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ORIGINAL RESEARCH article

Front. Appl. Math. Stat., 26 May 2022
Sec. Mathematical Biology
This article is part of the Research Topic Modelling and Numerical Simulations with Differential Equations in Mathematical Biology, Medicine and the Environment View all 11 articles

On the Dynamics of Sexually Transmitted Diseases Under Awareness and Treatment

\nSuares Clovis Oukouomi Noutchie
Suares Clovis Oukouomi Noutchie*Ntswaki Elizabeth MafatleNtswaki Elizabeth MafatleRichard GuiemRichard GuiemRodrigue Yves M&#x;pika MassoukouRodrigue Yves M'pika Massoukou
  • Pure and Applied Analytics, School of Mathematical and Statistical Sciences, North-West University, Potchefstroom, South Africa

In this paper, we develop and extend the work of Jia and Qin on sexually transmitted disease models with a novel class of non-linear incidence. Awareness plays a central role both in the susceptible and the infectious classes. The Existence, uniqueness, boundedness, and positivity of solutions are systematically established. Concavity arguments and the occurrence of a vertical asymptote are essential in the proof of the existence of a unique endemic equilibrium. Conditions for the stability of all steady states are investigated. In particular, numerical simulations are performed in order to capture the asymptotic behavior of solutions.

AMS Classification: 92D30, 34D23.

1. Introduction

Disease incidence plays a crucial role in mathematical epidemiology and it is essential in the computation of the basic reproduction number. Non-linear incidences are known to induce complex or chaotic behavior as oppose to standard incidences frequently used in classical infectious disease models [16]. A class of non-linear incidences particularly useful in the modeling of sexually transmitted diseases was introduced in [7] by the authors in the modeling of HIV/AIDS epidemic. The model considered however was not properly conceptualized as the density of individuals with full-blown AIDS not receiving ARV treatment did not bear any influence on the infection rate of the disease. In addition a number of inaccuracies are displayed in this paper like the unknown variable T missing in the third equation of system (2.1) and also a mistake occurred in the computation of the sign of a3 in the proof of the stability of the endemic equilibrium. The purpose of this paper is to develop and extend the work on [7] by deriving a realistic model for sexually transmitted diseases with a proper non-linear incidence rate with a valid biological significance and perform a full analysis of the resulting model. In Section 2, the model is derived and presented. Well-posedness analysis, positivity and boundedness are considered in Section 3 followed by stability analysis of the critical points of the system in Section 4, numerical simulations in Section 5 and the conclusion.

2. The Model

In this paper, a model with five compartments is formulated with non-linear incidence Sg(t, I) incorporated into it. The incidence is presumed to be a time dependent non-linear response to the size of the infectious population.

The compartments are denoted by S(t), I(t), T(t), A(t) and R(t) which represent the number of susceptible individuals, the number of infected individuals with the potential of transmitting the disease as they are not under treatment and do not take any form of protection while engaging in sexual activities, the number of individuals under treatment, the number of infectious individuals engaging in safe sex, and heathy individuals that engage in safe sex, respectively, at time t. The model represented in Figure 1 is governed by the system of nonlinear ordinary differential equations

{dSdt=Γ-Sg(t,I)-(ω1+d)S,dIdt=Sg(t,I)+ν1T-(d+τ1+τ2)I,dTdt=τ2I-ν2T-(d+ν1)T,dAdt=τ1I-dA+ν2T,dRdt=ω1S-dR,    (1)

endowed with initial conditions

S(0) ≡ S0 > 0, I(0) ≡ I0 > 0, T(0) ≡ T0 ≥ 0, A(0) ≡ A0 ≥ 0, R(0) ≡ R0 ≥ 0.

FIGURE 1
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Figure 1. Flow diagram.

The parameters in the evolution system (1) are described in Table 1:

The total population N(t) is given by S(t) + I(t) + T(t) + A(t) + R(t). By adding all the equations of the system (1), we obtain the rate of change of N(t), which is given by

dNdt=Γ-dN    (2)

and N(t) varies over time and is nearing a stable fixed point Γd as t → ∞. Therefore, the biologically feasible region for the system (1) is given by

Ψ={(S,I,T,A,R)+5|0<S(t)+I(t)+T(t)+A(t)+R(t)Γd}.

