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Article

Mathematical analysis and numerical simulation of co-infection of TB-HIV

, , ORCID Icon, &
Pages 431-441 | Received 18 Jul 2020, Accepted 17 Oct 2020, Published online: 29 Oct 2020

Abstract

In this article, we consider the model having co-infection of TB and HIV for numerical analysis and modelling. For this purpose, used non-standard finite difference scheme with Mickens approach ϕ(h)=h+O(h2) rather than h to control this disease. Furthermore, we analyse the well-posedness and stability of the system. Also, check the sensitivity analysis of the verse condition R0t and R0h as well as analyzed qualitatively. Finally represents the numerical solution of the model which supports the theoretical results.

1. Introduction

Human immunodeficiency virus is a global health problem which is a lentic virus and causes HIV infection. It is one of the most studied infectious diseases in the world. If an infected individual does not use medicines against HIV, then the total survival time of that individual is 9–11 years (Lawn & Zumla, Citation2011; Tahir, Inayat, & Zaman, Citation2019). After discovery of the virus, the models for HIV infection was discovered at late 1980s. In the 1900, SIR and SIS model by Kendrick and McCormack as well as bread-and-butter models of mathematical epidemiologists were discovered and this model for HIV was inspired from these models. These models were used to investigate infections between persons and population (Anderson & May, Citation1991). Viruses can investigate in person’s body by ‘viral dynamics’ model (Nowak & May, Citation2000). These models have since been used to describe many other human virus infections, such as Hepatitis B and C, influenza, dengue and herpes simplex virus (Alison, Citation2018). A system of nonlinear ordinary differential equation is used to made viral dynamic model which further used to investigate clinical parameters of HIV patient (Huang, Wu, & Acosta, Citation2010).

The outbreak of HIV was considered to wellbeing debacle at current times. HIV considered to most exasperating disease to different parts of the world, this made scientists to study about infection and its affects on human body during second pandemic of disease. This decrease in overspread of disease. But spread of the disease remains continue and treatment remains inaccessible to the mind-boggling standard of the individuals who require it (Sadegh & Miehran, Citation2015). Accordingly, various mathematical modelling have been arranged in the past time frames for HIV/AIDS spread elements. Global stability of equilibrium point for scientific models of HIV/AIDS spread elements have been pondered by various creators. It is normal that the HIV scourge feasts both through horizontal and vertical transmission (Silva & Torres, Citation2018).

Numerical mix of differential conditions was logically practiced by NSFD technique that was discovered by Mickens (Citation2005, Citation2007). NSFD scheme was applied to discretized SIRS outbreak by Sekiguchi and Ishiwata. Gonzalez-Parra, Arenas, and Charpentier (Citation2010) explained the durability of a SIRS distinct pandemic model through the NSFD scheme. Pandemic model was explained by Moghadas et al. to put forward NSFD defensive scheme (Arenas, Parra, & Charpentier, Citation2010). Here, we will demonstrate that a distinct pandemic model with inoculation built by NSFD wholeheartedly affirmation the inspiration of arrangements and the worldwide undercurrents of the identical nonstop model. Different models are studies for different numerical techniques to analysis the epidemic model to understand actual behaviour of the disease (Alexander, Summers, & Moghadas, Citation2006; Jordan, Citation2003; Mickens, Citation1994). A test problem of predator-prey model with two different cases are examined to determined the capability of our proposed methods in Kumar, Kumar, Cattani, and Samet (Citation2020) and Odibat and Kumar (Citation2019), and the proposed algorithm suggests a new optimal construction of the homotopy that reduces the computational complexity and improves the performance of the method in Kumar, Nisar, Kumar, Cattani, and Samet (2020) and Kumar, Kumar, Agarwal, and Samet (2020). A new fractional derivative with a non-singular kernel involving exponential and trigonometric functions is proposed in Alshabanat, Jleli, Kumar, and Samet (Citation2020), Kumar, Ghosh, Lotayif, and Samet (Citation2020), Veeresha, Prakasha, and Kumar (Citation2020), and Kumar, Ghosh, Samet, and Goufo (Citation2020) and some related new approaches for epidemic models are illustrated here (Farman, Ahmad, Akgul, & Imtiaz, Citation2020; Farman, Akgul, Baleanu, Imtiaz, & Ahmad, Citation2020; Farman, Saleem, A. Ahmad, & M. O. Ahmad, 2018; Farman, Saleem, et al., Citation2020; Farman, Saleem, M. O. Ahmad, & A. Ahmad, 2018; Farman, Saleem, Tabassum, Ahmad, & Ahmad, 2019; Raza, Farman, Akgul, Iqbal, & Ahmad, Citation2020; Saleem, Farman, Ahmad, Ehsan, & Ahmad, Citation2020; Saleem, Farman, Ahmad, & Rizwan, Citation2017; Saleem, Farman, Rizwan, Ahmad, & Ahmad, Citation2018). Some properties related to this new operator are established and some examples are provided (Baleanu, Jleli, Kumar, & Samet, Citation2020; Kumar, Kumar, Abbas, Al Qurashi, & Baleanu, 2020; Kumar, Kumar, Odibat, Aldhaifallah, & Nisar, 2020).

