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. 2023 Feb 28;11:1145. Originally published 2022 Oct 7. [Version 2] doi: 10.12688/f1000research.123693.2

Qualitative analysis of HIV and AIDS disease transmission: impact of awareness, testing and effective follow up

Oluwakemi E Abiodun 1,a, Olukayode Adebimpe 2, James Ndako 1, Olajumoke Oludoun 1, Benedicta Aladeitan 1, Michael Adeniyi 3
PMCID: PMC9997043  PMID: 36910027

Version Changes

Revised. Amendments from Version 1

Based on reviewer feedback, the abstract section's result and conclusion were rewritten. New literature were incorporated, and the study's uniqueness was re-examined for more clarity. The reproduction number was investigated once more, and the relationship between the reproduction number and the stability analysis of the disease free equilibrium was demonstrated. The effect of infants born to infected mothers was lengthened to three steps (@ 0.02, 0,04, and 0.06). The conclusion was paraphrased, and the major finding was highlighted as the reviewer advised. Grammatical errors were also verified.

Abstract

Background: Since the early 1980s, human immunodeficiency virus (HIV) and its accompanying acquired immunodeficiency syndrome (AIDS) have spread worldwide, becoming one of the world's major global health issues. From the beginning of the epidemic until 2020, about 79.3 million people became infected, with 36.3 million deaths due to AIDS illnesses. This huge figure is a result of those unaware of their status due to stigmatization and invariably spreading the virus unknowingly.

Methods: Qualitative analysis through a mathematical model that will address HIV unaware individuals and the effect of an increasing defaulter on the dynamics of HIV/AIDS was investigated. The impact of treatment and the effect of inefficient follow-up on the transmission of HIV/AIDS were examined. The threshold for the effective reduction of the unaware status of HIV through testing, in response to awareness, and the significance of effective non-defaulting in treatment commonly called defaulters loss to follow-up as these individuals contribute immensely to the spread of the virus due to their increase in CD4+ count was determined in this study. Stability analysis of equilibrium points is performed using the basic reproduction number $R_0$, an epidemiological threshold that determines disease eradication or persistence in viral populations.  We tested the most sensitive parameters in the basic reproduction numbers.

Results: The results portray that early identification and treatment only are inadequate for the illness to be eradicated, but effectively used of condom, strict adherence to treatment and counseling of and testing of pregnant women contribute to a decrease in infected HIV individuals.

Conclusions: Other control techniques, such as treatment adherence and effective condom usage, and reduction in vertical transmission cannot be over-emphasis to lessen the disease's burden. Policymakers must address these strategies through a series of public awareness campaigns about the dangers of not adhering to treatment procedures and patterns.

Keywords: HIV/AIDS, infection-free equilibrium, defaulter lost to follow-up, endemic equilibrium, next generation matrix, basic reproduction number, stability.

1. Introduction

Human immunodeficiency virus (HIV) is a sexually transmitted infection (STI) and a blood-borne illness in humans with a wide range of clinical manifestations. 1 , 2 HIV and its accompanying acquired immune deficiency syndrome (AIDS) have spread rapidly around the world since its discovery in the early 1980s, and it remains the world’s most serious global health and development challenges. There is, however, a global devotion to avoiding new infections and making sure that all patients diagnosed have access to treatment. In addition, 79.3 million individuals have been infected with HIV since the pandemic began, with 36.3 million people dying due to AIDS diseases. About five million individuals contracted HIV for the first time in 2003, the largest number in any one year since the pandemic began. 3 Globally, the figure of persons living with HIV/AIDS has risen from 35 million in 2001 to 37.7 million in 2020, with around 3 million people dying from the illness in that year. 4 , 5 Around 84 percent [68 − 98 percent] of HIV-positive persons in the globe know their status in 2020, and the remaining 16 percent (about 6 million people) [4.8 million-7.1 million] need to be tested for HIV. HIV testing is an important initial step in HIV prevention, treatment, care, and support. 6 , 7 Under Sustainable Development Goal 3, the international community pledged to work to end the AIDS pandemic by 2030. While progress has been made, it has been inconsistent, and the intermediate targets of “90-90-90” have been missed. 7 , 8 New diseases continue to wreak havoc on communities and undermine vital socioeconomic infrastructure all across the planet. According to the United Nations Joint Program on HIV and AIDS, the number of HIV-positive people in 2021 was 37.6 million, up from 33.2 million in 2010. 9 1.5 million [1.1 million-2.1 million] people contracted HIV for the first time in 2020, 690,000 [480,000-1 million] people died of AIDS-related illnesses, and antiretroviral medication was available to 27.4 million [26.5 million-27.7 million] patients in December 2020, up from 7.8 million [6.9 million-7.9 million] in 2010. 9 11 HIV can be spread horizontally or vertically from one infected individual to another. Horizontal HIV transmission occurs when an individual comes into direct contact with an HIV-positive person, including sexual contact, or when they use a needle and syringe that has recently been utilized by an HIV-positive individual. Contrastingly, vertical transmission occurs when the virus is passed directly from an infected mother to her pregnant or newborn child. 12 HIV/AIDS transmission dynamics has piqued the interest of applied mathematicians, epidemiologists 13 16 and biologists 17 22 due to the disease’s worldwide menace. Various improvements have been made to May and Anderson’s early models, 23 25 and particular issues have been discussed by researchers. 12 , 26 48 In Lu et al. 2020 27 fostered a compartmental model for the yearly revealed HIV/AIDS MSM in the Zhejiang Region of China between 2007 to 2019 and anticipated that 90 percent of people tested for HIV/AIDS will have received treatment by 2020 neglecting those that fall out of treatment, while the screened extent will remain as low as 40 percent, and that antiretroviral treatment (ART) can control the transmission of HIV, even within the sight of medication opposition. Rana and Sharma, 2020 30 presented a simple Likely to be exposed-Infected (i.e.SI) form of the HIV/AIDS mathematical model, given the supposition that changing from an AIDS-infected to an HIV-infected individual is conceivable, to understand disease dynamics and develop strategies to reduce or control disease transmission among individual. In Ref. 30, HIV positive individual were not placed on treatment until they developed full blown AIDS. Mushanyu 32 built a mathematical model for HIV acquisition using nonlinear ordinary differential equations to analyse the influence of delayed HIV diagnosis on the transmission of HIV in the year 2020. To prevent HIV from spreading further, the researchers advocated for early HIV treatment and the expansion of HIV self-testing initiatives, which would allow more people who have not been tested for HIV to learn their status. Teng 12 proposed and investigated a time-delay compartmental framework for HIV transmission in a sexually active cohort with press coverage, a disease that can result in a developed phase of infection known as acquired immunodeficiency syndrome (AIDS), as well as vertical transmission in the enrollment of people infected in 2019. 33 Saad et al. (2019) developed and considered an HIV + mathematical model with the next-generation matrix, the infection-free and endemic equilibrium points were identified, and the basic reproduction ratio R 0 was determined. The Lyapunov function was utilized to analyze the equilibria’s global stability, and it was observed that the equilibria’s stability is reliant on the magnitude of the fundamental reproduction ratio. 37 Developed an HIV/AIDS epidemic model with a generic nonlinear rate of occurrence and therapy and was able to obtain the basic reproductive number R 0 using the next generating matrix technique.

Researchers have employed numerous tools to manage and eradicate HIV/AIDS diseases. 3 , 11 , 12 In order to study the combined effects of three control measures, 49 presented an innovative and workable human-bat (host-vector) model that predicts the spread and severity of the Ebola virus from bats to humans. To demonstrate the model’s epidemiological viability, among other things, disease-free equilibrium, the endemic equilibrium, local and global stability, positivity, and boundedness were established. In order to understand the dynamics of the disease’s transmission and its long-term repercussions, 50 created a novel deterministic model of Lassa Hemorrhagic fever (LHF) with nonlinear force of infection. The Cauchy’s differential theorem, Birkhoff & Rota’s theorem, and other well-known approaches used in the qualitative studies of the model both confirm and make clear how well-posed it is.