It is easy to see that the set Ψ is positively invariant. Next we present a systematic analysis of our evolution equation.

TABLE 1
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Table 1. Biological meaning of parameters.

3. Mathematical Analysis

We start by investigating the well-posedness of the model (1). Given the fact that the variables represent biologically densities, it is important to show that all the variables remain positive at all time.

Lemma 1. For any non-negative initial conditions (S0, I0, T0, A0, R0), system (1) has a local solution which is unique.

Proof: Let x = (S, I, T, A, R), system (1) can be rewritten as x′(t) = f(t, x(t)), where f : ℝ6 → ℝ5 is a C1 vector field. By the classical differential equation theory, we can confirm that system (1) has a unique local solution defined in a maximum interval [0, tm).

Lemma 2. For any non-negative initial conditions (S0, I0, T0, A0, R0), the solution of (1) is non-negative and bounded for all t ∈ [0, tm).

Proof: We start by showing positivity of the local solution for any non-negative initial conditions. It is easy to see that S(t) ≥ 0 for all t ∈ [0, tm). Indeed, assume the contrary and let t1 > 0 be the first time such that S(t1) = 0 and S(t1)<0. From the first equation of the system (1), we have S(t1)=Γ>0, which presents a contradiction. Therefore S(t) ≥ 0 for all t ∈ [0, tm). Using the same argument, positivity I(t), T(t), A(t) and R(t) in the interval [0, tm) are established. Furthermore from (2), we have that

N(t)=Γd+N(0)e-dtΓd+N(0).    (3)

Therefore the solution N(t) is bounded in the interval [0, tm).

Theorem 1 For any non-negative initial conditions (S0, I0, T0, A0, R0), system (1) has a unique global solution. Moreover, this solution is non-negative and bounded for all t ≥ 0.

Proof: The solution does not blow up in a finite time as it is bounded, it is therefore defined at all time t ≥ 0. Other properties of the solution follow from lemma (1) and lemma (2).

Setting m = d + τ1 + τ2 and n = d + ν1 + ν2, system (1) transforms into a reduced system

{dSdt=Γ-Sg(t,I)-(ω1+d)S,dIdt=Sg(t,I)+ν1T-mI,dTdt=τ2I-nT,dAdt=τ1I-dA+ν2T,dRdt=ω1S-dR.    (4)

4. Models With Time Independent Non-linear Response

In this section, we assume that the non-linear response function is not time dependent, ie g(t, I) ≡ g(I). Following [7], it is further assumed that

(H1) : g(0)=0,g(0)>0,g(I)0 for I0,(H2) : limI0+g(I)I=k,0<k<.

4.1. The Basic Reproduction Number

In this section, we use the next generation method [8] to obtain the basic reproduction number. Let z be the transpose of (I, A, T, S, R). We rewrite the system (4) in the matrix form

dzdt=F(z)-V(z),

where

F(z)=(Sg(I)0000)

and

V(z)=(mI-ν1TdA-τ1I-ν2TnT-τ2ISg(I)+(ω1+d)S-ΓdR-ω1S).

The disease free equilibrium of system (4) takes the form

E0=(I0,A0,T0,S0,R0)=(0,0,0,Γω1+d,ω1Γd(ω1+d)).

Following [8], we compute the basic reproduction number using the formula below

R0=ρ(FV-1),

where

F=[F1EF1IF1T000000]|(E0,I0,T0,S0,R0)= [αΓω1+d00000000]

and

V=[V1EV1IV1TV2EV2IV2TV3EV3IV3T]|(E0,I0,T0,S0,R0)[m0ν1τ1dν2τ20n]

and ρ is the spectral radius of the matrix FV−1. Given the fact that

V-1=1d(mn-ν1τ2)[nd0-ν1dτ1n-ν2τ2mn-ν1τ2ν2m-ν1τ1τ2d0md],

it follows that

R0=αnΓ(ω1+d)(mn-ν1τ2).    (5)

4.1.1. Stability of the Disease-Free Equilibrium

The stability of the disease-free equilibrium will be investigated in this subsection.

