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. 2021 Mar 24;24:104053. doi: 10.1016/j.rinp.2021.104053

Modeling the transmission dynamics of middle eastern respiratory syndrome coronavirus with the impact of media coverage

BiBi Fatima a, Manar A Alqudah b,, Gul Zaman a, Fahd Jarad c,d, Thabet Abdeljawad e,d,f,
PMCID: PMC7987584  PMID: 33777666

Abstract

Middle East respiratory syndrome coronavirus has been persistent in the Middle East region since 2012. In this paper, we propose a deterministic mathematical model to investigate the effect of media coverage on the transmission and control of Middle Eastern respiratory syndrome coronavirus disease. In order to do this we develop model formulation. Basic reproduction number R0 will be calculated from the model to assess the transmissibility of the (MERS-CoV). We discuss the existence of backward bifurcation for some range of parameters. We also show stability of the model to figure out the stability condition and impact of media coverage. We show a special case of the model for which the endemic equilibrium is globally asymptotically stable. Finally all the theoretical results will be verified with the help of numerical simulation for easy understanding.

Keywords: SIHRS model, Media coverage, Backward bifurcation, Stability analysis

Introduction

Infectious diseases are responsible for a quarter of all death in the world annually, such as SARS, MERS, and now COVID-19, that exhibit some distinct features such as rapid spread and visible symptoms [1], [2], [3]. One of the initiatives is to inform individuals through media and education as quickly as possible the right preventive understanding of the disease. We understand from experience that the more preventive the inhabitants understand, the better they can stop the disease from spreading.

In recent years, there have been global fears over viruses. Outbreaks of MERS, SARS, or influenza A are deadly and spread fast. It is one area where the media can play a life-saving role. Timely, accurate information, under the umbrella of risk communication or disaster communication, can help curb outbreaks and drive people to seek treatment early[5], [4]. Mass media reports can induce individual behaviour change during a disease outbreak, which has been found to be useful as it reduces the force of infection.

In May 2015, South Korea was hit by a massive, deadly outbreak of the MERS virus [6], [7], [8]. It was a little known virus that started with the patient suffering symptoms of a common cold, but could kill within two weeks. The virus had first spread in Saudi Arabia, where 40 percent of those who contracted it died, [9], [10], [11]. In South Korea 186 people were infected and 38 of those died within two months of falling ill. A lack of information about the nature of the illness, and about where the outbreaks were occurring, led to a widespread panic. The research focused on media coverage of the 2015 Middle East respiratory syndrome (MERS) crisis in South Korea.

In particular by the country’s three major terrestrial television stations: KBS and MBC, both public broadcasters, and SBS, a commercial channel. Coverage of the MERS outbreak by these three television stations between May and July 2015 was examined. The author also interviewed eleven journalists and editors, via email and the messaging app ‘Kakao talk’ voice function, between 7th April to 7th June 2017. Other interviews were conducted in the UK, via events at the Refuters Institute for the Study of Journalism in Oxford. Mathematical modeling and analysis are used for the dynamics of infectious diseases, see for instance [12], [13], [14], [15], [16], [17], [18], [19]. There have been mathematical modeling studies to analyze the impact of media coverage on the spread and control of infectious disease in a given population. In mathematical epidemiology the role of media communication in alerting the outcome of infectious disease outbreak, continuously having a place. The paper aimed to analyse the flow of information during an epidemic and to understand the impact of media coverage on the transmission of infectious and hospitalized individuals.

In [20], the authors extend the classical SEI model by considering a new incidence functional which reflects the impact of the media coverage to the spreading and control of the disease. The incidence function has been considered to play a key role in ensuring that the model indeed give reasonable qualitative description of the transmission dynamics of the diseases. We consider the model of [20], by taking the hospitalize class.

