-lnEC-lnIC-lnLTC-lnITC-lnR.

Graph

Implementing the Itô's technique to Φ6, we have

58 LΦ6(Λ)-S-ψTSLT-ψCSEC-φ1ECIC-ς1ηLTCIC-θ1ξITCIC-λψCLTLTC-ϵψTECLTC-ρLTCITC-ς3ITITC-νICITC-ϖLTR-φ2ECR-δITR-φ3ICR+(ψT+ψC+7β)+(μ+λψC+ϖ+ϵψT+φ1+φ2+2ζC+ν+φ3+ρ+η+ζTC+ξ)+12(12+22+32+42+52+62+72+82).

Graph

Again, we describe

59 Φ7(Λ)=1μ+1(S+LT+IT+EC+IC+LTC+ITC+R)μ+1,

Graph

where μ(0,1) fulfilling

(β+ψT)(β+ψC)-μ2(1222324252627282)>0.

Graph

Employing the Itô's technique to Φ7, we have

60 LΦ7(Λ)=(S+LT+IT+EC+IC+LTC+ITC+R)μ×[-(β+ψT)(S+EC+IT+LT)-βIT-(β+ψC)(IC+LTC+ITC+R)-βIC]+μ2(S+LT+IT+EC+IC+LTC+ITC+R)μ-1×(12S2+22LT2+32IT2+42EC2+52IC2+62LTC2+72ITC2+82R2)(S+LT+IT+EC+IC+LTC+ITC+R)μ×[-[(β)+ψT(β+ψC)](S+LT+IT+EC+IC+LTC+ITC+R)]+μ2(S+LT+IT+EC+IC+LTC+ITC+R)μ+1×(1222324252627282)Q-μ~2(S+LT+IT+EC+IC+LTC+ITC+R)μ+1,

Graph

where

61 Q=supΛR+8{(S+LT+IT+EC+IC+LTC+ITC+R)μ-μ~2(S+LT+IT+EC+IC+LTC+ITC+R)μ+1},

Graph

and

62 μ~=(β+ψT)(β+ψC)-μ2(1222324252627282).

Graph

Here, introducing a C2 -function Φ8 on R+8R

63 Φ8(Λ)=MΦ5(Λ)+Φ6(Λ)+Φ7(Λ),

Graph

where M is a sufficiently significant non-negative constant that satisfies

64 -M(R0S-1)(β+ϵψT+φ1+φ2+422)+W-2,

Graph

and

65 W=supΛR+8{(ψT+ψC+7β)+(μ+λψC+ϖ+ϵψT+φ1+φ2+2ζC+ν+φ3+ρ+η+ζTC+ξ)+12(12+22+32+42+52+62+72+82)+Q+α1IT+α2IC-μ~2(S+LT+IT+EC+IC+LTC+ITC+R)μ+1}.

Graph

Examine that the minimal point Λ~R+8 of Φ8(Λ) appears to exist, therefore we conclude

66 Φ(Λ)=Φ8(Λ)-Φ8(Λ~).

Graph

Merging (57), (59) and (61), we have

67 LΦ(Λ)-M(R0S-1)(β+ϵψT+φ1+φ2+422)+W+M[α1(d1+b1d2)+α2(a2d1+d2)(β+ς3+ζT+δ)θ2ξ]IT-S-ψTSLT-ψCSEC-φ1ECIC-ς1ηLTCIC-θ1ξITCIC-λψCLTLTC-ϵψTECLTC-ρLTCITC-ς3ITITC-νICITC-ϖLTR-φ2ECR-δITR-φ3ICR-μ~4(S+LT+IT+EC+IC+LTC+ITC+R)μ+1.

Graph

Next, we construct the following for a bounded closed set:

68 Dϵ={ΛR+8:S[ϵ,1/ϵ],LT[ϵ3,1/ϵ3],IT[ϵ,1/ϵ],EC[ϵ2,1/ϵ2],IC[ϵ,1/ϵ],LTC[ϵ4,1/ϵ4],ITC[ϵ2,1/ϵ2],R[ϵ3,1/ϵ3]},

Graph

where ϵ is a non-negative constant that is small enough to meet the subsequent variants

69 -ψCα1ψξβϵ+F4-1,M[α1(d1+b1d2)+α2(a2d1+d2)(β+ς3+ζT+δ)θ2ξ]ϵ1,-μ~+8F4ϵμ+1-8ϵμ+1,-μ~+8F4ϵ3μ+3-8ϵ3μ+3,-μ~+8F4ϵ2μ+2-8ϵ2μ+2,-μ~+8F4ϵ4μ+4-8ϵ4μ+4,

Graph

having

70 F4=supITR+{M[α1(d1+b1d2)+α2(a2d1+d2)(β+ς3+ζT+δ)θ2ξ]IT-μ~8ITμ+1}.

Graph

For the sake of simplicity, we can split R+8\Dϵ into the subsequent sixteen regions:

71 Dϵ1={ΛR+8:S(0,ϵ]},Dϵ2={ΛR+8:LT(0,ϵ]},Dϵ3={ΛR+8:IT(0,ϵ3],S>ϵ,LT>ϵ},Dϵ4={ΛR+8:EC(0,ϵ2],S>ϵ},Dϵ5={ΛR+8:IC(0,ϵ]},Dϵ6={ΛR+8:LTC(0,ϵ4],EC>ϵ3},Dϵ7={ΛR+8:ITC(0,ϵ2],IT>ϵ},Dϵ8={ΛR+8:R(0,ϵ3],R>ϵ2},Dϵ9={ΛR+8:S1/ϵ},Dϵ10={ΛR+8:LT1/ϵ3},Dϵ11={ΛR+8:IT1/ϵ},Dϵ12={ΛR+8:EC1/ϵ2},Dϵ13={ΛR+8:IC1/ϵ},Dϵ14={ΛR+8:LTC1/ϵ4},Dϵ15={ΛR+8:ITC1/ϵ2},Dϵ16={ΛR+8:R1/ϵ3}.

Graph

Evidently, R+8\Dϵ=ȷ=116Dϵȷ. Consequently, it is easy to demonstrate that

72 LΦ(Λ)-1ΛR+8\Dϵ.

Graph

This verifies assumption (H1) of Lemma 1.

The diffusion matrix for model (28) is presented as follows:

73 Q=12S20000000022LT20000000032IT20000000042EC20000000052IC20000000062LTC20000000072ITC20000000082R2.

Graph

It is evident that, matrix Q is positive definite ΛD. This verifies assumption (H1) of Lemma 1. Thus, the model (28) has a unique stationary distribution π(.) and ergodic. This puts the proof to its conclusion.

Remark 2

For system (28), if R0>1, the illness always endures. According to Theorem 8, if R0S>1 , the sickness will continue in the stochastic framework (28). In particular, in the absence of noise, that is, κ=0,(κ=1,...,8). Observe that S¯=ψT+ψC+βS¯=ψC+β.

Next, the equation is S¯=S10. On the same instance, obtaining

74 R0S=α2R0T(R0T(ζC+φ1+φ3)-K8/2+R0T(R0TK82+4μα1)/2)(R0T(R0TK82+4μα1)/2+(φ1+φ3)R0T-K8R0T/2)(R0T(R0TK82+4μα1)/2+(ζC+φ3)R0T-K8R0T/2)>1.

Graph

Stochastic COVID-19 model without TB infection

By utilizing the identical technique from probabilistic framework (28) to incorporate random perturbation, we obtain the subsequent stochastic model:

75 dS=[-α2N1(EC+IC)-βS]dτ+4ȷ-3SdB4ȷ-3(τ),dEC=[α2N1(EC+IC)-(β+φ1+φ2)EC]dτ+4ȷ-2ECdB4ȷ-2(τ),dIC=[φ1EC-(β+ζC+φ3)IC]dτ+4ȷ-1ICdB4ȷ-1(τ),dR=[φ2EC+φ3IC-βR]dτ+4ȷRdB4ȷ(τ).