These studies revealed that awareness creation/information can help to control the disease burden but cannot eliminate the disease. Furthermore, there are other techniques and tools available that can be applied to study the dynamics of disease transmission and to provide suitable control interventions. The use of mathematical modeling is foremost among these techniques. 16 19 Although many articles 20 have studied the impact of different controls; however, none of them have incorporated human behaviour in response to information. Hence, the aim of this study is to identifies the threshold for effective reduction of HIV/AIDS, as a result of HIV-unaware individuals becoming aware with counseling and testing and placed on treatment afterwards. The consequent effective follow-up in the use of treatment, immediate treatment of HIV positive diagnosed, the inclusion of effective condoms usage by susceptible and infectious individual on the transmission dynamics cannot be over-emphasis in the eradication of HIV/AIDS as proposed by WHO and UNAID come 2030.

According to the literature, no one has proposed a model that takes into account both vertical and horizontal transmission of susceptible into unaware populations, as well as undiagnosed and diagnosed HIV/AIDS-infected individuals, with preventive measures on transmission dynamics, screening, treatment controlling mechanisms, and the consideration of non-adherence to therapy. This model takes into account the rate of becoming conscious and unaware as a consequence of counselling and testing as variables rather than constants, as well as the rising effect of non-adherence to treatment. Thus, according to the author’s knowledge, this work is unique.

The following is the structure of the paper: Section 2 describes the model, while Section 3 examines the model’s basic features, the basic reproduction number, and equilibrium points. Section 4 employs a parameter sensitivity index on the reproduction number to conduct a stability study of the equilibria (local and global), and the findings are generated from numerical simulations of data from previously published studies in Section 5. Finally, the research is examined and completed in Section 6.

2. Model formulation and description

A mathematical model on the mechanisms of horizontal and vertical transmission of HIV/AIDS was developed, by incorporating the effect of testing, defaulter loss to follow-up on treatment, and effective use of condoms on the existing model. The model is available from GitHub and is archived with Zenodo. 68 The model is depicted schematically in Figure 1. The model contains six (6) state variables, namely: Susceptible ( S), representing people who are likely to become infected with HIV; Unaware HIV infectives ( H U ), Aware HIV infectives ( H A ), Treated HIV infectives ( H T ); AIDS individuals ( A A ) and AIDS on treatment individuals ( A T ). The rate of effective contact with HIV-positive people either by immigration or emigration is given by Λ. A percentage of newborns get infected with HIV during birth at a rate of (1 − ζ) and are therefore directly enrolled into the unaware infected population H U , at a rate ζΛ, with 0 ≤ ζ ≤ 1. λH=c1ψξβ1HU+β2HA+β3AAN is the HIV transmission contact rate. Parameter c represents the average number of sexual partners acquired by people who are vulnerable to HIV annually. To simulate the influence of condom usage as a significant preventive intervention, the amount of condom protection (usage and effectiveness) is given as ψξ[0, 1] based on assumption. If ξ = 0, condom use provides no protection, but ξ = 1 denotes complete protection, where ψ is the condom use. The parameters β 1, β 2 and β 3 account for the HIV transfer rates between persons at risk and (HIV unaware, HIV aware and full blow AIDS) infectives individuals, respectively. Both the HIV-infected and the AIDS-infected groups are thought to be active in the spread of HIV/AIDS amongst susceptible. 51 Because infected patients with AIDS symptoms have a greater viral load than HIV-positive people (pre-AIDS) in the H U and H A classes, and because viral load and infectiousness have a positive connection, we must have β 1 < β 2 < β 3. There is evidence to suggest that individuals who know their HIV status H A change their sexual behaviour (i.e. adopt safer-sex practices), resulting in reduced transmission. 25 Most HIV pandemic models disregard the role of AIDS patients in HIV transmission by applying simplistic assumptions such as AIDS death being immediate or AIDS patients being incapable of mingling and gaining new sex partners. However, epidemiological data show that AIDS patients participate in hazardous sexual activities, such as seldom wearing condoms or having several sex partners. 52 As shown in the findings of Ref. 21 research of HIV-1-infected transfusion men and their women sex partners, severe AIDS patients are more likely to infect their partners than non-advanced immuno-compromised receivers. 51 , 53 Also reported similar findings. HIV-positive individuals with and without AIDS signs are likely to have access to antiretroviral therapy (ART). Unaware HIV-infected persons, H U , progress to the category of aware HIV infection H A , after testing at a rate of α, while an unaware infected individuals who did not go for testing progress to stage IV of AIDS, A A ; at a rate of ρ. HIV-infected aware people with no symptoms of AIDS; H A , proceed to the group of HIV infection under ART therapy, H T , whereas HIV-infected people with AIDS symptoms, A A , are treated for AIDS at a rate of θ 2 on reaching the class of A T. We presume that HIV-infected people on treatment do not spread the virus. 54 , 55 HIV-infected people who are receiving therapy but do not have AIDS symptoms, H T , who default during treatment and become resistant to the drug, will return to the HIV-infected aware individuals, H A , and that HIV-infected persons with AIDS symptoms, A A , who default during treatment in class A T , become re-infected with HIV with symptoms of AIDS individuals, A A , at a rate υ 1 and υ 2 respectively. 56 It is assumed that only HIV-infected people with AIDS symptoms, A A and A T , die of AIDS-related causes at a rate of d a. The following mathematical model is based on these assumptions and that the system has a natural death in each class at a rate μ.

Figure 1. HIV/AIDS compartmental flow diagram.

Figure 1.

In order to contribute to the arduous aim of ending HIV/AIDS by 2030 there is need to foresee the epidemic’s behaviour. One of the most significant tools we’ll utilize to attain our aim is mathematical modeling of HIV infection. Based on Ref. 57, the following model was developed by the inclusion of AIDS on treatment compartment (by considering treatment of both individual not showing and showing symptoms of AIDS), individual who fall-out of treatment, considering AIDS individual are able to transmit infection, condom use to control transmission rate and average number of sexual partners acquired on force of infection. A system of ordinary differential equations (ODEs) can be used to express the mathematical equations that correspond to the schematic diagram:

dSdt=Λ1ζHUλH+μSadHUdt=ΛζHU+λHSα+ρ+μHUbdHAdt=αHU+v1HTθ1+μHAcdHTdt=θ1HAv1+μHTddAAdt=ρHU+v2ATθ2+da+μAAedATdt=θ2AAv2+da+μATf (1)

with the positive initial conditions given as:

S0=S0,HU0=HU0,HA0=HA0,HT0=HT0,AA0=AA0,AT0=AT0 (2)

3. Model investigation

3.1 Region of invariant

All of the parameters in the model are considered to be non-negative. System (1), on the other hand, keeps track of the human populace, hence, the state variables are always positive for all time t ≥ 0. Thus, the total human populace is given as

Nt=St+HUt+HAt+HTt+AAt+ATt (3)

Here equation (1) is changing at a rate

dNdt=dSdt+dHUdt+dHAdt+dHTdt+dAAdt+dATdt=ΛμNdaAAdaAT+φHU (4)

In the non-existence of infection i.e. for H U = H A = H T = A A = A T = 0 we have,

dNdtΛμ (5)

We must have (6) by separating the variables of differential inequality.

dNΛμNdt (6)

Integrating the above equation we have

ΛμNCeμt

where C is a constant to which to be determined. Let at t = 0, N = N 0. So we have,

C=ΛμN0 (7)

From (7) we have

ΛμNΛμN0eμtNtΛμΛμN0μeμt

As t,0NtΛμ

As a result, the system (1) feasible solutions set enters the region.

Ω=SHUHAHTAAATe+6:0NΛμ

when NΛμ every solution with an initial condition in e+6 stays in that region for t > 0. As a result, the model is well posed and epidemiologically relevant in the domain Ω.