The paper is arrange as follow: In Section “A SIHRS model of MERS-CoV with media coverage”, we discuss formulation of the model, disease free equilibria and reproductive number. In Section “Endemic equilibria and backward bifurcation”, we discuss endemic equilibria and the existence of backward bifurcation for some range of parameter. In Section “Sensitivity analysis”, we discuss sensitivity analysis of the model. In Section “Stability analysis”, we find local and global stability analysis. In Section “A Special case of model (1) with γ=0”, we discuss a special case of the model and obtained global asymptotic stability of the proposed model. In Section “Numerical simulation”, we discuss numerical simulation of the proposed model. In Section “Discussion”, we give discussion on the obtained results.

A SIHRS model of MERS-CoV with media coverage

We examine the transmission of MERS CoV in a specified region. We distribute the population into the following compartments. The susceptible S(t).

  • All new born will goes to the susceptible class only,

  • The infected I(t) who are infectious,

  • The hospitalize H(t),

  • The recovered population R(t).

To incorporate the effect of the behavioral changes of the susceptible individuals, we used a non-linear incidence rate.

The mathematical model based on SIHR model with the incident of mass action is given by:

dSdt=π-(β1-β2Im+I)SI-(β3-β4Hm+H)SH+γR-μ0S,dIdt=(β1-β2Im+I)SI+(β3-β4Hm+H)SH-(q+κ+μ0)I,dHdt=qI-(α+μ0)H,dRdt=κI+αH-(μ0+γ)R, (1)

with

S(0)>0,I(0)0,H(0)0R(0)0. (2)

In model (1).

  • π is the recruitment rate of susceptible population.

  • μ0 represent natural death rate and κ is death rate occur due to disease.

  • β1,β3 are the contact rate before media alert.

  • β1-β2Im+I, and β3-β4Hm+H are the contact rate after media alert.

Disease free equilibrium and basic reproductive number

The model (1) have a disease free equilibrium denoted by E0 and given by E0=(S0,0,0,0), where the components are define as; S0=πμ0. Basic reproductive number a threshold representing how many secondary infections results from the introduction of one infected individuals in a susceptible population. For the basic reproductive number R0, we use the method of Driessche and Watmough [21].

F=β1πμ0β3πμ000,V=(q+κ+μ0)0-q(α+μ0), (3)
FV-1=β1πμ0(q+κ+μ0)+β3qπμ0(α+μ0)(q+κ+μ0)β3πμ0(α+μ0)00, (4)

then R0 is the spectral radius of FV-1, that is

R0=β1πμ0(κ+q+μ0)+β3qπμ0(α+μ0)(q+κ+μ0). (5)

The basic reproduction number R0 of this model consists of two parts, representing the two different transmission routes; i.e., from the infected individuals, from hospitalized individuals before media alert. Where β1,β3 show contact rate before media alert.

Theorem 1

The solution of the model (1) is bounded.

Proof

The total population is represented by N(t) that is N(t)=S(t)+I(t)+H(t)+R(t). Differentiation N(t) with time and setting the expression for dSdt,dIdt,dHdt,dRdt, we get

dN(t)dt=π-μ0S-μ0I-μ0H-μ0R. (6)
Ωh=(S(t),I(t),H(t),R(t)R+4,0<S(t)+I(t)+H(t)+R(t)πμ0.

 □

Endemic equilibria and backward bifurcation

Suppose the left hand side of each differential Eq. (1) be zero, the endemic (S,I,H,R) satisfies S>0,I>0,H>0,R>0 and

S=q+κ+μ0β1-β2Im+I+β3(α+μ0)-β4(q)2(α+μ0)(m(α+μ0)+q)I,H=qα+μ0,R=κ(α+μ0)+qα(μ0+γ)(α+μ0),

putting the above expression into the first equation of model (1) and after simplification, we have

aB2+bB+c. (7)
a=(β1-β2)γ(κ+μ0)+q(q+κ+μ0)(R0-1)(μ0+γ)+(β2-β3)γ(κ+μ0)(μ0+γ),b=-γβ1m-β3m(q+κ+μ0)-γβ1m(γ+μ0)-(1-R0),c=μ0m(q+κ+μ0)(R0-1).