Graph

Then, we state

Rȷκ=α2βϑ3ϑ3ϑ2(ϑ4ϑ1-φ2φ3).

Graph

The values of the parameters have similar significance within the system (75). Indicate

76 ϑ1=β+4ȷ-322,ϑ2=(β+φ2+φ1)+4ȷ-222,ϑ3=(β+ζC+φ3)+4ȷ-122,ϑ4=β+4ȷ-322.

Graph

The two theorems that proceed are derived from "Codynamics model and preliminaries" and "Stochastic configuration of codynamics of TB-COVID-19 model" section using a similar methodology.

Theorem 9

Suppose there are initial values (S(0),EC(0),IC(0),R(0))R+4 have unique solution (S(τ),EC(τ),IC(τ),R(τ))R+4 of the model (75) with τ>0 and the solution will exist in R+4 having probability 1 (a.s).

Theorem 10

Suppose that Rȷκ>1, then model (75) possesses the ergodic functionality and yields a unique stationary distribution π(.).

Probability density function (P.D.F)

In what follows, we present a mathematical principle pertaining to the P.D.F associated with the subsequent probabilistic framework as:

77 dΛ(τ)=c^(Λ,τ)dτ+d^(Λ,τ)dQ(τ),

Graph

where Λ indicates the parameter whilst c^(Λ,τ),d^(Λ,τ) are some functions and Q(τ) is the Wiener technique.

Lemma 2

([50]) Suppose there is a mapping p~(Λ) states the P.D.F associated to the formula (77):

τp~(Λ,τ|Λ0,τ0)=-Λ[c^(Λ,τ)p~(Λ,τ|Λ0,τ0)]+12Λ2(d^(Λ,τ)2p~(Λ,τ|Λ0,τ0)).

Graph

Following that, we provide the prerequisites required to find the positive definite (P-D) 4D real symmetric matrix.

Lemma 3

Assume that there is a 4D real algebraic equation Ξ02+QΥ+ΥQT=0 having Ξ0=diag(1,0,0,0), while Υ indicates the real symmetric matrix.

• If

  • Q=-ϑ1ϑ2-ϑ3-ϑ4100001000010,

Graph

  • containing with ϑ1>0,ϑ3>0,ϑ4>0 and ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4>0, then
  • 78 Υ=ϑ2ϑ3-ϑ1ϑ42(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)0-ϑ32(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)00ϑ32(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)0-ϑ12(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)-ϑ32(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)0ϑ12(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)00-ϑ12(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)0-ϑ1ϑ2-ϑ32(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)

Graph

  • is a P-D.

• If

  • Q=-ϑ1ϑ2-ϑ3ϑ410000100001ϑ5,

Graph

  • containing ϑ1>0,ϑ3>0 and ϑ1ϑ2-ϑ3>0, then
  • 79 Υ=ϑ22(ϑ1ϑ2-ϑ3)0-12(ϑ1ϑ2-ϑ3)0012(ϑ1ϑ2-ϑ3)00-12(ϑ1ϑ2-ϑ3)0ϑ12ϑ3(ϑ1ϑ2-ϑ3)00000,

Graph

  • is a semi P-D matrix.

• If

  • Q=-ϑ1ϑ2ϑ3ϑ4100000ϑ5ϑ600ϑ7ϑ8,

Graph

  • containing ϑ1>0 and ϑ2>0, then
  • 80 Υ=(2ϑ1)-10000(2ϑ1ϑ2)-10000000000,

Graph

  • is a semi P-D matrix.
Proof

Indicate the -th significant main component of Υ is Υ(), which is expressed as

  • Observe that ϑ1(ϑ2ϑ3-ϑ1ϑ4)>ϑ32>0, then
  • Υ(k)=ϑ2ϑ3-ϑ1ϑ42(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)>0,k=1ϑ3(ϑ2ϑ3-ϑ1ϑ4)4(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)2>0,k=2ϑ38(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)2>0,k=3116(ϑ1ϑ2ϑ3-ϑ32-ϑ12ϑ4)2>0,k=4.

Graph

  • Furthermore, assertions (ii) and (iii) can be obtained in the same way.

Here, the precise representation of the density function of system (75) at a quasi-equilibrium point will be derived. In relation to analytical importance, it is important to note that the P.D.F can represent the majority of the unpredictable features of a probabilistic process.

Initially, we apply an analogous change to illustrate (75). For this, consider ζ4ȷ-3=lnS,ζ4ȷ-2=lnEC,ζ4ȷ-1=lnIC and ζ4ȷ=lnR. Thus, system (75)'s corresponding expression is provided by

81 dζ4ȷ-3=[e-(4ȷ-3)-α2(e4ȷ-2e-(4ȷ-3)-e4ȷ-1e-(4ȷ-3))-ϑ1]dτ+4ȷ-3dB4ȷ-3(τ),dζ4ȷ-2=[α2(ϑ2-e4ȷ-1e-(4ȷ-2))-ϑ2]dτ+4ȷ-2dB4ȷ-2(τ),dζ4ȷ-1=[φ1e4ȷ-2e-(4ȷ-1)-ϑ3]dτ+4ȷ-2dB4ȷ-2(τ),dζ4ȷ=[φ2e(4ȷ-1)e-4ȷ+φ3e(4ȷ-1)e-4ȷ-ϑ4]dτ+4ȷdB4ȷ(τ),

Graph

When R0κ>1, we illustrate a quasi steady state Uȷ=(Sȷ,ECȷ,ICȷ,Rȷ), where

82 Sȷ=ϑ2ϑ3α2,ECȷ=ϑ3ITȷα2,ITȷ=ϑ2(R0κ-1)(ϑ2ϑ4-φ2φ3)α2ϑ4(β+φ2+φ1+4ȷ-222)-φ2φ3,Rȷ=φ2ECȷ+φ3ICȷϑ4.

Graph

Assume that g=ζ-ζ,(=1,...,8). Thus, system (81) can be expressed as

83 dg4ȷ-3=(-χ11g4ȷ-3+χ12g4ȷ-2-χ13g4ȷ-1-χ14g4ȷ)dτ+4ȷ-3dB4ȷ-3(τ),dg4ȷ-2=(χ22g4ȷ-3+χ22g4ȷ-2-χ22g4ȷ-1)dτ+4ȷ-2dB4ȷ-2(τ),dg4ȷ-1=(χ33g4ȷ-2-χ33g4ȷ-2)dτ+4ȷ-1dB4ȷ-1(τ),dg4ȷ=(χ41g4ȷ-3+χ42g4ȷ-2-(χ41+χ42)g4ȷ)dτ+4ȷdB4ȷ(τ),

Graph

where χ11=-α2(ECȷ+ICȷ)Sȷ,χ12=α2ECȷSȷ,χ13=α2ICȷSȷ,χ14=ϑ1Sȷ,χ22=α2ECȷECȷ,χ33=φ1ECȷICȷ,χ41=φ2ECȷRȷ,χ42=φ3ICȷRȷ.

Furthermore, χ11=ϑ1χ22+χ13=χ33ϑ2=ϑ3 and χ44=ϑ4.

Define Ψ(τ)=(g4ȷ-3(τ)....g4ȷ(τ)) and Q(τ)=(Q4ȷ-3(τ)....Q4ȷ(τ)), we have

dΨ(τ)=QΨ(τ)dτ+ΞdQ(τ),

Graph

where

84 Q=-χ11χ12-χ13χ14χ22-χ22χ2200χ33-χ330χ41χ420-(χ14+χ42),andΞ=4ȷ-300004ȷ-200004ȷ-100004ȷ.

Graph

Next, we confirm that the real components of each of Q 's eigenvalues are negative. The characteristic polynomial of Q that corresponds to it is χQ(υ)=a~4+a~3ψ1+a~2ψ12+a~1ψ13+ψ14, where

85 a~1=χ11+χ22+χ33+χ41+χ42>0,a~2=(χ11-χ12)χ22+(χ11-χ14)χ41+(χ33+χ42)χ11+(χ22+χ33)(χ41+χ42)>0,a~3=(χ13-χ12)χ22χ33+(χ11-χ12-χ14)(χ41+χ42)χ22+(χ11-χ14)χ33χ41+χ11χ33χ42>0,a~4=((χ13-χ12-χ14)(χ41+χ42)+χ14χ41)χ22χ33.