Theorem 2 The disease free equilibrium E0 is globally asymptotically stable if 0<R0<1, and unstable if R0>1.

Proof: The Jacobian matrix (JE0), evaluated at E0, is given by

JE0=(-(ω1+d)-αΓω1+d0000αΓω1+d-mν1000τ2-n000τ1ν2-d0ω1000-d).    (6)

The characteristic equation that results from the Jacobian matrix (JE0) is given by det(JE0-λI) = 0. Thus, we get

(d+λ)2[(ω1+d)+λ][(m-αΓω1+d+λ)(n+λ)-ν1τ2]=0.    (7)

The characteristic equation (7) has three negative real roots, which are

          λ1=-d,λ2=λ3=-(ω1+d),

and the other 2 roots, λ4 and λ5, are roots of the equation

f(λ)=[(m-αΓω1+d)+λ](n+λ)-ν1τ2λ2+a1λ+a2=0,    (8)

where

a1=m+n-αΓω1+d,a2=mn-ν1τ2-αnΓω1+d.

We now need to consider the signs of λ4 and λ5. Note that

mn-ν1τ2>0.

Assuming

R0=αnΓ(ω1+d)(mn-ν1τ2)<1,

we have that

mn-ν1τ2-αnΓω1+d=a2>0.

Moreover

αnΓω1+d<mn-ν1τ2<mn.

It implies that

m-αΓω1+d>0.

It follows that a1 > 0. As a result the roots λ4 and λ5 are strictly negative. We can conclude that all roots of (7) have negative real parts, therefore, the disease free equilibrium is locally asymptotically stable [810]. Furthermore assuming that

R0=αnΓ(ω1+d)(mn-ν1τ2)>1,

we have that a2 < 0, it follows that the characteristic equation f(λ) = 0 has a least a strictly positive root. Therefore, the disease free equilibrium E0 is unstable.

4.2. Existence of an Endemic Equilibrium

In this subsection, we investigate the existence of an endemic equilibrium for the system (4).

Proposition 1. The system of differential equations (4) admits a unique endemic equilibrium if and only if R0>1.

Proof: Let E* = (S*, I*, T*, A*, R*) be an equilibrium point. Then the components of E* satisfy the following set of equations

{Γ-S*g(I*)-(ω1+d)S*=0,S*g(I*)+ν1T*-mI*=0,τ2I*-nT*=0,τ1I*-dA*+ν2T*=0,ω1S*-dR*=0.    (9)

From the last three equations of the system (9), we have that

T*=τ2I*n,A*=τ1+ν2τ2ndI*,R*=ω1S*d.

Substituting T*, A* and R* into the first two equations, we obtain

Γ-S*g(I*)-(ω1+d)S*=0,      S*g(I*)-(ν1τ2n-m)I*=0.

It follows that

S*=(m-ν1τ2n)I*g(I*)    (10)

and

Γ-(m-ν1τ2n)I*-(ω1+d)(m-ν1τ2n)I*g(I*)=0.    (11)

Next we set

h(I):=(ω1+d)(m-ν1τ2n)IΓ-(m-ν1τ2n)I.    (12)

It is enough to show that there exists a point I* ∈ ℝ+ such that h(I*) = g(I*). In other words, we will show that the curves of the functions h and g intersect at a point I*.

Note that

I=nΓmn-ν1τ2

is a vertical asymptote of the function h(I). For all

0<I<nΓmn-ν1τ2,

we have that

h(I)=(ω1+d)(m-ν1τ2n)[Γ-(m-ν1τ2n)I]+(ω1+d)(m-ν1τ2n)2I[Γ-(m-ν1τ2n)I]2=Γ(ω1+d)(m-ν1τ2n)[Γ-(m-ν1τ2n)I]2>0

and

h(I)=2[Γ-(m-ν1τ2n)I](m-ν1τ2n)2Γ(ω1+d)[Γ-(m-ν1τ2n)I]4=2Γ(ω1+d)(m-ν1τ2n)2[Γ-(m-ν1τ2n)I]3>0.