3.2 Non-negativity of solutions

This section discusses the positivity of the solutions, which describes the system’s non-negativity of solutions (1).

Lemma 1: S( t) ≥ 0, H U ( t) ≥ 0, H A ( t) ≥ 0, H T ( t) ≥ 0, A A ( t) ≥ 0, A T ( t) ≥ 0 and N( t) ≥ 0 satisfied by the solutions of system (1) with initial conditions (2) for all t ≥ 0. The region Ωe+06 is positively invariant and attracts in terms of system (1).

Proof: Take a look at the first equation (a) in (1)

dSdt=Λ1ζHUλH+μS

we have;

dSdtΛζHU+λH+μS1SdSΛζHU+λH+μdt
SS0eΛζHU+λH+μ0

provided ΛζHU+λH+μ<

As a result, S ≥ 0

Likewise, for system (1)’s second equation (b), we have

dHUdt=ΛζHU+λHSα+ρ+μHU
dHUdtα+ρ+μHU1HUdHUα+ρ+μdt
HUHU0eα+ρ+μ0

provided α+ρ+μ<

Hence, H U ≥ 0

Similarly it can be shown that H A ≥ 0, H T ≥ 0, A A ≥ 0, A T ≥ 0 for all t > 0.

Thus, the solutions S, H U , H A , H T , A A , A T remain positive forever.

3.3 Equilibrium point and basic reproduction number; R 0

The model (1) has exactly one disease-free equilibrium (DFE) point and the equilibrium point E 0 is given by S0HU0HA0HT0AA0AT0=Λμ00000. In the absence of infection, the total population changes in proportion to the ratio of recruitment rate to the death rate.

The total population dynamics can be altered when an individual with an HIV/AIDS is introduced into a population. For the endemic equilibrium, there is an existence of infection hence H U H A H T A A A T ≠ 0. It is denoted by E *. Setting equation (1a-1f) equal to zero which exist when R 0 > 1 we have

S=M1ζΛM4M5υ2θ2λρM5AA (8)
HU=M4M5υ2θ2ρM5AA (9)
HA=αM3υ2θ2+M4M5M2M3υ1θ1AA (10)
HT=θ1αM3υ2θ2M4M5M3M2M3υ1θ1AA (11)
AA=ΛρM5λM1M4M5υ2θ2λ+μM1ζΛM4M5υ4θ2 (12)
AT=θ2M5AA (13)

M 1 = α + ρ + μ, M 2 = θ 1 + μ, M 3 = υ 1 + μ, M 4 = θ 2 + d a + μ, M 5 = υ 2 + d a + μ.

Theorem 1: There exists a positive endemic equilibrium if R 0 > 1

Reference 58 presented a better method for determining R 0 which was an improved technique of solving the reproduction number firstly developed by Ref. 59 that is widely accepted because it represents the biological meaning of R 0. By considering only the infective classes, we were able to obtain the system’s (1) basic reproduction number, R0, which is the spectral radius ( ρ) of the next generation matrix, NGM, i.e. R0=ρFV1 . The rate of emergence of new infections in compartments i, while V denotes the rate of transfer of individual into and out of the compartment i by all other means. Where F and V are the m × m matrices defined as:

F=FixoxjandV=Vixoxjwithii,jm

F is non-negative and V is non-singular matrix.

Then,

F=c1ψξβ1c1ψξβ20c1ψξβ3000000000000000000000andV=M1Λζ0000αM2υ1000θ1M300ρ00M4υ2000θ2M5V1=1ΛζM10000αM3ΛζM2M3Λζθ1υ1M1M2M3+M1θ1υ1M3M2M3θ1υ1υ1M2M3θ1υ100αθ1ΛζM2M3Λζθ1υ1M1M2M3+M1θ1υ1θ1M2M3θ1υ1M2M2M3θ1υ100ρM5ΛζM4M5Λζθ2υ2M1M4M5+M1θ2υ200M5M4M5θ2υ2υ2M4M5θ2υ2ρθ2ΛζM4M5Λζθ2υ2M1M4M5+M1θ2υ200θ2M4M5θ2υ2M4M4M5θ2υ2FV1=c1ψξβ1ΛζM1+c1ψξβ2αM3ΛζM2M3Λζθ1υ1M1M2M3+M1θ1υ1+c1ψξβ3ρM5ΛζM4M5Λζθ2υ2M1M4M5+M1θ2υ2c1ψξβ2M3M2M3θ1υ1c1ψξβ2υ1M2M3θ1υ1c1ψξβ3M5M4M5θ2υ2c1ψξβ3υ2M4M5θ2υ200000000000000000000 (14)

where M 1 = α + μ + ρ, M 2 = θ 1 + μ, M 3 = v 1 + μ, M 4 = θ 2 + d a + μ, M 5 = v 2 + d a + μ

The model reproduction number, denoted by R 0 is thus given by R0=ρFV1=R=R1+R2+R3 , the spectral radius of the NGM FV −1.

Here,

R1=c1ψξβ1ζΛM1R2=c1ψξβ2αM3M2M3θ1υ1ζΛM1R3=c1ψξβ3ρM5M4M5θ2υ2ζΛM1

Equivalently,

R0=ρFV1=c1ψξαβ2M3M4M5αβ2M3θ2υ2+β3ρM2M3M5β3ρM5θ1υ1+M2M3M4M5β1M2M3β1θ2υ2M4M5β1θ1υ1+β1θ1θ2υ1υ2M4M5θ2υ2M2M3θ1υ1ΛζM1 (*)

4. Equilibria stability analysis

4.1 Disease-free equilibrium stability on a local and global scale, E 0

Theorem 2: For all R 0, the disease-free equilibrium E 0 exists, and it is locally asymptotically stable for R 0 < 1 and unstable otherwise.

Proof: The resulting matrix from linearized model dxdt=AX, where X=x1x2x3x4x5x6T,x1x2x3x4x5x6R+6 , and

A=g1μg2Λζg5c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2g7c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2g3ζΛα+g4μρg6c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2g8c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT20αθ1μυ10000θ1υ1μ000ρ00θ2daμυ20000θ2υ2daμ (15)
g1=c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2c1ψξβ2HA+β3AA+HUβ1S+HU+HA+HT+AA+AT,
g2=c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2c1ψξβ1SS+HU+HA+HT+AA+AT,
g3=c1ψξβ2HA+β3AA+HUβ1S+HU+HA+HT+AA+ATc1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2,
g4=c1ψξβ1SS+HU+HA+HT+AA+ATc1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2,
g5=c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2c1ψξβ2SS+HU+HA+HT+AA+AT,
g6=c1ψξβ2SS+HU+HA+HT+AA+ATc1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2
g7=c1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2c1ψξβ3SS+HU+HA+HT+AA+AT,
g8=c1ψξβ3SS+HU+HA+HT+AA+ATc1ψξβ2HA+β3AA+HUβ1SS+HU+HA+HT+AA+AT2