Graph

Following that, if R0κ>1, then

86 χ13-χ12=(1-α2β+φ2+φ1+4ȷ-222)α2IC>0.(χ13-χ12-χ14)(χ41+χ42)+χ14χ41=(S-ϑ1)+φ2φ3=ϑ1ϑ4(R0κ-1)>0.a~1a~2χ33[(χ11-χ12)χ22+(χ11-χ14)χ41+χ11χ42]+χ11χ22(χ41+χ42)a~3+a~1(a~2a~3-a~1a~4)a~1{[(χ11(χ41+χ42))+χ22(χ11-χ12+χ41+χ42)-χ14χ41]χ22(χ11-χ12-χ14)(χ41+χ42)+[χ11(χ22+χ33+χ41+χ42)+χ33(χ41+χ42)-χ12χ22-χ14χ41]χ33(χ11-χ14)(χ41+χ42)+χ14χ33χ42a~2}[χ22(χ41+χ42)(χ11-χ12-χ14)+(χ13-χ12)χ22χ33+(χ11-χ14)χ33χ41+χ11χ33χ42]×χ22(χ11-χ12-χ14)(χ41+χ42)+[(χ11-χ12-χ14)(χ41+χ42)χ22+(χ13-χ12)χ22χ33+(χ11-χ14)χ33χ41+χ11χ33χ42](χ13-χ12)χ22χ33+[(χ11-χ12-χ14)(χ41+χ42)χ22+(χ13-χ12)χ22χ33+(χ11-χ41)χ33χ41+χ11χ33χ42]χ33(χ11-χ14)(χ41+χ42)+χ14χ33χ42a~1a~2>a~32.

Graph

Thus, a~ȷ>0,(ȷ=1,...,4)(a~1a~2-a~3)>0 and a~1a~2a~3-a~32-a~12a~4>0. Subsequently it appears that A possesses every negative real-part eigenvalues that correspond to the Routh-Hurwitz stability condition[51].

With reference to Lemma 2, the Fokker–Planck equation below is satisfied by the relevant P.D.F U(Ψ) to the Quasi-stationary condition of the system (81) can be expressed as

ȷ=12(4ȷ-3222Ug4ȷ-32+4ȷ-2222Ug4ȷ-22+4ȷ-1222Ug4ȷ-12+4ȷ222Ug4ȷ2)=ȷ=12{g4ȷ-3(χ14g4ȷ-χ13g4ȷ-1-χ11g4ȷ-3)U+g4ȷ-2(χ22g4ȷ-3-χ22g4ȷ-2+χ22g4ȷ-1)U+g4ȷ-1(χ33g4ȷ-2-χ33g4ȷ-2)U+g4ȷ(χ41g4ȷ-3+χ42g4ȷ-2-(χ41+χ42)g4ȷ)U}.

Graph

Given that Ξ is an invariant matrix, one can determine that U(Ψ) is potentially identified as having a Gaussian distribution by incorporating the pertinent findings of Roozen[52]:

U(Ψ)=c~exp(-12ΨTMΨ),

Graph

where c~ justifying R+4c~exp(-12ΨTMΨ)dΨ=1 and M=(θ1ȷκ)4×4 is a real symmetric matrix fulfilling

87 MΞ2M+MQ+QTM=0.

Graph

If M-1 holds, we indicate Π=M-1, M can be found to possess the equivalent degree of positive definiteness. Following this, (87) has the structure that follows.

88 Ξ2+QΠ+ΠQT=0.

Graph

The mathematical structure of (88) is obtained by employing a finitely autonomous coherence theory, which gives us Ξ==14Ξ and Π==14, then we have

Ξ2+QΠ+ΠQT=0,=1,...,4,

Graph

where

Ξ1=4ȷ-32000000000000000,Ξ2=000004ȷ-220000000000,Ξ3=00000000004ȷ-1200000,Ξ4=0000000000000004ȷ2,

Graph

and Π are decided upon thereafter.

Taking into account g=υ-υ and the transformation between the frameworks (75) and (81) yields the following:

U(Ψ~)=14φ22|Π|-1/2exp(-12Ψ~Π-1Ψ~T),

Graph

where Ψ~=(lnSS,lnECEC,lnICIC,lnRR).

Theorem 11

Surmising that R0κ>1, for any (S(0),EC(0),IC(0),R(0))R+4, then the solution (S(τ),EC(τ),IC(τ),R(τ))R+4 model (75) possess a log-normal P.D.F U(Ψ~) about Uȷ as follows Ψ~=(lnSS,lnECEC,lnICIC,lnRR) having Π=Π,(=1,...,4) is a positive definite matrix and the components Π1,Π2,Π3 and Π4 are described as

89 Π1=(χ22χ33χ414ȷ-3)2(U1H1)-1Υ1[(U1H1)-1]T,ifϖ1=0,(χ22χ334ȷ-3)2(U2H2H1)-1Υ2[(U2H2H1)-1]T,ifϖ10,ϖ2=0,(χ22χ33ϖ24ȷ-3)2(U3H2H1)-1Υ1[(U3H2H1)-1]T,ifϖ10,ϖ20,Π2=(χ124ȷ-2)2(U4H3)-1Υ3[(U4H3)-1]T,ifϖ3=0,ϖ4=0,(χ14χ33ϖ34ȷ-2)2(U5H3)-1Υ1[(U5H3)-1]T,ifϖ30,ϖ4=0,(χ13χ42ϖ44ȷ-2)2(U6H4H3)-1Υ1[(U6H4H3)-1]T,ifϖ3=0,ϖ40,ϖ30,ϖ4=0,(χ12ϖ44ȷ-2)2(U7H5H3)-1Υ4[(U7H5H3)-1]T,ifϖ30,ϖ40,ϖ5=0,(χ12ϖ4ϖ54ȷ-2)2(U8H5H3)-1Υ1[(U8H5H3)-1]T,ifϖ30,ϖ40,ϖ50,Π3=(χ134ȷ-1)2(U9H6)-1Υ5[(U9H6)-1]Tifϖ6=0,(χ13χ42ϖ64ȷ-1)2(U10H6)-1Υ1[(U10H6)-1]Tifϖ60,Π4=(χ14χ22χ334ȷ)2(U11H7)-1Υ1[(U11H7)-1]T,

Graph

where

90 ϖ1=(χ22-χ41)(χ41+χ42)/χ22,ϖ2=ϖ1-χ41-(χ41+χ42)ϖ1/χ33,ϖ3=(χ41χ122-χ14χ422+χ11χ12χ42+χ31χ33χ42-χ12χ42(χ41+χ42))/χ122,ϖ4=χ33(χ11χ12-χ12χ33+χ13χ33-χ14χ42)/χ122,ϖ5=-χ14χ33/χ12+ϖ4λ3/ϖ3-χ13χ42ϖ42/χ12ϖ32,ϖ6=(χ132-χ12χ22-χ11χ13+χ13χ22)χ22/χ132,λ3=(χ13-χ12)χ22χ33-χ14χ33χ41+χ14(χ41-χ22)(χ41+χ42),

Graph

and the matrices Uς1,(ς1-1,...,11),Hς2,(ς2=1,...,7) and ϖs,(s=1,...,5) are illustrated in the subsequent result.

Proof

Case A: Considering

91 Ξ12+QΠ1+Π1QT=0.

Graph

In view of the elimination matrix H1 as

H1=1000010000100-χ41/χ2201.

Graph

Consequently, we get

Q1=H1QH1-1=-χ11χ12χ22+χ41χ41/χ22-χ13χ14χ22-χ22χ2200χ33-χ3300ϖ1-χ41-(χ41+χ42),

Graph

where ϖ1=(χ22-χ41)(χ41+χ42)/χ22.