If R0>1, then c>0,a>0, it follow that the model (1) get a unique endemic equilibrium E(S,I,H,R). If R0<1, we obtain a<0,b<0,c<0 which does not have any endemic equilibrium.

The significance of backward bifurcation in the epidemiological model is that of the classical requirement of the basic reproduction number R0 to be less than one [22], [23], while necessary for the elimination of the MERS CoV virus from population. The presence of backward bifurcation in the proposed model suggests that the feasibility of MERS virus elimination, when the basic reproduction number is less than one, depends on the initial size of the sub population of the model. For R0=1, the following result holds (Fig. 1 ).

Lemma 1

If R0=1 , the model (1) posses the phenomena of backward bifurcation if c<0 .

Fig. 1.

Fig. 1

Bifurcation diagram of model (1) showing backward bifurcation.

Sensitivity analysis

We bring out sensitivity analysis of parameters using in the proposed model. This analysis will make it easy to know the parameters that have a essentially effect on reproductive number. We apply the technic given in [24], [25] and given by, ΔhR0=R0hhR0 where h is parameter.

Δβ1R0=R0β1β1R0=πμ0(q+κ+μ0)=0.99900099>0,ΔR0=R0R0=β3qπμ0(α+μ0)(q+κ+μ0)=0.000999899>0,ΔkR0=R0kkR0=-β1π(α+μ0)+β3qπμ0(α+μ0)(q+k+μ0)=-0.64516294<0,ΔqR0=R0qqR0=β1π(α+μ0)+β3qπμ0(α+μ0)(q+k+μ0)=-0.0321580<0,ΔαR0=R0ααR0=β1πμ0(α+μ0)(q+k+μ0)-β1π(α+μ0)+β3qπμ0(α+μ0)2(q+k+μ0)=-0.0016665050<0,Δμ0R0=R0μ0μ0R0=-1.3226639<0,Δβ3R0=R0β3β3R0=qπμ0(α+μ0)(q+k+μ0)=0.000999899>0,ΔπR0=R0ππR0=β1μ0(q+κ+μ0)=0.99900099>0.

Stability analysis

To examine the local and global stability analysis of the model (1) about E0=(S0,0,0,0), we use the following results. Fig. 2 .

Parameter Sensitivity indices Parameter Sensitivity indices
β1 + +
κ q
α μ0
β3 + π +

Theorem 2

We take the model (1) with all positive parameters. For R0>1 the model (1) possess a unique endemic equilibrium E(S,I,H,R) and is locally asymptotically stable. For R0<1 the model (1) get a unique disease free equilibrium E0(S0,I0,H0,R0) and is globally asymptotically stable.

Proof

The Jacobian matrix of the suggested model (1) about the DFE point E0 is

J(πμ0,0,0,0)=-μ0-β1πμ0-β3πμ0γ0-(q+κ+μ0)(1-R0)β3πμ000q-(α+μ0)00κα-(μ0+γ). (8)

The first two eigen values have already negative real part λ1=-μ0<0,λ2=-(μ0+γ)<0 for the rest of eigenvalue we take 2×2 matrix, by Routh–Hurwitz criteria [26], we have to prove that trace of A is negative and determinant of A is positive, if R0<1,

J0=-(q+κ+μ0)(1-R0)β3πμ0q-(α+μ0). (9)
Trace(A)=-[(q+κ+μ0)(1-R0)+(α+μ0)],

thus Trace(A)<0 if R0<1.

det(A)=[(q+κ+μ0)(1-R0)][(α+μ0)]-[β3πμ0(q)].

Hence det(A)>0 if R0<1 and β30, which implies that det(A) is positive, if R0<1. Therefore, Trac(A)<0 and det(A)>0 if and only if R0<1. Thus the disease free equilibrium is locally asymptotically stable at E0.