The resulting Jacobian matrix of (15) at E 0 is

|AλI|=μλΛζc1ψξβ1c1ψξβ20c1ψξβ300Λζ+c1ψξβ1αρμλc1ψξβ20c1ψξβ300αθ1μλυ10000θ1υ1μλ000ρ00θ2daμλυ20000θ2υ2daμλ (16)

from (16) the first eigenvalue is given as λ1=μ then the matrix reduces to the 5×5 matrix below

|AλI|=Λζ+c1ψξβ1M1λc1ψξβ20c1ψξβ30αM2λυ1000θ1M3λ00ρ00M4λυ2000θ2M5λ=0

and the characteristics equation of the above matrix is obtained as:

f(λ)=λ5+(ξβ1Λζcβ1+M1+M2+M3+M4+M5)λ4+(αβ2ξ+β3ρξ+ξM2β1+ξM3β1+ξM4β1+ξM5β1ΛζM2ΛζM3ΛζM4ΛζM5αβ2cβ3cM2β1cM3β1cM4β1cM5β1+M1M2+M1M3+M1M4+M1M5+M2M3+M2M4+M2M5+M3M4+M3M5+M4M5θ1υ1θ2υ2)λ3+(αβ2ξM3+αβ2ξM4+αβ2ξM5+β3ρξM2+β3ρξM3+β3ρξM5+ξM2M3β1+ξM2M4β1+ξM2M5β1+ξM3M4β1+ξM3M5β1+ξM4M5β1ξβ1θ1υ1ξβ1θ2υ2ΛζM2M3ΛζM2M4ΛζM2M5ΛζM3M4ΛζM3M5ΛζM4M5+Λζθ1υ1+Λζθ2υ2αβ2cM3αβ2cM4αβ2cM5β3M2β3M3β3M5cM2M3β1cM2M4β1cM2M5β1cM3M4β1cM3M5β1cM4M5β1+cβ1θ1υ1+cβ1θ2υ2+M1M2M3+M1M2M4+M1M2M5+M1M3M4+M1M3M5+M1M4M5M1θ1υ1M1θ2υ2+M2M3M4+M2M3M5+M2M4M5M2θ2υ2+M3M4M5+M3θ2υ2M4θ1υ1M5θ1υ1)λ2+(αβ2ξM3M4+αβ2ξM3M5+αβ2ξM4M5αβ2ξθ2υ2+β3ρξM2M3+β3ρξM2M5+β3ρξM3M5β3ρξθ1υ1+ξM2M3M4β1+ξM2M3M5β1+ξM2M4M5β1ξM2β1θ2υ2+ξM3M4M5β1ξM3β1θ2υ2ξM4β1θ1υ1ξM5β1θ1υ1ΛζM2M3M4ΛζM2M3M5ΛζM2M4M5+ΛζM2θ2υ2ΛζM3M4M5+ΛζM3θ2υ2+ΛζM4θ1υ1+ΛζM5θ1υ1αβ2cM3M4αβ2cM3M5αβ2cM4M5+αβ2cθ2υ2β3M2M3β3M2M5β3M3M5+β3θ1υ1cM2M3M4β1cM2M3M5β1cM2M4M5β1+cM2β1θ2υ2cM3M4M5β1+cM3β1θ2υ2+cM4β1θ1υ1+cM5β1θ1υ1+M1M2M3M4+M1M2M3M5+M1M2M4M5M1M2θ2υ2+M1M3M4M5M1M3θ2υ2M1M4θ1υ1M1M5θ1υ1+M2M3M4M5M2M3θ2υ2M4M5θ1υ1+θ1θ2υ1υ2)λ+αβ2cM3θ2υ2αβ2cM3M4M5β3M2M3M5+β3M5θ1υ1cM2M3M4M5β1+cM2M3β1θ2υ2+cM4M5β1θ1υ1Λζθ1θ2υ1υ2cβ1θ1θ2υ1υ2+β3ρξM2M3M5β3ρξM5θ1υ1+ξM2M3M4M5β1ξM2M3β1θ2υ2ξM4M5β1θ1υ1+αβ2ξM3M4M5αβ2ξM3θ2υ2+ξβ1θ1θ2υ1υ2+M1M2M3M4M5M1M2M3θ2υ2M1M4M5θ1υ1+M1θ1θ2υ1υ2ΛζM2M3M4M5+ΛζM2M3θ2υ2+ΛζM4M5θ1υ1=0 (17)

The above characteristic equation in (17) is of the form

fλ=a0λ4+a1λ3+a2λ2+a3λ+a4
αβ2cM3θ2υ2αβ2cM3M4M5β3M2M3M5+β3M5θ1υ1cM2M3M4M5β1+cM2M3β1θ2υ2+cM4M5β1θ1υ1Λζθ1θ2υ1υ2cβ1θ1θ2υ1υ2+β3ρξM2M3M5β3ρξM5θ1υ1+ξM2M3M4M5β1ξM2M3β1θ2υ2ξM4M5β1θ1υ1+αβ2ξM3M4M5αβ2ξM3θ2υ2+ξβ1θ1θ2υ1υ2+M1M2M3M4M5M1M2M3θ2υ2M1M4M5θ1υ1+M1θ1θ2υ1υ2ΛζM2M3M4M5+ΛζM2M3θ2υ2+ΛζM4M5θ1υ1=0

By Descartes rule of sign

c1ψξαβ2M3M4M5αβ2M3θ2υ2+β3ρM2M3M5β3ρM5θ1υ1+M2M3M4M5β1M2M3β1θ2υ2M4M5β1θ1υ1+β1θ1θ2υ1υ2<M4M5θ2υ2M2M3θ1υ1ΛζM1
1<c1ψξαβ2M3M4M5αβ2M3θ2υ2+β3ρM2M3M5β3ρM5θ1υ1+M2M3M4M5β1M2M3β1θ2υ2M4M5β1θ1υ1+β1θ1θ2υ1υ2M4M5θ2υ2M2M3θ1υ1ΛζM1

Let

R0=1<c1ψξαβ2M3M4M5αβ2M3θ2υ2+β3ρM2M3M5β3ρM5θ1υ1+M2M3M4M5β1M2M3β1θ2υ2M4M5β1θ1υ1+β1θ1θ2υ1υ2M4M5θ2υ2M2M3θ1υ1ΛζM1

Then,

R0=c1ψξαβ2M3M4M5αβ2M3θ2υ2+β3ρM2M3M5β3ρM5θ1υ1+M2M3M4M5β1M2M3β1θ2υ2M4M5β1θ1υ1+β1θ1θ2υ1υ2M4M5θ2υ2M2M3θ1υ1ΛζM1

Because all parameters of the model are assumed to be positive, λ 2 < 0, λ 3 < 0, λ 4 < 0, λ 5 < 0, λ 6 < 0. Evidently, if R 0 < 1, the roots of f( λ) have negative real parts, implying that E 0 is locally asymptotically stable (LAS) when R 0 < 1; if R 0 > 1, the roots of f( λ) are real and some are positive, implying that E 0 is unstable.

Theorem 3: If R 0 < 1, the disease free equilibrium is asymptotically stable globally for system (1).

Proof: The comparison theorem, as demonstrated by Ref. 60 proves the global stability of the disease-free equilibrium. We rename the infected class: dxdt=FVXJX,X=HUHAHTAAAT where,

F=c1ψξβ1c1ψξβ20c1ψξβ3000000000000000000000,V=M1Λζ0000αM2υ1000θ1M300ρ00M4υ2000θ2M5 (18)