The subsequent sub-stages are then taken out of the appropriate evaluation.

Subphase AI Choose ϖ1=1 and N=(0,0,0,1), then there is U1Q1U1-1=Q1, where U1=(NQ13,NQ12,NQ1,N)T and

Q1=-a1~-a2~-a3~-a4~100001000010.

Graph

Consequently, it is possible to write the appropriate formula of (91) as

(U1H1)Ξ12(U1H1)T+Q1((U1H1)Π1(U1H1)T)+((U1H1)Π1(U1H1)T)Q1T=0.

Graph

By making the use of Lemma 3, we determine (U1H1)Π1(U1H1)T=(χ22χ33χ414ȷ-3)2Υ1, where

Υ1=a~2a~3-a~1a~42(a~1a~2a~3-a~32-a~12a~4)0-a~32(a~1a~2a~3-a~32-a~12a~4)00a~32(a~1a~2a~3-a~32-a~12a~4)0-a~12(a~1a~2a~3-a~32-a~12a~4)-a~32(a~1a~2a~3-a~32-a~12a~4)0a~312(a~1a~2a~3-a~32-a~12a~4)00-a~12(a~1a~2a~3-a~32-a~12a~4)0-a~1a~2-a~32(a~1a~2a~3-a~32-a~12a~4),

Graph

is a P-D symmetric matrix. Therefore, Π1=(χ22χ33χ414ȷ-3)2(U1H1)-1Υ1((U1H1)-1)T is also a P-D matrix.

Subcase AII Taking ϖ10 and also suppose that Q2=H2Q1H2-1, where

H2=10000100001000-ϖ1χ331,andQ2=H2Q1H2-1=-χ11χ12χ22+χ14χ41χ22χ14χ41-χ13χ22χ33χ22χ33χ14χ22-χ22χ2200χ33-χ33000ϖ2-(χ41+χ42),

Graph

containing ϖ2=ϖ1-χ41-(χ41+χ42)ϖ1/χ33.

Subcase AIII Taking ϖ10 and ϖ2=0. Moreover, suppose that Q2=U2Q2U2-1, where

U2=χ22χ33-χ33(χ22+χ33)χ332+χ22χ3300χ33-χ33000100001,andQ2=-λ1-λ2-λ3χ14χ22χ3310000100000-(χ41+χ42),

Graph

containing λ2=χ11+χ22+χ33>0,λ2=(χ11-χ12)χ22+χ11χ33-χ14χ41>0 and λ3=(χ13-χ12)χ22χ33-χ14χ33χ41+χ14(χ41-χ22)(χ41+χ42)>0. Hence, we get

(U2H2H1)Ξ12(U2H2H1)T+Q2((U2H2H1)Π1(U2H2H1)T)+((U2H2H1)Π1(U2H2H1)T)Q2T=0.

Graph

By making the use of Lemma 3, we determine (U2H2H1)Π1(U2H2H1)T=(χ22χ33χ414ȷ-3)2Υ2, where

Υ2=λ22(λ1λ2-λ3)0-12(λ1λ2-λ3)0012(λ1λ2-λ3)00-12(λ1λ2-λ3)0λ12(λ1λ2-λ3)00000,

Graph

is a symmetric, semi P-D matrix. Thus, Π1=(χ22χ334ȷ-3)2(U2H2H1)-1Υ2((U2H2H1)-1)T.

Subcase AIV Taking ϖ10 and ϖ20, employing the analogous technique as we did in Subcasee AI. Suppose that U3=(NQ23,NQ22,NQ2,N)T so that U3Q2U3-1=Q1. Hence, we have (U3H2H1)Ξ12(U3H2H1)T+Q2((U3H2H1)Π1(U3H2H1)T)+((U3H2H1)Π1(U3H2H1)T)Q3T=0, where (U3H2H1)Π1(U3H2H1)T=(χ22χ33ϖ24ȷ-3)2Υ1. Thus, we conclude that Π1=(χ22χ33ϖ24ȷ-3)2(U3H2H1)-1Υ1((U3H2H1))T is a P-D matrix.

Case B Considering

Ξ22+QΠ2+Π2QT=0.

Graph

Assume that H3QH3=Q3, where

H3=01001000-χ42/χ12001-χ33/χ12010,Q3=-χ22χ12χ22+χ22χ33/χ120χ22χ12-(χ11χ12+χ13χ33+χ14χ42/χ12)χ14-χ130ϖ3-(χ12χ41+χ12χ42+χ14χ42/χ12)χ13χ42/χ120ϖ4-χ14χ23/χ12χ13χ33-χ33χ12/χ12,,

Graph

where ϖ3=(χ41χ122-χ14χ422+χ11χ12χ42+χ13χ33χ42-χ12χ42(χ41+χ42)/χ122) and ϖ4=χ33(χ11χ12-χ12χ33+χ13χ33-χ14χ42/χ122).

Subcase BI When ϖ3=0=ϖ4 and suppose that Q3=U4Q3U4-1, where

U4=χ12-(χ11χ12+χ13χ33+χ14χ42/χ12)χ14-χ13010000100001,Q3=-λ4-λ5-λ6-λ7100000-(χ12(χ41+χ42)+χ14χ42/χ12)χ13χ42/χ1200-χ14χ33/χ12χ13χ33-χ33χ12/χ12,

Graph

containing λ4=(χ11χ12+χ12χ22+χ13χ33-χ14χ42/χ12)>0, λ5=((χ11-χ12)χ12χ22+(χ13-χ12)χ22χ33-χ14χ42χ22/χ12)>0, λ6=((χ13-χ12)χ12χ23+(χ23-χ12)χ22χ31-χ14χ42χ23/χ12)>0, and λ7=((χ33-χ12)χ12χ13+(χ42-χ12)χ22χ13-χ14χ42χ14/χ12)>0.

In this way, we have

(U4H3)Ξ22(U4H3)T+Q3((U4H3)Π2(U4H3)T)+((U4H3)Π2(U4H3)T)Q3T.

Graph

Taking into account Lemma 3, we have (U4H3)Π2(U4H3)T is a semi P-D matrix and

(U4H3)Π2(U4H3)T=(χ124ȷ-2)2Υ3Υ3=(2λ4)-10000(2λ4λ5)-10000000000.

Graph

Finally, Π2=(χ124ȷ-2)2(U4H3)-1Υ3((U4H3)-1)T.

Subcase BII When ϖ30 and ϖ4=0, applying the analogous approach as we did in the Subcase AI, then we attain U5=(NQ33,NQ32,NQ3,N)T so that U5Q3U5-1=Q1. hence, we get

(U5H3)Ξ22(U5H3)T+Q1((U5H3)Π2(U5H3)T)+((U5H3)Π2(U5H3)T)Q1T,

Graph

where (U5H3)Π2(U5H3)T=(χ14χ33ϖ34ȷ-2)2Υ1. Thus,

92 Π2=(χ14χ33ϖ34ȷ-2)2(U5H3)-1Υ1((U5H3)-1)T,

Graph

is a P-D matrix.

Subcase BIII When ϖ3=0 and ϖ40 and suppose that Q4=H4Q3H4-1, where

H4=1000010000010010,Q4=-χ22χ12χ22+χ22χ33/χ12χ220χ12-(χ11χ12+χ13χ33+χ14χ42/χ12)-χ13χ140ϖ4χ13χ33-χ33χ12/χ12-χ14χ33/χ1200χ13χ42/χ12-(χ12(χ41+χ42)+χ14χ42/χ12).

Graph

Furthermore, we have U6=(NQ43,NQ42,NQ4,N)T so that U6Q4U6-1=Q1. Hence, we get

(U6H4H3)Ξ22(U6H4H3)T+Q1((U6H4H3)Π2(U6H4H3)+((U6H4H3)Π2(U6H4H3)T)Q1T,

Graph

where (U6H4H3)Π2(U6H4H3)T=(χ13χ42ϖ44ȷ-2)2Υ1. Thus,

Π2=(χ13χ42ϖ44ȷ-2)2(U6H4H3)-1Υ1((U6H4H3)-1)T,

Graph

is a P-D matrix.