Let us consider Lypunov function V=I. Differentiating V with the solution of model (1), we obtain

V.=I.=(β1-β2Im+I)SI+(β3-β4Hm+H)SH-(q+κ+μ0)Iβ1SI-(q+κ+μ0)I(q+κ+μ0)(R0-1)I<0.

Hence E0 is globally stable at disease free equilibrium point.

For R0>1, the jacobian matrix at the equilibrium E is

J(S,I,H,R)=-A-B-CγD-EG00q-(α+μ0)00κα-(μ0+γ), (10)

where

A=μ0-(β1-β2Im+I)I-(β3-β4Hm+H)H,B=β2mI[β1m+(β1-β2)I](m+I),C=β4mH[β3m+(β3-β4)I](m+H),D=(β1-β2Im+I)I+(β3-β4Im+I)H,G=β4mI(q)(α+μ0)[β2m+(β3-β4)H](m+H),E=β2mI(q+κ+μ0)[β1m+(β1-β2)I](m+I)-(q+κ+μ0).

The characteristic equation of the jacobian matrix is

ξ4+a1ξ3+a2ξ2+a3ξ+a4=0, (11)

where

a1=(A+2μ0+γ+q+κ),a2=(π+μ0+α+q)B+(A(α+μ0)+DM,a3=π(q+κ+μ0)A+M(α+μ0)C,a4=NG(π+μ0)β2m+(R0-1)+(γ+q+κ),

a1>0,a2>0,a3>0,a4>0, also a1a2a3>a32+a12a4. It follows from Routh Hurwtiz criteria all the eigen values (11) have negative real part if R0>1, which means that E is locally asymptotically stable. □

Fig. 2.

Fig. 2

The variation of different parameters and its effect on the basic reproductive number.

A Special case of model (1) with γ=0

Suppose γ=0 in model (1) we have the following SIHR model

dSdt=π-(β1-β2Im+I)SI-(β3-β4Hm+H)SH-μ0S,dIdt=(β1-β2Im+I)SI+(β3-β4Hm+H)SH-(q+κ+μ0)I,dHdt=qI-(α+μ0)H,dRdt=κI+αH-μ0R. (12)

The first three equations are independent of the fourth equation in the model (12). We consider the reduced model as:

dSdt=π-(β1-β2Im+I)SI-(β3-β4Hm+H)SH-μ0S,dIdt=(β1-β2Im+I)SI+(β3-β4Hm+H)SH-(q+κ+μ0)I,dHdt=qI-(α+μ0)H. (13)

The model (13) bear disease free equilibrium at E0=(πμ0). For endemic equilibrium point we put right hand side of (13) zero,

S=q+κ+μ0β1-β2Im+I+β3(α+μ0)-β4(q)2(α+μ0)(m(α+μ0)+q)I,I=q+κ+μ0β1-β2Im+I+β3α(R0-1)(α+μ0)(m(α+μ0)+πμ0,H=qα+μ0.

Theorem 3

We take the model (13) with all positive parameters. For R0>1 the model (13) possess a unique endemic equilibrium E(S,I,H,R) and is locally asymptotically stable. For R0<1 the model (13) get a unique disease free equilibrium E0(S0,I0,H0,R0) and is globally asymptotically stable.

Proof

Jacobian matrix of the suggested model (13) about the point E0 is

J(πμ0,0,0,0)=-μ0-β1πμ0β3πμ00(q+κ+μ0)(R0-1)β3πμ00q-(α+μ0). (14)

When R0<1, then (q+κ+μ0)(R0-1)<0, complete the proof.

Jacobian matrix at the point E=(S,I,H) is give by,

J(S,I,H)=-A-B-CD-EG0q-(α+μ0). (15)

where

A=μ0-(β1-β2Im+I)I-(β3-β4Hm+H)H,B=β2mI[β1m+(β1-β2)I](m+I),C=β4mH[β3m+(β3-β4)I](m+H),D=(β1-β2Im+I)I+(β3-β4Im+I)H,G=β4mI(q)(α+μ0)[β2m+(β3-β4)H](m+H),E=β2mI(q+κ+μ0)[β1m+(β1-β2)I](m+I)-(q+κ+μ0).