It follows that the function h is increasing and concave upward in the interval

[0,nΓmn-ν1τ2)

with a vertical asymptote at the right end of the interval. Note that the function g is increasing and concave downward in the closed interval

[0,nΓmn-ν1τ2].

As a result if

g(0)>h(0)=(ω1+d)(m-ν1τ2n)Γ,

which is equivalent to the condition R0>1, then Equation (12) has a unique root I* in the interval

(0,nΓmn-ν1τ2).

Furthermore if

I>nΓmn-ν1τ2,

then h(I) < 0. There is no intersection point with g(I) since g is a positive function. Therefore there exists a unique endemic equilibrium point E* = (S*, I*, T*, A*, R*) provided that R0>1. In addition if

g(0)h(0)=(ω1+d)(m-ν1τ2n)Γ,

equivalent to the condition R01, there is no endemic equilibrium for the system (4).

4.2.1. Stability of the Endemic Equilibrium

Lemma 3. Let g(I) be a positive smooth function defined on the interval [0, ∞). Suppose that assumptions H1 and H2 hold, then the following inequality is satisfied

1-Ig(I)g(I)0 for any I>0.    (13)

Proof:

We have that

d[g(I)-Ig(I)]dI=-Ig(I)0

as g″(I) ≤ 0. This implies that the function g(I) − Ig′(I) is increasing on the interval [0, ∞). Given the fact that g(0) − 0g′(0) = 0, it follows that g(I) − Ig′(I) ≥ 0.

Theorem 3 If R0>1, then the endemic equilibrium E* is locally asymptotically stable.

Proof: The Jacobian matrix of the endemic equilibrium is given by

JE*=(-g(I*)-(ω1+d)S*g(I*)000g(I*)S*g(I*)-mν1000τ2-n000τ1ν2-d0ω1000-d).    (14)

The characteristic equation that results from the Jacobian matrix (JE*) is given by det(JE*-λI) = 0. Thus, we get

(d+λ)2(λ3+b1λ2+b2λ+b3)=0,    (15)

where

b1=g(I*)+ω1+d+m+n-S*g(I*),b2=(m+n)[g(I*)+ω1+d]-S*g(I*)(ω1+d+n)+mn-ν1τ2,b3=(mn-ν1τ2)[g(I*)+ω1+d]-n(ω1+d)S*g(I*).

The characteristic Equation (15) has a negative real double root

λ1=λ2=-d,

and three other roots, λ3, λ4 and λ5, which are the roots of the equation

λ3+b1λ2+b2λ+b3=0.    (16)

From Lemma (3), we have that

1-I*g(I*)g(I*)0.    (17)

It follows that

m-S*g(I*)=m-(m-ν1τ2n)I*g(I*)g(I*)                         >m[1-I*g(I*)g(I*)]0.    (18)

Hence,

b1=g(I*)+ω1+d+m+n-S*g(I*)>0 using 18,b2=(m+n)[g(I*)+ω1+d]-S*g(I*)(ω1+d+n)+mn-ν1τ2     =(m+n)g(I*)+(ω1+d)[m+n-S*g(I*)]-nS*g(I*)+            mn-ν1τ2     =(m+n)g(I*)+(ω1+d)[m+n-S*g(I*)]+            n[m-(m-ν1τ2n)I*g(I*)g(I*)]-ν1τ2     =(m+n)g(I*)+(ω1+d)[m+n-S*g(I*)]+            (mn-ν1τ2)[1-I*g(I*)g(I*)]>0 using 17,

and

b3=(mn-ν1τ2)[g(I*)+ω1+d]-n(ω1+d)S*g(I*)     =(mn-ν1τ2)[g(I*)+ω1+d]     -(ω1+d)[(mn-ν1τ2)I*g(I*)g(I*)]     =(mn-ν1τ2)[g(I*)+ω1+d-(ω1+d)I*g(I*)g(I*)]     =(mn-ν1τ2){g(I*)+(ω1+d)[1-I*g(I*)g(I*)]}>0using 17.

Moreover we have that

b1b2-b3  =b1{(m+n)g(I*)+(ω1+d)[m+n-S*g(I*)]}           -(mn-ν1τ2)g(I*)           +b1{(mn-ν1τ2)(1-I*g(I*)g(I*))}           -{(mn-ν1τ2)[(ω1+d)(1-I*g(I*)g(I*))]}.