In this article, brief introduction of the model is given in Section 2, also discussed the stability, well-posedness and qualitative analysis in Section 3. Furthermore, the system is analyzed by local asymptotically stable. Also, check the sensitivity analysis of the verse condition R0t and R0h as well as analyzed qualitatively. We proposed the NSFD scheme for co-infection of TB-HIV model. Numerical simulations are carried out to support the analytical results in Sections 4 and 5.

2. Mathematical model

In this analysis of co-infection of HIV and TB, we suppose that total population is homogeneous and closed. Let N denotes the total number of population. Next, we divide this N into six different classes and parameters used in model, where the state space parameters and associate parameters and their description is presented in and respectively.

Table 1. Description of associate parameters with their values for disease free equilibrium point.

Table 2. Description of associate parameters with their values for endemic equilibrium point.

The mathematical model of co-infection HIV-TB can be represented as follows, (1) dSdt=IhSβh+Λ+δ(S)SItβt+α1μ1It,dItdt=IhItϕβh+SItβtα1μ1ItδIt,dIhdt=γ1Ih(1μ2)δIh+IhSβhIhσ1Itβt+α2Ihtμ1,dIhtdt=Ihσ1Itβt+IhItϕβhα2Ihtμ1γ2Iht(1μ2)δIht,dAhdt=Ah(δ+μ1)σ2ItAhβt+α3μ1Aht+γ1Ih(1μ2),dAhtdt=σ2ItAhβtα3μ1AhtAht(δ+μ2)+γ2Iht(1μ2),(1) along with initial condition S(0)>0,It(0)>0,Ih(0)>0,Ah(0)>0,Aht(0)>0. Here S(t) is susceptible human, It(t) is infectious human with TB, Ih(t) is infectious human with HIV, Iht(t) is I = infectious human with co-infection of HIV-TB, Ah(t) is infectious human with only HIV and susceptible to TB, Aht(t) is Infectious human with both HIV and TB in time (Fatmawati, Citation2016). While area of biological interest of model (1) is Ω={(S,It,Ih,Iht,Ah,Aht)R+6,0NΛδ}.

3. Well-Posedness of the model

Theorem 3.1.

Assumed that the modelEquation(1) enclosing all possible results with respect to non-negative initial solution then it is non-negative over the whole time.

Proof.