The characteristic equation of the above jacobian matrix is

ξ3+a1ξ2+a2ξ+a3=0. (16)

where

a1=(A+2μ0+γ+q+κ),a2=(π+μ0+α+q)B+(A(α+μ0)+DM,a3=π(q+κ+μ0)A+M(α+μ0)(R0-1)C,a1a2=Aπ+γπ+κμ0+A(α+μ0)+qκ+(R0-1)+2Dμ0,

a1>0,a2>0,a3>0, also a1a2>a3. From Routh Hurwtiz criteria [26] all the eigen values (16) have negative real part if and only if R0>1, which means that E is locally asymptotically stable. □

Global stability of disease free equilibrium

For global stability at DFE, we use Lyapunov function theory [27].

Theorem 4

For R0<1 the disease free equilibrium of model (13) is stable globally, if S=S0 other wise unstable if R0>1 .

Proof

We define the following Lyapunov function is given by

F(t)=12[(S-S0)+I+H+(R-R0)]2+w1(S-S0)+w2I(t)+w3H(t)+w4(R-R0). (17)

where’s wii=1,2,3,4 are positive constant taking time derivative of (17), we have

dFdt=[(S-S0)+I+H+(R-R0)][π-μ0S-μ0I-μ0R]+w1dSdt+w2dIdt+w3dHdt+w4dRdt.

By using w1=w2=w3=μ0,w4=δ

dFdt=-[(S-S0)+I(t)+H(t)+(R-R0)][μ0(S-S0)+μ0(I(t)+H(t)+R(t)+μ0(R-R0)-μ0q2(S-S0)-q2q3(1-R0)H(t)-β1S0H(t)-μ0(R-R0),

dFdt is negative if S>S0 and R0<1 and dFdt=0if and only if S=S0. By Lasala inverience principle [28], [29], the disease free equilibrium is globally asymptotically stable.

For global stability at endemic equilibrium we used the geometrical approach [30], [31]. □

Proof

The linearized matrix and second additive compound matrix is denoted by J and J2| model (13), which becomes

J=-a11a12a13a21a22a230qγ-a33,J2|=-(a11+a22)a23-a13a32-(a11+a33)a12-a31a21-(a22+a33). (18)

Consider the function G(χ)=G(S,I,H)=diagSI,SI,SI, then, G-1(χ)=diagIS,IS,IS, taking derivative of, Gf(χ), we get

Gf(χ)=diagS˙I-SI˙I2,S˙I-SI˙I2,S˙I-SI˙I2. (19)

GfG-1=diagS˙S-I˙I,S˙S-I˙I,S˙S-I˙I, GJ22|G-1=J22| and take N=GfG-1+GJ22|G-1, which can be written as

N=N11N12N21N22, (20)

where

N11=S˙S-I˙I-(β1-β2Im+I)I-(β3-β4Hm+H)H-μ0,
N12=-β1S+β2(m+I)2I-I2(m+I)2-β3S+β4(m+H)2H-H2(m+H)2,N21=(β1-β2Im+I)I+(β3-β4Hm+H)0,
N22=S˙S-I˙I-β1S-β2(m+I)2I-I2(m+I)2-(q+κ+μ0)β3S-β4(m+H)2H-H2(m+H)2qγS˙S-I˙I-2d0-(α+μ0).