Then all of the matrix FV eigenvalues have negative real parts, i.e. so that

J=1SNc1ψξβ1+ΛζM1λc1ψξβ20c1ψξβ30αM2λυ1000θ1M3λ00ρ00M4λυ2000θ2M5λ=0 (19)
λ5cβ1cψξβ1+ΛζM1M2M3M4M5λ4(ΛζM2+ΛζM3+ΛζM4+ΛζM5ξcψβ2αcψρξβ3cψξM2β1cψξM3β1cψξM4β1cψξM5β1+cβ2α+ρcβ3+cM2β1+cM3β1+cM4β1+cM5β1M2M1M3M1M4M1M1M5M3M2M2M4M2M5M3M4M3M5M4M5+υ1θ1+θ2υ2)λ3(ΛζM2M3+ΛζM2M4+ΛζM2M5+ΛζM3M4+ΛζM3M5+ΛζM4M5αcψξM3β2αcψξM4β2αcψξM5β2cψρξM2β3cψρξM3β3cψρξM5β3cψξM2M3β1cψξM2M4β1cψξM2M5β1cψξM3M4β1cψξM3M5β1cψξM4M5β1+cψξβ1θ1υ1+cψξβ1θ2υ2Λζθ1υ1Λζθ2υ2+αcM3β2+αcM4β2+αcM5β2+M2β3+M3β3+M5β3+cM2M3β1+cM2M4β1+cM2M5β1+cM3M4β1+cM3M5β1+cM4M5β1cβ1θ1υ1cβ1θ2υ2M1M2M3M1M2M4M1M2M5M1M3M4M1M3M5M1M4M5+M1θ1υ1+M1θ2υ2M2M3M4M2M3M5M2M4M5+M2θ2υ2M3M4M5+M3θ2υ2+M4θ1υ1+M5θ1υ1)λ2(αcψξβ2θ2υ2αcψξM3M4β2αcψξM3M5β2αcψξM4M5β2cψρξM2M3β3cψρξM2M5β3cψρξM3M5β3+cψρξβ3θ1υ1cψξM2M3M4β1cψξM2M3M5β1cψξM2M4M5β1+cψξM2β1θ2υ2cψξM3M4M5β1+cψξM3β1θ2υ2+cψξM4β1θ1υ1+cψξM5β1θ1υ1+ΛζM2M3M4+ΛζM2M3M5+ΛζM2M4M5ΛζM2θ2υ2+ΛζM3M4M5ΛζM3θ2υ2ΛζM4θ1υ1ΛζM5θ1υ1+αcM3M4β2+αcM3M5β2+αcM4M5β2αcβ2θ2υ2+M2M3β3+M2M5β3+M3M5β3cρβ3θ1υ1cM2M3M4β1+cM2M3M5β1+cM2M4M5β1cM2β1θ2υ2+cM3M4M5β1cM3β1θ2υ2cM4β1θ1υ1cM5β1θ1υ1M1M2M3M4M1M2M3M5M1M2M4M5+M1M2θ2υ2M1M3M4M5+M1M3θ2υ2+M1M4θ1υ1+M1M5θ1υ1M2M3M4M5+M2M3θ2υ2+M4M5θ1υ1θ1θ2υ1υ2)λ+αcψξM3M4M5β2αcψξM3β2θ2υ2+cψρξM2M3M5β3cψρξM5β3θ1υ1+cψξM2M3M4M5β1cψξM2M3β1θ2υ2cψξM4M5β1θ1υ1+cψξβ1θ1θ2υ1υ2ΛζM2M3M4M5+ΛζM2M3θ2υ2+ΛζM4M5θ1υ1Λζθ1θ2υ1υ2αcM3M4M5β2+αcM3β2θ2υ2M2M3M5β3+M5β3θ1υ1cM2M3M4M5β1+cM2M3β1θ2υ2+cM4M5β1θ1υ1cβ1θ1θ2υ1υ2+M1M2M3M4M5M1M2M3θ2υ2M1M4M5θ1υ1+M1θ1θ2υ1υ2 (20)

Equation (20) has four (4) negative roots by Descartes rule of signs if

(αcψξM3M4M5β2αcψξM3β2θ2υ2+cψρξM2M3M5β3cψρξM5β3θ1υ1+cψξM2M3M4M5β1cψξM2M3β1θ2υ2cψξM4M5β1θ1υ1+cψξβ1θ1θ2υ1υ2ΛζM2M3M4M5+ΛζM2M3θ2υ2+ΛζM4M5θ1υ1Λζθ1θ2υ1υ2αcM3M4M5β2+αcM3β2θ2υ2cρM2M3M5β3+cρM5β3θ1υ1cM2M3M4M5β1+cM2M3β1θ2υ2+cM4M5β1θ1υ11θ1θ2υ1υ2+M1M2M3M4M5M1M2M3θ2υ2M1M4M5θ1υ1+M1θ1θ2υ1υ2)<[(1cψξβ1+ΛζM1M2M3M4M5)×(ΛζM2+ΛζM3+ΛζM4+ΛζM5ξcψβ2αcψρξβ3cψξM2β1cψξM3β1cψξM4β1cψξM5β1+2α+ρcβ3+cM2β1+cM3β1+cM4β1+cM5β1M2M1M3M1M4M1M1M5M3M2M2M4M2M5M3M4M3M5M4M5+υ1θ1+θ2υ2)(ΛζM2M3+ΛζM2M4+ΛζM2M5+ΛζM3M4+ΛζM3M5+ΛζM4M5αcψξM3β2αcψξM4β2αcψξM5β2cψρξM2β3cψρξM3β3cψρξM5β3cψξM2M3β1cψξM2M4β1cψξM2M5β1cψξM3M4β1cψξM3M5β1cψξM4M5β1+cψξβ1θ1υ1+cψξβ1θ2υ2Λζθ1υ1Λζθ2υ2+αcM3β2+αcM4β2+αcM5β2+cρM2β3+cρM3β3+cρM5β3+cM2M3β1+cM2M4β1+cM2M5β1+cM3M4β1+cM3M5β1+cM4M5β11θ1υ11θ2υ2M1M2M3M1M2M4M1M2M5M1M3M4M1M3M5M1M4M5+M1θ1υ1+M1θ2υ2M2M3M4M2M3M5M2M4M5+M2θ2υ2M3M4M5+M3θ2υ2+M4θ1υ1+M5θ1υ1)(αcψξβ2θ2υ2αcψξM3M4β2αcψξM3M5β2αcψξM4M5β2cψρξM2M3β3cψρξM2M5β3cψρξM3M5β3+cψρξβ3θ1υ1cψξM2M3M4β1cψξM2M3M5β1cψξM2M4M5β1+cψξM2β1θ2υ2cψξM3M4M5β1+cψξM3β1θ2υ2+cψξM4β1θ1υ1+cψξM5β1θ1υ1+ΛζM2M3M4+ΛζM2M3M5+ΛζM2M4M5ΛζM2θ2υ2+ΛζM3M4M5ΛζM3θ2υ2ΛζM4θ1υ1ΛζM5θ1υ1+αcM3M4β2+αcM3M5β2+αcM4M5β2αcβ2θ2υ2+cρM2M3β3+cρM2M5β3+cρM3M5β3cρβ3θ1υ1+cM2M3M4β1+cM2M3M5β1+cM2M4M5β1cM2β1θ2υ2+cM3M4M5β1cM3β1θ2υ2cM4β1θ1υ1cM5β1θ1υ1M1M2M3M4M1M2M3M5M1M2M4M5+M1M2θ2υ2M1M3M4M5+M1M3θ2υ2+M1M4θ1υ1+M1M5θ1υ1M2M3M4M5+M2M3θ2υ2+M4M5θ1υ1θ1θ2υ1υ2)]

Since StΛμ in the invariant set, J is a non-negative matrix. Hence, it follows that

dxdtFVX

When R 0 < 1, the eigenvalues of the matrix FV are negative. As a result, the linearized. Since HUHAHTAAAT00000 as t . According to the comparison theorem, HUHAHTAAAT00000 as t . Substituting H U = H A = H T = A A = A T = 0 in (1) gives StS0 as t . Thus, SHUHAHTAAATS000000 as t for R 0 < 1.

4.2 The endemic equilibrium’s local and global stability; E *

Theorem 4: The endemic steady state ESHuHAHTAAAT of the model is locally asymptotically stable (LAS). If R 0 > 1.

Proof: We must now demonstrate the local stability of the endemic steady state. Assume R 0 > 1.

The Jacobian matrix for the variables of system (1) is computed in the proof of Theorem 2 as in (14).

Hence, for the endemic equilibrium SHUHAHTAAAT) , the Jacobian matrix and the determinantal equation at the endemic equilibrium is given as matrix in (15)

Clearly, the equation reduces to:

θ1μλv1μλv2daμλθ2daμλg1μλΛζ+g2g3Λζα+g4μρλ=0 (21)

The first four eigenvalues of (21) are given as:

λ1=θ1+μ,λ2=v1+μ,λ3=v2+da+μ,λ4=θ2+da+μ

The eigenvalue of the remaining 2 × 2 is obtained from the characteristics equation below:

λ2++αΛζg1g4+2μ+ρλ+Λζg1+Λζg3Λζμαg1+αμ+g1g4g1μg1ρg2g3g4μ+μ2+μρ (22)

The determinants of the characteristic polynomial from (22) yield the following result:

f(λ)=λ2+a1λ+a0.