Assume that we have non-native initial solution of the model Equation(1), that is (2) S(0)0,Ih(0)0,It(0)0,Iht(0)0,Ah(0)0,Aht(0)0(2) By model Equation(1), the principal condition is evaluated as follows, (3) dSdt=Λ+α1μ1ItSD, where D=Ihβh+δ+Itβt(3) The solution of S can be evaluated by following expression, (4) S=S(0)eB+eB0tπeA(u)du0(4) where B=0tB(s)ds and A(u)=0uB(w)dw. Therefore, S(0)0 for all time t0. The non-negativity of rest parameters, the model Equation(1) can be demonstrated as follows, (5) dItdt=IhItϕβh+SItβtα1μ1ItδIt,dIhdt=γ1Ih(1μ2)δIh+IhSβhIhσ1Itβt+α2Ihtμ1,dIhtdt=Ihσ1Itβt+IhItϕβhα2Ihtμ1γ2Iht(1μ2)δIht,dAhdt=Ah(δ+μ1)σ2ItAhβt+α3μ1Aht+γ1Ih(1μ2),dAhtdt=σ2ItAhβtα3μ1AhtAht(δ+μ2)+γ2Iht(1μ2),(5) The above system Equation(5) can be demonstrated in the form of matrix as follows, (6) d Y(t)dt=B(t)+MY(t),(6) where Y(t)=[It(t)Ih(t)Iht(t)Ah(t)Aht(t)],    B(t)=[00ϕβh+σ1βt00] and M=[δ+Sβtα1μ100000δ+Sβh+γ1(μ21)α2μ10000δα2μ1+γ2(μ21)000γ1(1μ2)0δμ1α3μ100γ2(1μ2)0δα3μ1μ2]=[3.1×108S0.08000004.5×108S0.960.03600000.1030000.9400.050.03000.04700.11] It is clear that the matrix M is a Matzler matrix (a matrix whose all diagonal entries are strictly negative and non-diagonal entries are non-negative). From this fact, we investigate R+5 is invariant along with the stream of model Equation(6), which completes the proof.□

Theorem 3.2.

Suppose that the underlying circumstances for considered modelEquation(1), the following conditions holds, H(0)Hm,Ah(0)Ahm,Aht(0)Ahtm

Here, (7) Hm=γ1+δβh,Ahm=γ1(δβh2+γ1βhβt+δβhβt+γ1σ1βt2+δσ1βt2)ϕβh2(δβh+μ1βh+γ1σ2βt+δσ2βt),Ahtm=((γ1+δ)(δβh2+(γ1+δ)βhβt+σ1(γ1+δ)βt2))ϕ(δ+μ2)βh4(γ1σ2βhβt(δ+μ1)βh+σ2(γ1+δ)βt+γ2(ϕβh+σ1βt)γ2+δ).(7) Then, when the zeros of considered model exists on an interval J, it holds for subsequent a priori limits H(t)Hm,Ah(t)Ahm,Ath(t)Ahtm

Proof.

The result can be proved by three cases,

Case: 1 Subsequently, It(t)0 we have the following transformation by using first and second equation of model Equation(1), (8) H=S+ItdH(t)dt=dSdt+dItdt,=ΛδHβhIh[S+ϕIt].(8) Since, Ih0,It0.

So, we have, dHdtΛδH. Applying Gronwall inequality, we get H(t)γ1+δβh+(H(0)γ1+δβh)eδt This gives us, H(t)Hm  whenever  H(0)Hm Consequently, It(t)Hm. Replacing this in fifth equation of model, we have dAhdt(1μ2)γ1Hm+μ1α3Ahtσ2βtAhHm(δ+μ1)Ah This implies that, Ah(t)Ahm  if  Ah(0)Ahm Case: 2 Subsequently, Ih(t)0 we have the following transformation by using first and third equation of model (1), (9) H=S+IhdH(t)dt=dSdt+dIhdt,=Λγ1Ih(1μ2)δIhIhσ1Itβt+α2Ihtμ1δSSItβt+α1μ1It=ΛδHγ1Ih(1μ2)Itβt(S+Ihσ1)+α2Ihtμ1+α1μ1It.(9) Since, Ih0,It0,Iht0.