Subcase BIV When ϖ3=ϖ40 and suppose that Q5=H5Q3H5-1, where

H5=10000100001000-ϖ4/ϖ31,Q5=-χ22χ12χ22+χ22χ33/χ12χ22ϖ4/ϖ3χ22χ12-(χ11χ12+χ13χ33+χ14χ42/χ12)χ14-χ13ϖ4/ϖ3-χ130ϖ4-λ8χ13χ42/χ1200ϖ5ϖ3(χ13χ33-χ33χ12)-χ13χ32ϖ4ϖ3χ12.

Graph

Furthermore, we have U6=(NQ43,NQ42,NQ4,N)T so that U6Q4U6-1=Q1. Hence, we get

(U6H4H3)Ξ22(U6H4H3)T+Q1((U6H4H3)Π2(U6H4H3)+((U6H4H3)Π2(U6H4H3)T)Q1T,

Graph

where (U6H4H3)Π2(U6H4H3)T=(χ13χ42ϖ44ȷ-2)2Υ1. Thus,

Π2=(χ13χ42ϖ44ȷ-2)2(U6H4H3)-1Υ1((U6H4H3)-1)T,

Graph

is a P-D matrix.

Subcase BV When ϖ3=ϖ40 and ϖ5=0, applying the identical technique from Subcase AIII), we obtain U7Q5U7-1=Q4, where

U7=χ12ϖ4-λ9λ1000ϖ4-λ8000100001,,Q4=-λ11-λ12-λ13λ14100λ150110λ16000λ17,

Graph

having

λ9=(χ12χ11+χ13χ33-χ14χ42χ12+λ8),λ10=λ82+(ϖ3χ14+χ13ϖ4ϖ3)ϖ4,λ11={(χ11χ41χ122+χ12χ42χ112-χ11χ14χ422+χ22χ41χ122-χ14χ22χ422+(χ41χ122-χ14χ422-χ12χ22χ42)(χ41+χ42)-χ12χ42(χ41+χ42)2+χ11χ12χ22χ42+χ11χ13χ33χ41+χ13χ22χ33χ42+χ13χ332χ42)χ122/ϖ3}>0,λ12={χ132χ332χ41-χ122χ412χ14+χ142χ422χ41-χ123χ22χ41-χ11χ122χ22χ42+χ11χ122χ22χ41+χ112χ12χ22χ42-χ11χ14χ22χ422+χ12χ14χ22χ422+χ11χ122χ41(χ41+χ42)-χ122χ22χ33χ41-χ11χ12χ42(χ41+χ42)2+χ112χ12χ42(χ41+χ42)-χ13χ22χ42χ332-χ11χ14χ422(χ41+χ42)+χ14χ22χ33χ422+χ122χ22χ42(χ41+χ42)+χ122χ22χ41(χ41+χ42)-χ12χ22χ42(χ41+χ42)2-χ14χ22χ422(χ41+χ42)-χ13χ33χ42(χ41+χ42)2+χ11χ12χ13χ33χ41-χ11χ12χ14χ42χ41-χ11χ12χ22χ33χ42+χ11χ13χ22χ33χ42-χ12χ13χ22χ33χ42+χ12χ13χ22χ33χ41-χ12χ13χ33χ33χ41+χ11χ13χ33χ42(χ41+χ42)+χ12χ13χ33χ41(χ41+χ42)-2χ13χ14χ33χ41χ42+χ13χ22χ33χ33χ42+χ12χ14χ41χ42(χ41+χ42)+χ12χ22χ33χ42(χ41+χ42)+χ13χ33χ33χ42(χ41+χ42)χ122/ϖ3}>0,λ13=-{(χ112χ22χ12χ33χ42-χ112χ22χ12χ42(χ41+χ42)+χ122χ11χ22χ33χ41-χ122χ11χ22χ41(χ41+χ42)+χ122χ11χ22χ42(χ41+χ42)-χ22χ11χ12χ13χ33χ41-χ22χ11χ12χ13χ33χ42+χ22χ11χ12χ14χ41χ42+χ22χ11χ12χ14χ422-χ22χ33χ11χ12χ33χ42+χ22χ11χ12χ13χ42(χ41+χ42)2+χ22χ11χ13χ332χ42-χ22χ11χ13χ33χ42(χ41+χ42)-χ22χ11χ14χ33χ422+χ22χ11χ14χ422(χ41+χ42)+χ22χ123χ41(χ41+χ42)+χ22χ122χ14χ412+χ22χ14χ41χ42χ122+χ22χ122χ33χ41(χ41+χ42)-χ22χ33χ122χ33χ41-χ22χ42χ122(χ41+χ42)2+χ22χ12χ13χ41χ332-χ22χ12χ13χ33χ41(χ41+χ42)+χ22χ33χ12χ13χ33χ41+χ22χ12χ13χ33χ42(χ41+χ42)+χ22χ33χ12χ13χ33χ42-χ22χ12χ14χ41χ42(χ41+χ42)-2χ22χ12χ14χ422(χ41+χ42)-χ22χ12χ33χ42(χ41+χ42)2+χ22χ13χ33χ42(χ41+χ42)2-χ22χ33χ13χ33χ42(χ41+χ42)-χ22χ41χ22χ144χ422χ423-χ22χ14χ33χ422(χ41+χ42)+χ22χ33χ14χ33χ422)χ122/ϖ3}>0.

Graph

Moreover, λ13-λ11λ12<0,λ14,λ15,λ16 and λ17 will be determined later.

Then, we obtain

(U7H5H3)Ξ22(U7H5H3)T+Q4((U7H5H3)Π2(U7H5H3)+((U7H5H3)Π2(U7H5H3)T)Q4T=0,

Graph

where (U7H5H3)Π2(U7H5H3)T=(χ12ϖ44ȷ-2)2Υ4 and

Υ4=(λ12/2(λ11λ12-λ13))0-(1/2(λ11λ12-λ13))00(1/2(λ11λ12-λ13))00-(1/2(λ11λ12-λ13))0(λ11/2(λ11λ12-λ13))00000.

Graph

Therefore, Π2=(χ12ϖ44ȷ-2)2(U7H5H3)-1Υ4((U7H5H3)-1)T.

Subcase BVI If ϖ3=ϖ4=ϖ50 and applying the analogous approach as we did in Subcase AIV. Assume that U8=(NQ53,NQ52,NQ5,N)T so that U8Q5Q8-1=Q1. Hence, we have

(U8H5H3)Ξ22(U8H5H3)T+Q1((U8H5H3)Π2(U8H5H3)+((U8H5H3)Π2(U8H5H3)T)Q1T=0,

Graph

where (U8H5H3)Π2(U8H5H3)T=(χ12ϖ4ϖ54ȷ-2)2Υ1=0. Therefore, Π2=(χ12ϖ4ϖ54ȷ-2)2(U8H5H3)-1Υ1((U8H5H3)-1)T is a P-D matrix.

Case C Surmise that Ξ32+QΠ3+Π3QT=0.

Assume that Q6=H6QH6-1, where

H6=00101000χ22/χ131000001,andQ6=-χ33-χ22χ33/χ13χ330-χ13-(χ11χ13+χ12χ22/χ13)χ12χ140ϖ6(χ12χ22-χ22χ12/χ13)χ14χ22/χ1300χ42-(χ41+χ42),

Graph

having ϖ6=(χ132-χ12χ22-χ11χ13+χ13χ22)χ22/χ132.

Subcase CI When ϖ6=0, employing the identical approach as we applied in Subcase AIII and consider that Q5=U9Q6U9-1, where

93 U9=-χ13-(χ11χ13+χ12χ22/χ13)χ12χ14010000100001,andQ5=-λ18-λ19-λ20-λ22100000(χ12χ22-χ22χ13/χ13)χ14χ22/χ1300χ42-(χ41+χ42),

Graph

containing λ18=(χ11χ13+χ12χ22+χ13χ33)/χ13,λ19=(χ11χ13χ33+χ12χ22χ33-χ13χ33χ22)/χ13,λ20 and λ22 will be computed later.