Polynomials of order 2 satisfy the Routh-Hurwitz criterion, We know that f( λ) = 0 using Routh-Hurwitz criterion polynomials of order 2 is stable if and only if both coefficients in (22) satisfy the following conditions: a i > 0 From Eq. (22) the condition is satisfied. Therefore, EE is locally asymptotically stable.

Theorem 5: When R 0 < 1, the equations of the model have a positive distinct endemic equilibrium, which is said to be globally asymptotically stable.

Proof: Considering the Lyapunov function, which is defined as

LSHUHAHTAAAT=SSlnSS+HUHUlnHUHU+HAHAlnHAHA+HTHTlnHTHT+AAAAlnAAAA+ATATlnATAT

where L directly takes its derivative along the system as:

dLdt=1SSdSdt+1HUHUdHUdt+1HAHAdHAdt+1HTHTdHTdt+1AAAAdAAdt+1ATATdATdt
dLdt=1SSΛ1ζHUcbh1ψξβ1HU+β2HA+β3AAN+μS+1HUHUcbh1ψξβ1HU+β2HA+β3AANS(α+ρ+μ)HU+ΛζHU+1HAHAαHU+υ1HTθ1+μHA+1HTHTθ1HAυ+μHT+1AAAAρHU+υ2ATθ2+da+μAA+1ATATθ2AAυ2+da+μAT

At equilibrium

Λ1ζHU=cbh1ψξβ1HU+β2HA+β3AANS+μS
α+ρ+μ+Λζ=cbh1ψξβ1HU+β2HA+β3AAHUNS
θ1+μ=αHU+υ1HTHA
υ1+μ=θ1HAHT
θ2+da+μ=ρHUAA+υ2ATAA
υ2+da+μ=θ2AAAT
dLdt=1SScbh1ψξβ1HU+β2HA+β3AANS+μScbh1ψξβ1HU+β2HA+β3AAN+μS+1HUHUcbh1ψξβ1HU+β2HA+β3AANScbh1ψξβ1HU+β2HA+β3AAHUNSHU1HAHAαHU+υ1HTαHUHA+υ1HTHAHA+1HTHTθ1HAθ1HAHTHT+1AAAAρHU+υ2ATρHUAA+υ2ATAAAA+1ATATθ2AAθ2AAATAT
=1SScbh1ψξβ1HUNS+cbh1ψξβ2HANS+cbH1ψξβ3AANS+μScbh1ψξβ1HUNScbh1ψξβ2HANScbh1ψξβ3AANSμS+1HUHUcbh1ψξβ1HUNS+cbh1ψξβ2HANS+cbh1ψξβ3AANScbh1ψξβ1HUSHUHUNcbh1ψξβ2HASHUHUNcbh1ψξβ3AASHUHUNS+1HAHAαHU+υ1HTαHUHAHAυ1HTHAHA+1HTHTθ1HAθ1HAHTHT+1AAAAρHU+υ2ATρHUAAAAυ2ATAAAA+1ATATθ2AAθ2AAATAT
=1SScbh1ψξβ1HUSN1HUSNHUSNcbh1ψξβ2HAS1HASNHASNcbh1ψξβ3AAS1HASNAASNμS(1SS)+1HUHUcbh1ψξβ1HUSN1HUSNHUSN+cbh1ψξβ2HASN1HASHUHASHUN+cbh1ψξβ3AASN1AASHUAASHUN+(1HAHA)αHU1HUHU1HAHA+υHT1HTHT1HAHA+1HTHT(θ1HA1HAHA1HTHT+(1AAAA)ρHU1HUHU1AAAA+υ2AT(1ATAT)1AAAA+1ATATθ2AA1AAAA1ATATAT=μS1SS2+P1SHUHAHTAAAT+P2SHUHAHTAAAT

where

P1SHUHAHTAAAT=cbh1ψξβ1HUSN1SS1HUSNHUSNcbh1ψξβ2HASNHASN1SS1HASNHASNcbh1ψξβ3AASN1SS1AASNAASN
P2SHUHAHTAAAT=All others
P10wheneverHUSNHUSN,HASNHASN,AASNAASN (23)
P20wheneverHUSNHUSN,HASHUNHASHU,AASHUNAASHU,HUHAHUHA,HTHA, (24)

Thus

dLdt0

if (23) and (24) holds.

Hence, by Lasalle theorem, the equilibrium is globally asymptotically stable in the feasible region R+6 .

4.3 Sensitivity indices

Knowing the relative relevance of the different factors involved in HIV transmission and prevalence is vital for deciding how effectively to minimize human morbidity and mortality rate due to HIV infections. Sensitivity analysis is performed in this sub-section to assess the resilience of factors that have a strong impact on the basic reproduction number, R 0, so that suitable intervention strategies may be implemented.

The effect of HIV testing and treatment on HIV/AIDS dynamics was studied using the elasticity of ReH with respect to α and θ. Using the method described in Refs. 61 64 to compute the elasticity 65 of R eH with respect to α and θ as shown in Equation (25)

αθReHReHαθ=c1ψξζΛM1+c1ψξαM3M2M3θ1υ1ζΛM1+c1ψξρM4M42θ2υ2ζΛM1 (25)

Interpretation of the sensitivity indices

Table 1’s sensitivity indices are read as follows: Positive indices indicate that the corresponding basic reproduction number increases (decreases) as those parameters increase (decrease). Negative indices, on the other hand, indicate that increasing (decreasing) those parameters reduces the associated basic reproduction number (increases).

Table 1. Sensitivity indices of R 0.

Parameter Sensitivity index Parameter Sensitivity index
Λ +2.403314920 α -1.668175411
ζ +2.403314919 μ -0.6142854995
β 1 +0.6078964848 ρ -0.7905498030
β 2 +0.2655262466 d a -0.002219932464
β 3 +0.1265772695 θ 1 -0.2354014199
c +1 θ 2 -0.1120071499
υ 1 +0.01834155833
υ 2 +0.0009827457838

The endemicity of HIV infection increases when the values of β i , i = 1, 2, 3, υ, and c are increased; when the values of α and μ are decreased, the endemicity of HIV infection decreases.

As a result, interventions should aim to reduce the annual average number of sexual partners acquired, c, the number of defaulters lost to follow-up, υ, and the likelihood of HIV transmission per sexual contact, β i , i = 1, 2, 3, because the rate of progression from HIV to AIDS is increasing, ρ, indicates rapid progression to AIDS. In addition, effective condom use should be mandated as a precautionary measure to reduce the rate of HIV/AIDS transmission.

5. Numerical simulation

To affirm the model’s theoretical prognosis, simulation studies of the system (22) are run with the estimated parameter values listed below:

Simulation 1. Take into account the parametric data in Table 2 c = 3, ψ = 0, ξ = 0, β 1 = 0.050, β 2 = 0.055, β 3 = 0.060, μ = 0.2, Λ = 29, α = 0.7, ρ = 0.322, ζ = 0.02, υ 1 = 0.0169, υ 2 = 0.0169, θ 1 = 1.6949, θ 2 = 1.6949, d a = 0.0333: Hence, R 0 = 0.698 and the infection-free equilibrium is (145;0;0;0;0;0): We can see in Figure 2 that by changing the initial values, the solution trajectories intersect to (145.00;0;0;0;0;0): This confirms the fact that if R 0 < 1, the virus-free equilibrium is globally asymptotically stable:

Table 2. Definition of Parameters values for the HIV model.