So, we have, dHdtΛδH. Applying Gronwall inequality, we get H(t)γ1+δβh+(H(0)γ1+δβh)eδt This gives us, H(t)Hm  whenever  H(0)Hm Consequently, Ih(t)Hm. Replacing this in fifth equation of model, we have dAhdt(1μ2)γ1Hm+μ1α3Ahtσ2βtAhHm(δ+μ1)Ah This implies that, Ah(t)Ahm  if  Ah(0)Ahm Case: 3 Subsequently, Iht(t)0 we have the following transformation by using first and second equation of model Equation(1), (10) H=S+IhtdH(t)dt=dSdt+dIhtdt,=ΛIhSβh+Ihσ1Itβt+IhItϕβhα2Ihtμ1γ2Iht(1μ2)δIhtδSSItβt+α1μ1It,=ΛδHItβt(S+Ihσ1)+Ih(βh)(SItϕ)α2Ihtμ1γ2Iht(1μ2)+α1μ1It.(10) Since, Ih0,It0,Iht0.

So, we have, dHdtΛδH. Applying Gronwall inequality, we get H(t)γ1+δβh+(H(0)γ1+δβh)eδt This gives us, H(t)Hm  whenever  H(0)Hm Consequently, Iht(t)Hm. Replacing this in fifth equation of model, we have dAhdt(1μ2)γ1Hm+μ1α3Ahtσ2βtAhHm(δ+μ1)Ah This implies that, Ah(t)Ahm  if  Ah(0)Ahm The boundedness of Aht is proved similarly, which completes the proof.□

3.1. Qualitative analysis

In this section we present the stability analysis of considered model presented in EquationEquation (1). Furthermore, we investigate the model (1) is locally stable at disease free and endemic equilibrium points. The disease free equilibrium points of model (1) is computed as follows, Let E0=(S0,It0,Ih0,Iht0,Ah0,Aht0) be represent the disease free equilibrium points then by solving EquationEquation (1) in a well-known mathematical software MATHEMATICA, the solution is computed as follows, (11) S0=Λδ,It0=0,Ih0=0,Iht0=0,Ah0=0,Aht0=0.(11) Next, we find existence and evaluate the equilibrium points of considered model Equation(1). Assume that E(S,It,Ih,Iht,Ah,Aht) be an equilibrium point such that, we have following TB-HIV endemic equilibrium point Eht=(S,It,Ih,Iht,Ah,Aht), such that, (12) S=γ1+δ+σ1ItβtβhIh=δβhR0h+δβhR0t+σ1ItR0hβt2ϕβh2R0hIht=It(ϕβh+σ1βt)(δβh(R0tR0h)+σ1ItR0hβt2)(γ2+δ)ϕβh2R0hAh=γ1(δβh(R0tR0h)+σ1ItR0hβt2)ϕβh2R0h(δ+μ1+σ2Itβt)Aht=γ2It(ϕβh+σ1βt)(δβh(R0tR0h)+σ1ItR0hβt2)(γ2+δ)(δ+μ2)ϕβh2R0h+γ1σ2Itβt(δβh(R0tR0h)+σ1ItR0hβt2)(δ+μ2)ϕβh2R0h(δ+μ1+σ2Itβt)(12) Next we substitute the value of S,Ih,Iht in 3rd equation of system (1), (13) 0=Ih(γ1δμ2+γ1γ2μ2+α2μ1Itϕβh+α2μ1σ1Itβt)γ2+δ=(δβhR0tδβhR0h+σ1ItR0hβt2)(γ1δμ2+γ1γ2μ2+α2μ1Itϕβh+α2μ1σ1Itβt)ϕ(γ2+δ)βh2R0h,=1ϕ(γ2+δ)βh2R0h(γ1δ2μ2βhR0t+γ1γ2δμ2βhR0tγ1δ2μ2βhR0hγ1γ2δμ2βhR0h+It(α2δμ1ϕβh2R0t+α2δμ1σ1βhR0tβtα2δμ1σ1βhR0hβt+α2δμ1ϕβh2R0t+γ1δμ2σ1R0hβt2γ1γ2μ2σ1R0hβt2)+(It)2(α2μ1σ1ϕβhR0hβt2+α2μ1σ12R0hβt3))=(α2Λμ1σ1βhβt2(ϕβh+σ1βt)δ(γ1μ2+γ1+δ))(It)2+(Λβt(α2δμ1ϕβh2+α2δμ1σ1βhβt)δ(α1μ1+δ)Λβh(α2δμ1ϕβh2+α2δμ1σ1βhβtγ1δμ2σ1βt2γ1γ2μ2σ1βt2)δ(δγ1(μ21)))Itγ1Λμ2(γ2+δ)βh(α1μ1βh+δβh+γ1μ2βtγ1βtδβt)(α1μ1+δ)(γ1μ2+γ1+δ)(13) we have the term It satisfy the following quadratic equation, (14) B0(It)2+B1It+B2=0,(14) where (15) B0=α2Λμ1σ1βhβt2(ϕβh+σ1βt)δ(γ1μ2+γ1+δ),B1=Λβt(α2δμ1ϕβh2+α2δμ1σ1βhβt)δ(α1μ1+δ)Λβh(α2δμ1ϕβh2+α2δμ1σ1βhβtγ1δμ2σ1βt2γ1γ2μ2σ1βt2)δ(δγ1(μ21)),B2=γ1Λμ2(γ2+δ)βh(α1μ1βh+δβh+γ1μ2βtγ1βtδβt)(α1μ1+δ)(γ1μ2+γ1+δ).(15) Consider B1=B1(σ1βt+ϕβh) as follows (16) B1=Λβt(α2δμ1ϕβh2+α2δμ1σ1βhβt)δ(α1μ1+δ)Λβh(α2δμ1ϕβh2+α2δμ1σ1βhβtγ1δμ2σ1βt2γ1γ2μ2σ1βt2)δ(δγ1(μ21)),=Λβt(α2δμ1ϕβh2+α2δμ1σ1βhβt)δ(α1μ1+δ)Λβh(α2δμ1ϕβh2+α2δμ1σ1βhβt)δ(δγ1(μ21))+Λβh(γ1δμ2σ1βt2+γ1γ2μ2σ1βt2)δ(δγ1(μ21))=(α2δμ1ϕβh2+α2δμ1σ1βhβt)(Λβtδ(α1μ1+δ)Λβhδ(δγ1(μ21)))+(γ1δμ2σ1βt2+γ1γ2μ2σ1βt2)(Λβhδ(δ+γ1μ2γ1))=(α2δμ1ϕβh2+α2δμ1σ1βhβt)(R0tR0h)+(γ1δμ2σ1βt2+γ1γ2μ2σ1βt2)R0h(16) where R0h=Λβhδ(δγ1(μ21)),R0t=Λβtδ(α1μ1+δ) are represented the reproductive number.