Thus, we find

(U9H6)Ξ32(U9H6)T+Q5((U9H6)Π3(U9H6)T)+((U9H6)Π3(U9H6)T)Q5T=0.

Graph

Using the fact of Lemma 3, we have (U9H6)Π3(U9H6)T=(χ134ȷ-1)2Υ5, where

Υ5=(2λ18)-10000(2λ18λ19)-10000000000.

Graph

Consequently, Π3=(χ134ȷ-1)2(U9H6)-1Υ5((U9H6)-1)T.

Subcase CII When ϖ60, then applying Subcase AI with a similar technique, resulting in U10=(NQ63,NQ62,NQ6,N)T so that U10Q6U10-1=Q1, which leads to

(U10H6)Ξ32(U10H6)T+Q1((U10H6)Π3(U10H6)T)+((U10H6)Π3(U10H6)T)Q1T=0,

Graph

where

((U10H6)Π3(U10H6)T)Π3((U10H6)Π3(U10H6)T)T=(χ13χ42ϖ64ȷ-1)2Υ1.

Graph

Hence, we conclude that Π3=(χ13χ42ϖ64ȷ-1)2(U10H6)-1Υ1((U10H6)-1)T is a P-D matrix.

Case D Considering Ξ42+QΠ4+Π4QT=0, and also, we have Q7=H7QH7-1, where

H7=0001100001000010,Q7=-(χ41+χ42)χ41χ420χ41-χ11χ12-χ130χ22-χ22χ2200χ33-χ33.

Graph

Indicate U11=(NQ73,NQ72,NQ7,N)T so that U11Q7U11-1=Q1. Thus, we get

(U11H7)Ξ42(U11H7)T+B1((U11H7)Π4(U11H7)T)+((U11H7)Π4(U11H7)T)Q1T=0,

Graph

where

(U11H7)Π4((U11H7))T=(χ14χ22χ334ȷ)2Υ1.

Graph

This concludes that Π4=(χ14χ22χ334ȷ)2(U11H7)-1Υ1((U11H7)-1)T is a P-D matrix. Finally, the expression Π=Π,(=1,...,4) is a P-D matrix. So, the solution (S(τ),EC(τ),IC(τ),R(τ)) of model (75) possess a log-normal P.D.F U(Ψ~) about Uȷ as

U(Ψ~)=14φ22|Π|-1/2exp(-12Ψ~Π-1Ψ~T).

Graph

This yields the intended result.

Numerical solutions of co-dynamics model using random perturbations

The computation methods of stochastic perturbations influence whenever differentiating expressions involve fractional differential compositions involving singular or nonsingular kernels, and classical prescriptions include this component. The fractional notions have an order corresponding to 0 and 1.

Caputo fractional derivative operator

The main objective of this study is to investigate the co-infection of the TB and COVID-19 models involving integer-order (2), power-law (3) and stochastic strategy for (28). This scheme incorporates substantial pulmonary inflammation, which makes the circulatory mechanism a key battleground for numerous ailments. In the situation where is chosen as the final propagation period, the mathematical framework will be built using the classical-order expression in the beginning, the power-law memory considered in the next step, and the stochastic configuration in the stages that follow. After the fact that the subsequent number pattern is provided to explain the incidence.

Specifically, we analyze the sectionally divided frameworks (2), (3) and (28) quantitatively by using the procedure given in[29] in the context of CFD. In order to outline the procedure, we conducted what follows:

dι(τ)dτ=ϝ(τ,ι).ι(0)=ι,0,ι=1,2,...,nifτ[0,1],1cDτωι(τ)=ϝ(τ,ι),ι(1)=ι,1,ifτ[1,2],dι(τ)=ϝ(τ,ι)dτ+ιιdBι(τ),ι(2)=ι,2,ifτ[2,].

Graph

Thus, it implies that

ιv=ι(0)+κ=2v{2312ϝ(τκ,κ)Δτ-43ϝ(τκ-1,κ-1)Δτ+712ϝ(τκ-2,κ-2)Δτ},τ[0,1].ι(1)+(Δτ)ω-1Γ(ω+1)κ=2vϝ(τκ-2,κ-2)1~+(Δτ)ω-1Γ(ω+2)κ=2v{ϝ(τκ-1,κ-1)-ϝ(τκ-2,κ-2)}2~+ω(Δτ)ω-12Γ(ω+3)κ=2v{ϝ(τκ,κ)-2ϝ(τκ-1,κ-1)+ϝ(τκ-2,κ-2)}3~,τ[1,2],ι(2)+κ=v+3n{712ϝ(τκ-2,κ-2)Δτ-43ϝ(τκ-1,κ-1)Δτ+2312ϝ(τκ,κ)Δτ}+κ=v+3n{712(B(τκ-1)-B(τκ-2))κ-2-43(B(τκ)-B(τκ-1))κ-1+2312(B(τκ+1)-B(τκ))κ},τ[2,],

Graph

where

94 1~:=(v-κ-1)ω-(v-κ)ω,

Graph

95 2~:=(v-κ+1)ω(v-κ+2ω+3)-(v-κ)ω(v-κ+3ω+3),

Graph

and

96 3~:=(v-κ+1)ω(2(v-κ)2+(3ω+10)(v-κ)+2ω2+9ω+12)+(v-κ)ω(2(v-κ)2+(5ω+10)(v-κ)+6ω2+18ω+12).

Graph

Caputo–Fabrizio fractional derivative operator

The aim of this research is to examine the co-infection of the TB and COVID-19 models using integer-order (2), exponential decay kernel (4) and the ensuing stochastic scheme (28). This plan includes significant pulmonary inflammation, which means that the circulatory system is a major site of disease combat for a variety of diseases. The mathematical structure will be constructed using the classical-order formulation at first, the exponential decay memory at a later stage, and the stochastic setting in the phases that proceed in the case when is selected as the ultimate dissemination time. Following this, the following numerical pattern is given to clarify this occurrence.

At this point, we examine the sequential configurations (2), (4) and (28) analytically by using the method outlined in Ref.[29] in the context of the CFFD. In order to lay out the procedure, we did what follows:

97 dι(τ)dτ=ϝ(τ,ι).ι(0)=ι,0,ι=1,2,...,nifτ[0,1],1CFDτωι(τ)=ϝ(τ,ι),ι(1)=ι,1,ifτ[1,2],dι(τ)=ϝ(τ,ι)dτ+ιιdBι(τ),ι(2)=ι,2,ifτ[2,].

Graph

Thus, it implies that

98 ιv=ι(0)+κ=2v{2312ϝ(τκ,κ)Δτ-43ϝ(τκ-1,κ-1)Δτ+712ϝ(τκ-2,κ-2)Δτ},τ[0,1].ι(1)+1-ωM(ω)ϝ(τn,n)+ωM(ω)κ=2v{712ϝ(τκ-2,κ-2)Δτ-43ϝ(τκ-1,κ-1)Δτ+2312ϝ(τκ,κ)Δτ},τ[1,2],ι(2)+κ=v+3n{712ϝ(τκ-2,κ-2)Δτ-43ϝ(τκ-1,κ-1)Δτ+2312ϝ(τκ,κ)Δτ}+κ=v+3n{712(B(τκ-1)-B(τκ-2))κ-2-43(B(τκ)-B(τκ-1))κ-1+2312(B(τκ+1)-B(τκ))κ},τ[2,].