Let (n1,n2,n3) be a vector in R3 its norm . defined as

n1,n2,n3=max{n1,n2+n3}. (21)

Now by Martin et al. [31], (N)sup{g1,g2}=sup{(N11)+N12),(N22)+N21}, where gi=(Nii)+Nij) for i=1,2 and ij, which implies that

g1=(N11)+N12),g2=(N22)+N21), (22)

where (N11)=S˙S-I˙I-(β1-β2Im+I)I-(β3-β4Hm+H)H-μ0, (N22)=S˙S-I˙I-β1S-β2(m+I)2I-I2(m+I)2-(q+κ+μ0),β3S-β4(m+H)2H-H2(m+H)2=S˙S-I˙I-2μ0-(q+κ)-min{β1,β3}, N12)=1NβS and N21)=max{(β1-β2Im+I)I+(β3-β4Hm+H,0}=(β1-β2Im+I)I+(β3-β4Hm+H. Therefore g1 and g2 becomes, such that, g1S˙S-2μ0-(q+κ) and g2S˙S-2μ0-(q+κ)-min{(β1-β2Im+I)I+(β3-β4Hm+H,0}, which implies that (N)S˙S-2μ0-min{(β1,β3}. Hence (B)S˙S-2μ0. Now integrating the Lozinski measure (N) with respect to t in the interval [0,t] and taking limt, we obtain

limtsupsup1t0t(B)dt<-2μ0. (23)

So finally, we can write

q¯=limtsupsup1t0t(N)dt<0.

Thus the system (1) around (S,I,H). is globally asymptotically stable. □

Numerical simulation

In this section, we solved the proposed deterministic model by using Runge–Kutta method of order 4th, see for detail [32]. To further understand the dynamical behavior of the proposed model we used numerical simulation to verify our analytical findings. In order to do this, we assumed some value of parameters, and some are taken from publish data given in Table 1 . The choice of numerical values of the parameter are taken in such a way that would be more biologically feasible. We also assume the time interval is 10 days with initial population for susceptible S(t), infected I(t), hospitalised H(t), recovered from MERS-CoV R(t). Moreover, the biological interpretation of these results states that if the value of basic reproductive number is less than one, then the susceptible population decreases, while then become stable and shows that there will be always stable susceptible population, see Fig. 3 . The dynamics of I(t),H(t),R(t) reveals that the number of these populations will be decreases and reaches to zero as shown in Fig. 3a–d, which ensure the stability of the proposed model. One of the important factor is to find the relative impact of the basic reproductive number to epidemic parameters as shown in Fig. 3.

Table 1.

Description of parameter and its value.

π recruitment rate .09
μ0 natural Death rate .022
μ1 constant Death rate related to disease .022
β1 contact rate before media alert .026
β2 contact rate before media alert .026
β3 contact rate after media alert .026
β4 contact rate after media alert .026
q relative transmission rate .002
α rate at which individuals moves to recovered class .05
γ rate at which individuals move to susceptible class from recovered class .065
m media coverage .64
κ death rate due to MERS-CoV .004

Fig. 3.

Fig. 3

The plots demonstrate the time dynamics of different compartmental population (Susceptible, Infected, Hospitalize and Recover).

Discussion

We developed a mathematical model to analyze the impact of media coverage to the spread of infectious diseases in a given region. We get the following results from SIHRS, and SIHR model.

We calculate basic reproductive number R0 by the method of next generation method. When β2,β4=0, the media coverage does not effect the reproductive number R0. We discuss the stability of the proposed model. Stability analysis show that the disease free equilibrium is locally asymptotically stable if R0<1. If R0>1, it is shown that a unique endemic equilibrium appears and bifurcation can occur which cause oscillatory phenomena. We discuss the role of media coverage on the spreading of MERS-CoV. Though the media coverage itself is not a determined fact, to eradicate the infection of the diseases, the analysis of the model indicates that, to certain extent, the more media coverage in a given population, the less number of individuals will be infected. Our analytical results show that the susceptible S(t), infected I(t), hospitalize H(t), recovered R(t) converge to equilibrium point. Which ensure the stability of the proposed model. In future, we are planning to develop an optimal mechanism on the basis of local dynamics and sensitivity analysis. This control strategy will help that how to eradicate the infection from the community. Work on such issue is in progress and will be reported soon in the form of a new article.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Acknowledgement

This research was funded by the Deanship of Scientific Research at Princess Nourah bint Abdulrahman University through the Fast-track Research Funding Program.

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