Theorem 3.3.

For disease free equilibrium point E0 if real part of eigenvalues of Jacobian matrix J of considered systemEquation(1), then the systemEquation(1) is locally asymptotically stable otherwise it is unstable.

Proof.

Let J be a Jacobian matrix of system Equation(1) is and is computed by following expression, (17) J=[V1α1μ1SβtSβh000ItβtV2ϕItβh000IhβhIhβtσ1V3α2μ1000Ih(ϕβh+βtσ1)It(ϕβh+βtσ1)V4000Ahβtσ2γ1(μ21)0V5α3μ10Ahβtσ20γ2(μ21)Itβtσ2V6](17) where V1=δIhβhItβt,V2=δϕIhβh+Sβtα1μ1,V3=δ+Sβh+γ1(μ21)Itβtσ1,V4=δα2μ1+γ2(μ21),V5=δμ1Itβtσ2 and V6=δα3μ1μ2. For disease free equilibrium points E0=(S0,It0,Ih0,Iht0,Ah0,Aht0) the Jacobian matrix J0 becomes, (18) J0=[δα1μ1ΛβtδΛβhδ0000δα1μ1+Λβtδ000000δ+γ1(μ21)+Λβhδα2μ100000δα2μ1+γ2(μ21)0000γ1(μ21)0δμ1α3μ1000γ2(μ21)0δα3μ1μ2].(18) The eigenvalue of matrix J0 is computed by finding the solution of det(J0λI)=0, where I is an 6 × 6 identity matrix. Take |J0λI|=0, Thus the eigenvalues of J0 are follows, λ1=δ=0.02,λ2=δμ1=0.05,λ3=α1δμ1δ2+Λβtδ=0.0025,λ4=α3μ1δμ2=0.11,λ5=γ1δμ2γ1δδ2+Λβhδ=0.8475,λ6=α2μ1+γ2μ2γ2δ=0.103. All of the eigenvalues of considered Jacobian matrix J are strictly negative, therefore the system is locally asymptotically stable at disease free equilibrium.□