Parameters Description Parameters value Source
Λ Recruitment rate 29 yr 1 3
ζ Rate of newborns infected with HIV 0.02 [Assumed]
c Contact rate 3 patners/ yr 3
β i , i = 1, 2, 3 Transmission rate for the infective HIV and AIDS [0.050, 0.055, 0.060] Assumed
μ Natural mortality 0.2 [Assumed]
α Testing rate 0.7 [Assumed]
ρ Progression rate from Unaware HIV to AIDS 0.322 [Assumed]
υ i , i = 1, 2 HIV and AIDS defaulters from treatment 0.0169 56
θ 1, i = 1, 2 HIV and AIDS treatment rate 1.6949 27
d a Mortality due to AIDS 0.0333 [Assumed]
ψ condom effectiveness [0,1] [Assumed]
ξ condom usage [0,1] [Assumed]

Figure 2. (Simulation 1) if R 0 < 1, the infection-free equilibrium is asymptotically stable.

Figure 2.

Simulation 2. Let c = 6, ψ = 0, ξ = 0, β 1 = 0.080, β 2 = 0.085, β 3 = 0.090, μ = 0.2, Λ = 29, α = 0.7, ρ = 0.322, ζ = 0.02, υ 1 = 0.0169, υ 2 = 0.0169, θ 1 = 1.6949, θ 2 = 1.6949, d a = 0.0333: Hence, R 0 = 2.197. Moreover, the endemic equilibrium is (64.197;13.225;5.251;41.035;2.348;15.905): We can see in Figure 3 that by changing the initial conditions, the solution trajectories intersect to (64.197;13.225;5.251;41.035; 2.348;15.905): This proves Theorem 5: if R 0 > 1, the endemic stability is globally stable.

Figure 3. (Simulation 2) If R 0 > 1, the endemic stability is asymptotically stable.

Figure 3.

Figure 4. (Simulation 3) Take ψ = 1 and ξ = 1,to check the impact of condom use and effectiveness on the population when there’s no contact.

Figure 4.

Simulation 3 depicts the distribution of individual proportions over time in various classes where there are no new infected children ζ or recruitment Λ, and contact c i.e. taking c = 0, ζ = 0, Λ = 0 when ψ = 1 and ξ = 1, (condom usage and effectiveness) i.e. when there is full protection keeping every other values at endemic equilibrum constant, the value of R 0 = 0.

The impact of perinatal transmission in the system, i.e. the incidence of new recruits of infected children directly into the infective group, is pointedly demonstrated in simulation 4.

Figure 5(a) shows that as the proportion of infected newborns ( ζ) rises, so does the proportion of the general population who is unaware. Figure 5(b) shows that increasing the value of ( ζ) causes the proportion of the AIDS population to decrease over time, then raise until it reaches its stable state. As a result, if newborns infected with the virus are treated, the total infective group will be better controlled, minimizing the AIDS individuals. Figure 5(c) shows that as the number of infected children born rises, so does the treated populace.

Figure 5. (Simulation 4) Variation in the infected individual for different ζ values.

Figure 5.

A. Variation of Unaware HIV population for different values of ζ. B. Variation of Aware HIV population for different values of ζ. C. Variation of HIV on Treatment population for different values of ζ. D. Variation of AIDS population for different values of ζ. E. Variation of AIDS on Treatment population for different values of ζ.

The effect of defaulters on treatment lost to follow-up in the model is examined in simulation 5.

Figure 6(a) shows that as the rate of defaulters ( υ) increases, so does the proportion of the population that is aware, whereas the proportion of HIV patients on treatment decreases (b). Figure 6(c) shows how increasing upsilon causes the proportion of the AIDS population to increase over time while decreasing the proportion of the AIDS population on treatment until equilibrium is reached. As a result, if the HIV-aware infected population follows adheres therapy, the infectious individual as a whole would then remain under control, lowering the HIV-aware and AIDS number of individuals.

Figure 6. (Simulation 5) Variation of the infected individual for different fallout, υ values.

Figure 6.

A. Variation of HIV Aware population for different values of υ. B. Variation of HIV on Treatment population for different values of υ. C. Variation of AIDS population for different values of υ. D. Variation of AIDS on Treatment population for different values of υ.

The increasing effect of testing and treatment on the model is examined in simulation 6.

From Figure 7(a-d), it is observed that if testing rate and treatment rate is increase,the unaware HIV decrease, while aware HIV and AIDS individual decrease with time due to treatment. Furthermore, the susceptible individual increases, and as treatment increases, so does the population of HIV and AIDS patients on treatment. As a result, increasing HIV screening and treatment is the first procedure to UNAIDS’ 90-90-90 aspirations.

Figure 7. (Simulation 6) Proportion of different Population at the increased values of α and θ.

Figure 7.

A. Proportion of Population when α = 0.7 and θ = 1.6949. B. Proportion of Population when α = 0.9 and θ = 2.6949. C. Proportion of Population when α = 1.5 and θ = 4.6949. D. Proportion of Population when α = 1.9 and θ = 9.6949.

Figure 8 shows the effect of treatment fall out on the reproduction number. When the number of infected individual on treatment that fallout is 19.8 percent then R 0 = 0.041. The linear graphical representation also revealed that if 40.1 percent of the population drops out of treatment, the reproduction number rises to 0.043. This simply means that, as defaulters lost to follow-up increase, the reproduction number also increases. Hence, reducing high-risk habits, mainly through education, is the most effective way to reduce the overall number of HIV/AIDS patients.

Figure 8. Impact of treatment fall out on HIV reproduction number.

Figure 8.

6. Conclusions and recommendations

This study investigated the effect of testing and ART on the vertical and horizontal transmission dynamics of HIV/AIDS infection using an improved compartmental model and the dynamics theory of SI infectious diseases.

Reducing high-risk behaviours, primarily through education on the importance of HIV/AIDS status awareness and treatment adherence, is the best option for reducing the total number of HIV/AIDS patients.

Increased HIV testing is the first step toward UNAIDS’s 90-90-90 objectives, although many countries still face significant obstacles in attaining this goal. Early detection allows for prompt antiretroviral therapy, which lowers HIV viral load and hence slows the transmission of the virus. We believe that increasing HIV/AIDS diagnosis rates will increase the number of HIV/AIDS patients treated in the short term but decrease the number in the long term. WHO advises HIV self-testing as a complementary strategy, 66 which can improve the efficiency of HIV testing. 67

The following summarizes the paper’s key findings:

  • The discovery that increased screening rates will slow the spread of the disease suggests that the endemicity of the virus will rise in the absence of screening, which will lead to a constant rise in the number of people living with AIDS. When HIV infected people are aware of the consequences of not following treatment protocol strictly and taking preventative actions with their contacts in the community, the effects on the dynamics of HIV/AIDS are also examined.

  • The current research showed that these intervention strategies are effective in combating the HIV/AIDS epidemic. This also emphasizes the need of behavioral and biologic therapies in preventing HIV transmission among pregnant women as neglected by Ref. 33.

  • Finally, based on the study, it can be inferred that the best strategy to lower the infections rate and incidence level is to inform, counsel, and educate the public about HIV testing as well as the dangers of engaging in risky behavior such as having unsafe sex or failing to use condoms properly.

This study has flaws, as well. Homosexual transmission was not included in the model and certain characteristics were chosen on the basis of assumptions and may not reflect reality.

In conclusion, the model implies that the most effective strategy to lower the incidence rate, in light of our study's findings, is through HIV counseling and testing, behavioural and biological strategies, effective condom use, controlling vertical transmission and stringent adherence to ART are required for HIV prevention among individuals and pregnant women. Even in the face of medication resistance, ART procedure adherence and effective condom use can successfully limit the transmission of HIV. The 90-90-90 strategy may not be sufficient on its own to end the global HIV/AIDS outbreak, but educational campaign by policy maker on strict adherence to treatment by HIV/AIDS positive on treatment and effective use of condom by those who are vulnerable to the virus and unaware individual would go a long way in meeting this eradication strategies by WHO.