It follows that

b1b2-b3   >n{(m+n)g(I*)+(ω1+d)[m+n-S*g(I*)]}-mng(I*) + {(mn-ν1τ2)[(ω1+d)(1-I*g(I*)g(I*))][g(I*)+m-S*g(I*)]}>0.

As a result, by the Routh−Hurwitz stability criterion [11], all the roots of the characteristic polynomial (15) have strictly negative real parts. Therefore the endemic equilibrium is locally asymptotically stable.

5. Numerical Simulations

In this section, we provide numerical simulations for the evolution system of ordinary differential equations (1) to support the theoretical findings. Without loss of generality we set

g(I)=α(t)I1+β(t)I.

Note that conditions of assumptions (H1) and (H2) are satisfied. Furthermore we let

Γ=150,ω1=1,d=2,ν1=1,ν2=1,τ1=2,τ2=3.

Next we explore two scenarios involving static simulations and time-dependent simulations respectively.

5.1. Static Simulations

Picking α=112 and β = 1 and substituting in the expression of the basic reproduction number, we get that R0=23<1. According to Theorem 2 the disease-free equilibrium, E0 = (50, 0, 0, 0, 25), is globally asymptotically stable. In Figure 2, it clearly shows that the disease eventually dies out.

FIGURE 2
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Figure 2. Static simulation for disease-free equilibrium.

Picking α=15 and β = 0.1 and substituting in the expression of the basic reproduction number, we get that R0=1.6>1. According to Theorem 3 the endemic equilibrium, E* = (42.5, 3.6, 2.7, 4.9, 21.2), is locally asymptotically stable. In Figure 3, all the graphs converge to the endemic equilibrium.

FIGURE 3
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Figure 3. Static simulation for endemic equilibrium.

5.2. Time-Dependent Simulations

Picking α(t)=15+2t, it can be observed in Figure 4 that graphs converge to the disease free equilibrium as time increases. It therefore suggests the global asymptotical stability of the disease free equilibrium and the extension of the disease in time.

FIGURE 4
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Figure 4. Simulation with time dependence for disease-free equilibrium.

Picking α(t)=t2+54, Figure 5 clearly shows that the susceptible population vanishes in a short span of time and the disease essentially affects all people in the population.

FIGURE 5
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Figure 5. Simulation with time dependence for endemic equilibrium.

6. Concluding Remarks

In this paper, we formulated and investigated a mathematical model describing the dynamics on sexually transmitted disease models with a novel class of non-linear incidence. We showed that the derived non-autonomous system of differential equations governing the evolution of the process was well-posed and the solution happened to be positive and bounded. The role of awareness in the susceptible and infectious classes was explored and investigated. A vertical asymptote and concavity arguments were critical in the proof of existence of an endemic equilibrium for the system and its asymptotical stability. In particular, numerical simulations were performed in order to predict the asymptotic behavior of solutions and support the theoretical findings.

Data Availability Statement

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author/s.

Author Contributions

All authors contributed to all critical aspects of the analysis and simulations. All authors contributed to the article and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher's Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Keywords: stability, non-linear response, concavity, vertical asymptote, awareness, disease

Citation: Oukouomi Noutchie SC, Mafatle NE, Guiem R and M'pika Massoukou RY (2022) On the Dynamics of Sexually Transmitted Diseases Under Awareness and Treatment. Front. Appl. Math. Stat. 8:860840. doi: 10.3389/fams.2022.860840

Received: 23 January 2022; Accepted: 19 April 2022;
Published: 26 May 2022.

Edited by:

Ramoshweu Solomon Lebelo, Vaal University of Technology, South Africa

Reviewed by:

Appanah Rao Appadu, Nelson Mandela University, South Africa
Marin I. Marin, Transilvania University of Braşov, Romania

Copyright © 2022 Oukouomi Noutchie, Mafatle, Guiem and M'pika Massoukou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Suares Clovis Oukouomi Noutchie, 23238917@nwu.ac.za

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.