3.2. Sensitivity analysis

The sensitivity analysis of reproduction number R0t, R0t=Λβtδ(α1μ1+δ), with respect to each parameters is, (19) R0tΛ=βtδ(α1μ1+δ)=0.000019375>0R0tβt=Λδ(α1μ1+δ)=3.125×107>0R0tδ=Λβt(α1μ1+2δ)δ2(α1μ1+δ)2=60.5469<0R0tα1=Λμ1βtδ(α1μ1+δ)2=0.363281<0R0tμ1=α1Λβtδ(α1μ1+δ)2=24.2188<0(19) From above sensitivity analysis, we analyze that the R0t become sensitive by a very slight variation in parameters. The reproduction number R0t increase with increment of Λ,βt and decrease with decrease with parameters δ,α1,μ1.

The sensitivity of reproduction number R0h, R0h=Λβhδ(δγ1(μ21)), with respect to each parameters is, (20) R0hΛ=βhδ(δγ1(μ21))=2.34375×106>0R0hβh=Λδ(δγ1(μ21))=2.60416×106>0R0hδ=Λβh(2δγ1(μ21))δ2(δγ1(μ21))2=5.98145<0R0hγ1=Λ(1μ2)βhδ(δγ1(μ21))2=0.114746<0R0hμ1=γ1Λβhδ(δγ1(μ21))2=0.12207>0(20) From above sensitivity analysis, we analyze that the R0h become sensitive by a very slight variation in parameters. The reproduction number R0h increase with increment of Λ,βh and decrease with decrease with parameters δ,γ1,μ2.

4. Proposed NSFD scheme

The fundamental hypothesis of nonstandard finite difference (NSFD) displaying was set up by Micken’s with a portion of his articles from the eighties. An essential reference is the book (Mickens, Citation2000) which he altered, and where he gave the first section (Mickens, Citation2000). The discretized transformation of model Equation(1) in the form of NSFD scheme using first order forward method is discriminated as follows, Sk+1Skh=βhIhkSk+1δSk+1Sk+1Itkβt+α1μ1Itk+Λ This implies that (21) Sk+1=Sk+h(α1μ1Itk+Λ)1+h(δ+βhIhk+Itkβt)(21) Also, we have Itk+1Itkh=ϕβhIhkItk+1+Sk+1Itkβtα1μ1Itk+1δItk+1 This implies, (22) Itk+1=Itk(hSk+1βt+1)1+h(α1μ1+δ+ϕβhIhk)(22) Also, we have Ihk+1Ihkh=γ1(1μ2)Ihk+1δIhk+1+βhIhkSk+1σ1Ihk+1Itk+1βt+α2μ1Ihtk This implies, (23) Ihk+1=α2hμ1Ihtk+Ihk(hβhSk+1+1)1+h(γ1(1μ2)+δ+σ1Itk+1βt)(23) Also, we have Ihtk+1Ihtkh=σ1Ihk+1Itk+1βt+ϕβhIhk+1Itk+1α2μ1Ihtk+1γ2(1μ2)Ihtk+1δIhtk+1 This implies, (24) Ihtk+1=hIhk+1Itk+1(ϕβh+σ1βt)+Ihtk1+h(α2μ1+γ2(1μ2)+δ)(24) Also, we have Ahk+1Ahkh=(δ+μ1)Ahk+1σ2Itk+1βtAhk+1+α3μ1Ahtk+γ1(1μ2)Ihk+1 This implies, (25) Ahk+1=Ahk+h(α3μ1Ahtk+γ1(1μ2)Ihk+1)1+h(δ+σ2Itk+1βt+μ1)(25) Also, we have Ahtk+1Ahtkh=σ2Itk+1βtAhk+1+α3(μ1)Ahtk+1(δ+μ2)Ahtk+1+γ2(1μ2)Ihtk+1 This implies, (26) Ahtk+1=Ahtk+h(σ2Itk+1βtAhk+1+γ2Ihtk+1(1μ2))1+h(α3μ1+δ+μ2)(26)