Graph

Atangana–Baleanu–Caputo fractional derivative operator

The current research aims to investigate the co-infection of the stochastic technique (28) and the integer-order model (2) and the GML kernel TB and COVID-19 models (5). Significant pulmonary inflammation is present in this design, indicating that the circulatory system is a key area of illness defense for a number of illnesses. Initially, the classical-order interpretation will be used to build the computational framework; afterwards, the GML function will be implemented; and in the phases that follow, the stochastic configuration will be used in the scenario where is chosen as the eventual propagation time. After that, the subsequent numerical structure is provided to explain these instances. In particular, we analyze the sequential configurations (2), (5) and (28) numerically employing the algorithm defined in Ref.[29] in the framework of the ABCFD. In order to lay out the procedure, we did what follows:

dι(τ)dτ=ϝ(τ,ι).ι(0)=ι,0,ι=1,2,...,nifτ[0,1],1ABCDτωι(τ)=ϝ(τ,ι),ι(1)=ι,1,ifτ[1,2],dι(τ)=ϝ(τ,ι)dτ+ιιdBι(τ),ι(2)=ι,2,ifτ[2,].

Graph

Thus, it implies that

ιv=ι(0)+κ=2v{2312ϝ(τκ,κ)Δτ-43ϝ(τκ-1,κ-1)Δτ+712ϝ(τκ-2,κ-2)Δτ},τ[0,1].ι(1)+1-ωABC(ω)ϝ(τn,n)+ω(Δτ)ω-1ABC(ω)Γ(ω+1)κ=2vϝ(τκ-2,κ-2)1~+ω(Δτ)ω-1ABC(ω)Γ(ω+2)κ=2v{ϝ(τκ-1,κ-1)-ϝ(τκ-2,κ-2)}2~+ω(Δτ)ω-12ABC(ω)Γ(ω+3)κ=2v{ϝ(τκ,κ)-2ϝ(τκ-1,κ-1)+ϝ(τκ-2,κ-2)}3~,τ[1,2],ι(2)+κ=v+3n{712ϝ(τκ-2,κ-2)Δτ-43ϝ(τκ-1,κ-1)Δτ+2312ϝ(τκ,κ)Δτ}+κ=v+3n{712(B(τκ-1)-B(τκ-2))κ-2-43(B(τκ)-B(τκ-1))κ-1+2312(B(τκ+1)-B(τκ))κ},τ[2,],

Graph

where the previous values of 1~,2~ , and 3~ are found in (94)–(96).

Experimental outcomes and discussion

In order to support research ideas, we will demonstrate mathematical simulation techniques in the next part that make leverage of the Atangana and Araz approaches formerly mentioned in Ref.[29]. The appropriateness and usefulness of the planned TB-COVID-19 are demonstrated through a number of concrete instances, such as manpower reductions, delays in test result transformation, and limitations of analytical equipment. The accessibility and promptness of TB examinations have been severely impacted by these interruptions in the deterministic-probabilistic situation. Utilizing MATLAB 21, all quantitative and symbolic computations were performed.

Researchers are at present demonstrating a great deal of enthusiasm in the estimation of modeling characteristics from provided statistical information, and it is thought to be an essential component of quantitative disease investigations. The aforementioned section was added to the current investigation employing the popular nonlinear least squares method. Applying the previously described method, the settings were determined, and the structure was calibrated to actual codynamic situations found in Later research from the Philippines and South Africa revealed that, for a specific duration, COVID-19 patients having TB had a 2.17[53] and 2.7[54] worse probability of death, respectively, than COVID-19 individuals lacking TB[53]. Especially, the entire number of documented infections and fatalities over the time span between March 2020 (the initial incidence had been identified on March 12, 2020) and June 2022 were used to determine the characteristics of the model. Considering the implementation of (99), the Ordinary Least Square solution was employed to reduce the inaccuracy concepts, and the associated relative deviation is incorporated in assessing the quality of fit as

99 mink=1n(k-^k)2k=1nk2.

Graph

The documented accumulative infection rates are denoted by k in this particular instance, while the total number of contaminated occurrences determined by modeling execution is denoted by ^k . The people who are moved daily from the contaminated compartment to the confined compartment are added together to determine the estimated levels of progressive transmission. With the exception of ς1=0.0456 , which is envisioned, all the parameters are estimates. When τ=1 and ω=1 the data in Fig. 6 has been fitted to the model.

Graph: Figure 6 The codynamics of TB-COVID-19 fitting outcomes considering the data obtained from WHO[55] for weekly reported cases.

The parameters' projected estimates are displayed in Table 2.

Table 2 Details on the system's characteristic.

Notations

Values

References

500

Supposed

β

0.0477

53

α1

0.6

53

α2

0.659

54

φ1

0.02

Supposed

ς3

0.01

Estimated

ζC

0.023

54

ζT

0.01

54

φ3

0.05

Calculated

λ

0.03

Calculated

ϵ

0.03

Calculated

ξ

0.003

Calculated

ρ

0.021

Supposed

ϖ

0.09

53

ϵ

0.048

Estimated

μ

0.25

54

η

0.01

Estimated

ν

0.002

Estimated

ζTC

0.2

Assumed

φ2

0.05

53

δ

0.056

Estimated

θ2

0.95

Estimated

θ1

0.9

Estimated

ς2

0.25

53

Example 1

To illustrate our results, we quantitatively generate the paths for the probabilistic sickness structures (2), (3) and (28) and their corresponding deterministic components. The starting points are (S,LT,IT,EC,IC,LTC,ITC,R)(0)=(1000,100,10,1000,10,7,5,1) and the time range is [0, 100] units. Table 2 allows us to re-select the parameters to represent the piecewise methodology assessment of the naturally occurring factor process for (2), (3) and (28), respectively.

Here, we calculate the fundamental reproductive quantity R0=2.4563>1 for the deterministic framework (2), which suggests that co-infection of TB and COVID-19 will continue to exist in the average situation in both submodels. To observe how noise concentration affects the behavior of the probabilistic framework (28), we select random perturbations ȷ=0.03(ȷ=1,...,5). This yields R0S=ψCS~(β+ϵψT+φ1+φ2)+422=1.231>1. The existence of an ESD for the probabilistic model (28) is demonstrated by Theorem 8.

When a power-law-type kernel with a FO ω=0.98 is employed on (3), Fig. 7a–h illustrates how incorporating two propagation interprets enhances the occurrence of ailments in comparison to a single procedure. In view of the CFD operator and biological-nature strategy, we also find that certain combinations prove more deadly than others. A transmission surge is produced by all interactions comprising the effective collaboration rate connecting S and IT . This is followed by any coupling via the effective interface rate between S and ITC , and finally other procedures. The respective two ICs (S,LT,IT,EC,IC,LTC,ITC,R)(0)=(4000,100,40,1000,10,7,5,4) and (S,LT,IT,EC,IC,LTC,ITC,R)(0)=(5000,100,50,1000,10,7,5,5), are depicted in Figs. 8a–h and 9a–h, with various population schemes.

Graph: Figure 7 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (3) and (28) with the impacts of latent and active TB outbreaks using CFD operator having FO ω=0.98, low intensities and ICs (1000, 100, 10, 1000, 10, 7, 5, 1).

Graph: Figure 8 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (3) and (28) with the impacts of latent and active TB outbreaks using CFD operator having FO ω=0.98, low intensities and ICs (4000, 100, 40, 1000, 10, 7, 5, 4).

Graph: Figure 9 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (3) and (28) with the impacts of latent and active TB outbreaks using CFD operator having FO ω=0.98, low intensities and ICs (5000, 100, 50, 1000, 10, 7, 5, 5).

We employ the identical factors as in (3), when implementing the identical methodology to the CFFD operator of DEs (2), (4) and (28), respectively. However, we modify the ICs as previously mentioned. It is simple to compute the threshold factors R0S>1 and R0C<1. As seen in Fig. 10a–h, the co-infections are expected to continue in a typical way, supporting the result of Theorem 8 (see Figs. 11a–h, 12a–h). According to this research, co-infection will spread throughout the body and develop ineffective causative agents, whereas mycobacterium TB will go obsolete.

In light of the prevalent concentrations and parameterization fluctuations discussed above, an intervention plan based on the computational findings for (2), (5) and (28) seems to be effective. There is an ESD of a probabilistic framework (28), as shown by Theorems 8. These results suggest that co-infection will become increasingly permanent while TB will go extinct for ABCFD case. These are corroborated by Figs. 13a–h, 14a–h and 15a–h, respectively.