Data availability

The data in this article come from Mukandivire et al., 2010, Zu et al., 2016, Lu et al., 2020, and other assumed/estimated data.

Software availability

Source code available from: https://github.com/OE-Abiodun/release/tag/v3.1.2

Archived source code at the time of publication: https://doi.org/10.5281/zenodo.6894864. 68

License: GNU General Public License v3.0

Funding Statement

The author(s) declared that no grants were involved in supporting this work.

[version 2; peer review: 3 approved]

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F1000Res. 2023 Mar 13. doi: 10.5256/f1000research.143793.r164918

Reviewer response for version 2

Fatmawati Fatmawati 1

The authors have addressed most of the issues raised in my report, and improved the paper accordingly.

Is the work clearly and accurately presented and does it cite the current literature?

Partly

If applicable, is the statistical analysis and its interpretation appropriate?

Partly

Are all the source data underlying the results available to ensure full reproducibility?

No

Is the study design appropriate and is the work technically sound?

Partly

Are the conclusions drawn adequately supported by the results?

Partly

Are sufficient details of methods and analysis provided to allow replication by others?

Partly

Reviewer Expertise:

Mathematical modeling in life science, optimal control, fractional modelling.

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.

F1000Res. 2023 Mar 8. doi: 10.5256/f1000research.143793.r164917

Reviewer response for version 2

Adedapo Loyinmi 1

All observed lapses are corrected. The article is now fit for indexing.

Is the work clearly and accurately presented and does it cite the current literature?

Yes

If applicable, is the statistical analysis and its interpretation appropriate?

Yes

Are all the source data underlying the results available to ensure full reproducibility?

Yes

Is the study design appropriate and is the work technically sound?

Yes

Are the conclusions drawn adequately supported by the results?

Yes

Are sufficient details of methods and analysis provided to allow replication by others?

Yes

Reviewer Expertise:

Biological and computational Mathematics

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.

F1000Res. 2023 Jan 25. doi: 10.5256/f1000research.135825.r159237

Reviewer response for version 1

Ropo Ebenzer Ogunsakin 1

In this paper, the authors developed a new mathematical model for the transmission dynamics of HIV and AIDS and the model was rigorously analysed. The authors considered the impact of three major strategies (impact of awareness, testing and follow up) which are important in controlling the transmission dynamics of HIV/AIDS. The six- compartmental model of HIV/AID presented are: Susceptible, (S), representing people who prone to be infected with HIV in engage in risk habits/factors, those who are unaware of their HIV status (HU), those who become aware after testing (HA), those who are placed on treatment after becoming aware (HT); the AIDS individuals (AA) due to non-adherence to treatment and the AIDS on treatment population (AT). The author showed that the model is positive through a given region in their analyses and the reproduction number of the model was correctly worked out. The effects of the strategies were graphically represented in the numerical simulations. The title is peaks a volume to the context of the article.

The work is well organized and approved for indexing. I have the following observation/comment on the paper:

  1. The overall command of English looks good, however there are some grammatical errors in the paper. Also the authors should check for incomplete sentences in the paper.

  2. Some representation can be made to reduce the size of the matrices as they are big or boxes should be adjusted.

  3. It is necessary that the biological meaning of R0 be properly stated.

  4. In the sensitivity section, the authors can as well placed the real values of the indices.

  5. The conclusion looks good, the novelty of the work is discussed.

Is the work clearly and accurately presented and does it cite the current literature?

Yes

If applicable, is the statistical analysis and its interpretation appropriate?

Partly

Are all the source data underlying the results available to ensure full reproducibility?

Yes

Is the study design appropriate and is the work technically sound?

Yes

Are the conclusions drawn adequately supported by the results?

Yes

Are sufficient details of methods and analysis provided to allow replication by others?

Yes

Reviewer Expertise:

Statistician, Biological and Computational Mathematics

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.

F1000Res. 2023 Jan 5. doi: 10.5256/f1000research.135825.r158041

Reviewer response for version 1

Fatmawati Fatmawati 1

I have read this article. Some of my critical comments include:

  1. Please explore the novelty of this article. What is the difference between this article and previous research that already exists.

  2. I don't see the connection between the existence of the endemic equilibrium point and basic reproduction number (R0). Likewise to prove the stability of the disease-free equilibrium. The authors only mention that if R0 < 1 then the disease-free equilibrium is LAS, while depending on R0 cannot be proven exactly

  3. Please also check for proof of global stability of the disease-free equilibrium.

  4. The authors must proofread very carefully the language of the manuscript.

  5. Carefully check in whole manuscript, dot, and comma after each equation.

  6. Then numerical results need to be discussed in more details.

  7. The conclusion sections should highlight the main findings of this study.

  8. References should be up to date and must follow the style correctly.

Is the work clearly and accurately presented and does it cite the current literature?

Partly

If applicable, is the statistical analysis and its interpretation appropriate?

Partly

Are all the source data underlying the results available to ensure full reproducibility?

No

Is the study design appropriate and is the work technically sound?

Partly

Are the conclusions drawn adequately supported by the results?

Partly

Are sufficient details of methods and analysis provided to allow replication by others?

Partly

Reviewer Expertise:

Mathematical modeling in life science, optimal control, fractional modelling.

I confirm that I have read this submission and believe that I have an appropriate level of expertise to state that I do not consider it to be of an acceptable scientific standard, for reasons outlined above.

F1000Res. 2022 Nov 18. doi: 10.5256/f1000research.135825.r152688

Reviewer response for version 1

Adedapo Loyinmi 1

The article proposed a mathematical model for the transmission dynamics of HIV and AIDS considering three control/preventive strategies: the impact of awareness, testing and follow up. The work presented a six- compartmental model of HIV/AID which are Susceptible, ( S), representing people who are likely to become infected with HIV; Unaware HIV infective, ( HU), Aware HIV infective ( HA), Treated HIV infective, ( HT); AIDS individuals ( AA) and AIDS on treatment individuals ( AT). Analysis of the model showed that the model is positively invariant. Also, the reproduction number of the model was accurately worked out. The stability of the model showed that the disease free and endemic equilibrium is stable if necessary conditions are satisfied. The numerical simulations graphically showed the effect of the control strategies. The work is well organized and suitable for indexing.

However, a few issues should be addressed:

  1. The manuscript needs to be properly arranged as some of the matrices are too big. The boxes should be adjusted.

  2. Under stability analysis of the DFE, the R0 is not clearly shown. Since conclusion depends on the value of R0, it is necessary that R0 is properly substituted in the equation.

  3. In the sensitivity section, the sensitivity value need to be presented in order to know how sensitive each parameters are. The + and - signs are not enough

  4. Graphs are not bold enough.

  5. Revisit the conclusion under stability of DFE to drive home your findings

  6. In figure 5, I suggest that more than two values of   ζ  be used .

  7. In the conclusion, the novelty of the work is not elaborately discussed. Please rewrite this part to show what the contribution to knowledge is.

  8. There should be a paragraph discussing earlier work on diseases such as Ebola, covid-19 and the likes threatening global health. Such articles like, but not limited to 'qualitative analysis and dynamical behaviour of a Lassa haemorrhagic fever model with exposed rodents and saturated incidence rate' would help.

Is the work clearly and accurately presented and does it cite the current literature?

Yes

If applicable, is the statistical analysis and its interpretation appropriate?

Yes

Are all the source data underlying the results available to ensure full reproducibility?

Yes

Is the study design appropriate and is the work technically sound?

Yes

Are the conclusions drawn adequately supported by the results?

Yes

Are sufficient details of methods and analysis provided to allow replication by others?

Yes

Reviewer Expertise:

Biological and computational Mathematics

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard, however I have significant reservations, as outlined above.

Associated Data

    This section collects any data citations, data availability statements, or supplementary materials included in this article.

    Data Availability Statement

    The data in this article come from Mukandivire et al., 2010, Zu et al., 2016, Lu et al., 2020, and other assumed/estimated data.


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