5. Results and discussion

In this section, we present some numerical simulations of susceptible human S, infectious human with TB It, infectious human with HIV Ih, infectious human with both of HIV-TB Iht, infectious human with only HIV and susceptible to TB Ah and infectious human with both HIV and TB Aht for both case of R0h<1,R0t<1 and R0h>1,R0t>1 using values of associated parameters taken in and respectively. By analyzing the graphical results assure us to justify the theoretical literature review of stability and instability of co-infection of TB-HIV. The following graphical results are plotted by a well-known software MATLAB. By using the NSFD scheme, we draw the graphical solution of the system in which will approached to study state points for disease free and in for endemic point of the system.

Figure 1. Susceptible population S(t) in time t at different step size for DFE.

Figure 1. Susceptible population S(t) in time t at different step size for DFE.

Figure 2. Infected population with TB It(t) in time t at different step size for DFE.

Figure 2. Infected population with TB It(t) in time t at different step size for DFE.

Figure 3. Infected population with HIV only Ih(t) in time t at different step size for DFE.

Figure 3. Infected population with HIV only Ih(t) in time t at different step size for DFE.

Figure 4. Infected population with both TB and HIV Iht(t) in time t at different step size for DFE.

Figure 4. Infected population with both TB and HIV Iht(t) in time t at different step size for DFE.

Figure 5. Infected with AIDS only and susceptible to TB class Ah(t) in time t at different step size for DFE.

Figure 5. Infected with AIDS only and susceptible to TB class Ah(t) in time t at different step size for DFE.

Figure 6. Infected population with TB and AIDS both class Aht(t) in time t at different step size for DFE.

Figure 6. Infected population with TB and AIDS both class Aht(t) in time t at different step size for DFE.

Figure 7. Susceptible population S(t) in time t for EEP at different step size.

Figure 7. Susceptible population S(t) in time t for EEP at different step size.

Figure 8. Infected population with TB It(t) in time t for EEP at different step size.

Figure 8. Infected population with TB It(t) in time t for EEP at different step size.

Figure 9. Infected population with HIV only Ih(t) in time t for EEP at different step size.

Figure 9. Infected population with HIV only Ih(t) in time t for EEP at different step size.

Figure 10. Infected population with both TB and HIV Iht(t) in time t for EEP at different step size.

Figure 10. Infected population with both TB and HIV Iht(t) in time t for EEP at different step size.

Figure 11. Infected with AIDS only and susceptible to TB class Ah(t) in time t for EEP at different step size.

Figure 11. Infected with AIDS only and susceptible to TB class Ah(t) in time t for EEP at different step size.

Figure 12. Infected population with TB and AIDS both class Aht(t) in time t for EEP at different step size.

Figure 12. Infected population with TB and AIDS both class Aht(t) in time t for EEP at different step size.

6. Conclusion

In this article, we present a mathematical model for the co-infection of TB and HIV transmission along with variable aggregate population size. The well-posedness of the co-infection TB-HIV model is presented. Furthermore, we analyze the existence of a disease-free and endemic equilibrium for the co-infection of TB-HIV. Also, we present the basic reproduction number R0t and R0h for Tb and HIV infection respectively. The formulation and sensitivity analysis of fundamental reproduction numbers for Tb and HIV are analyzed. The formulation of the proposed co-infection TB-HIV model in terms of non-standard finite difference schemes is presented. Finally, we present the graphical representation of the solution using the Non-Standard Finite Difference scheme which provides the solution according to our steady-state for both disease-free and endemic equilibrium.

Disclosure statement

No potential conflict of interest was reported by the author(s).

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