Example 2

For probabilistic co-infection systems (28) involving community propagation, it is challenging to define appropriate criteria for virus extermination considering the limits of statistical approaches. Nonetheless, we provide a numerical model of the disappearance of illnesses where the noise is high for a thorough explanation. For instance, in the actual environment, individuals haphazardly raise vaccination or exterminating rates to stop co-infection from spreading. This successfully removes contamination.

To illustrate that high levels of environmental disturbance will eventually cause TB to disappear, we set 1=4=0.21, κ=0.11,κ=2,3,5,6,7 with the identical setting off rate as well as additional factors as in the aforesaid discussion. Following this, as Fig. 16a–h illustrates, co-infection will become extinct.

Example 3

For the probabilistic COVID-19 model in the absence of TB (75), the white noise ȷ=0.02,(ȷ=1,...,8) and the IC and the remaining arguments are the similar as in Example 1. Thus, we determine R0κ=2.83212>1. and the quasi-equilibrium (Sȷ,ECȷ,ITȷ,Rȷ)=(801867.49,6698439.45,10.768934.65,1387430.65). In view of Theorem 11.

100 Π=0.00110.0003-0.000550.00030.00030.00720.0070.0033-0.000610.00700.00780.00260.0030.00330.00260.0022.

Graph

As a result, the following is the relevant P.D.F U(Ψ~)=14φ22|Π|-1/2exp(-12Ψ~Π-1Ψ~T). where

Ψ~=(lnSȷ801867.49,lnECȷ6698439.45,lnITȷ10.768934.65,lnRȷ1387430.65).

Graph

Consequently, the four marginal D. Fs of Ψ~ are as follows:

USȷ=10.34267exp(-420.4235(lnSȷ-17.1893)),UECȷ=3.75123exp(-70.8992(lnECȷ-8.7834)),UIȷ=3.3410exp(-80.2341(lnIȷ-12.00345)),URȷ=9.2301exp(-235.9921(lnRȷ-5.5512)).

Graph

Finally, population concentrations oscillate according to the quasi-stable equilibrium U , as seen in Fig. 17.

Conclusions

In this article, a deterministic-stochastic model is being suggested to investigate the potential transmission of the codynamics of COVID-19 and TB. Taking into account the deterministic fractional model and stochastic approach, we have provided the qualitative characteristics such as positivity and boundedness, reproduction number and their allied outcomes for co-infection model (2), global positive solution and unique erogdicity for the co-dynamics of (28). Besides that, applying the Khasminskii notion and a suitable Lyapunov function, the existence of a stationary distribution in model (28) was analytically verified. Additionally, an accurate representation of the P.D.F regarding a quasi-equilibrium point of the random-perturbed COVID-19 model constitutes one of this research's particularly noteworthy discoveries. In fact, it has been determined that the validity and strength of our numerical outcomes and modeled estimates have been provided in a piecewise fractional DEs context. Furthermore, the outcomes of this study shed a spotlight on the P.D.F and stationary distribution of the probabilistic multidimensional framework at its quasi-equilibrium point. Although the ABCFD, CFFD and CFD have been demonstrated to be efficient in documenting various interaction practices, we contend that their ability to accomplish this effectively may be hindered by the vastness of biological systems. It follows that oscillation might eliminate signals that are widely dispersed, despite leaving infectious diseases uncontrolled.

Graph: Figure 10 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (3) and (28) with the impacts of latent and active TB outbreaks using CFFD operator having FO ω=0.98, low intensities and ICs (1000, 100, 10, 1000, 10, 7, 5, 1).

Graph: Figure 11 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (4) and (28) with the impacts of latent and active TB outbreaks using CFFD operator having FO ω=0.98, low intensities and ICs (4000, 100, 40, 1000, 10, 7, 5, 4).

Graph: Figure 12 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (4) and (28) with the impacts of latent and active TB outbreaks using CFFD operator having FO ω=0.98, low intensities and ICs (5000, 100, 50, 1000, 10, 7, 5, 5).

Graph: Figure 13 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (5) and (28) with the impacts of latent and active TB outbreaks using ABCFD operator having FO ω=0.98, low intensities and ICs (1000, 100, 10, 1000, 10, 7, 5, 1).

Graph: Figure 14 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (5) and (28) with the impacts of latent and active TB outbreaks using ABCFD operator having FO ω=0.98, low intensities and ICs (4000, 100, 40, 1000, 10, 7, 5, 4).

Graph: Figure 15 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 models (2), (5) and (28) with the impacts of latent and active TB outbreaks using ABCFD operator having FO ω=0.98, low intensities and ICs (5000, 100, 50, 1000, 10, 7, 5, 5).

Graph: Figure 16 Time evaluation plots for deterministic-probabilistic co-infection TB-COVID-19 model (2) and (28) with the impacts of latent and active TB outbreaks with low intensities and ICs (5000, 100, 50, 1000, 10, 7, 5, 5) using CFD when ω=0.95.

Graph: Figure 17 Numerical modeling of the outcome (S(τ),EC(τ),IC(τ),R(τ)) in system (75) is displayed in the upper portion row. The P.D.Fs and marginal D.Fs of S,EC,IC and R are displayed in the lower portion row, respectively, with ℘ȷ=0.02(ȷ=1,...,8) and R0κ=2.83212>1.

Predicting how TB is propagated by population mobility and random disturbances was challenging until this research was conducted. The research advances our knowledge of why TB still exists around the globe. Regarding stochastic TB systems, including community propagation, it is challenging to define adequate requirements for infection eradication considering the restrictive nature of computational approaches. On the other hand, we also offer a simulation of the disease's disappearance. To determine the necessary requirements for TB's endurance and extermination, additional investigation needs to be performed.

Numerous fascinating and open-ended, high-dimensional models deserve further consideration. It is vital for inquiry into phenomena that are impacted by additional factors, such as neural networking with stochastic resonance or oscillatory spectrum disruption, while examining the unpredictable nature of this form of contention. Such studies may include certain specific but complex concepts, including evaluating the effects of Lévy and Poisson noise or Markov processes. These pertinent issues might be covered in the upcoming analysis.

Acknowledgements

The authors extend their appreciation to Taif University, Saudi Arabia, for supporting this work through project number (TU-DSPP-2024-127).

Author contributions

All authors read and approved the final manuscript.

Funding

This research was funded by Taif University, Saudi Arabia, Project No.(TU-DSPP-2024-127).

Data availability

The datasets used and/or analyzed during the current study available from the corresponding author on reasonable request.

Competing interests

The authors declare no competing interests.

Publisher's note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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By Saima Rashid; Sher Zaman Hamidi; Saima Akram; Muhammad Aon Raza; S. K. Elagan and Beida Mohsen Tami Alsubei

Reported by Author; Author; Author; Author; Author; Author

Titel:
Enhancing the trustworthiness of chaos and synchronization of chaotic satellite model: a practice of discrete fractional-order approaches.
Autor/in / Beteiligte Person: Rashid, S ; Hamidi, SZ ; Akram, S ; Alosaimi, M ; Chu, YM
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Zeitschrift: Scientific reports, Jg. 14 (2024-05-09), Heft 1, S. 10674
Veröffentlichung: London : Nature Publishing Group, copyright 2011-, 2024
Medientyp: academicJournal
ISSN: 2045-2322 (electronic)
DOI: 10.1038/s41598-024-60268-3
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  • Nachgewiesen in: MEDLINE
  • Sprachen: English
  • Publication Type: Journal Article
  • Language: English
  • [Sci Rep] 2024 May 09; Vol. 14 (1), pp. 10674. <i>Date of Electronic Publication: </i>2024 May 09.
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  • Contributed Indexing: Keywords: Bifurcation; Chaotic attractors; Fractional calculus; Fractional difference equation; Lyapunov exponent; Sample entropy; Satellite model
  • Entry Date(s): Date Created: 20240509 Latest Revision: 20240509
  • Update Code: 20240510

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