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. 2018 Mar 27;2018(1):42. doi: 10.1186/s13661-018-0961-7

Global stability analysis of an SVEIR epidemic model with general incidence rate

Da-peng Gao 1, Nan-jing Huang 2,, Shin Min Kang 3, Cong Zhang 4,
PMCID: PMC7149115  PMID: 34171003

Abstract

In this paper, a susceptible-vaccinated-exposed-infectious-recovered (SVEIR) epidemic model for an infectious disease that spreads in the host population through horizontal transmission is investigated, assuming that the horizontal transmission is governed by an unspecified function f(S,I). The role that temporary immunity (vaccinated-induced) and treatment of infected people play in the spread of disease, is incorporated in the model. The basic reproduction number R0 is found, under certain conditions on the incidence rate and treatment function. It is shown that the model exhibits two equilibria, namely, the disease-free equilibrium and the endemic equilibrium. By constructing a suitable Lyapunov function, it is observed that the global asymptotic stability of the disease-free equilibrium depends on R0 as well as on the treatment rate. If R0>1, then the endemic equilibrium is globally asymptotically stable with the help of the Li and Muldowney geometric approach applied to four dimensional systems. Numerical simulations are also presented to illustrate our main results.

Keywords: Epidemic model, Reproduction number, Lyapunov function, Geometric approach, Global stability, Susceptible–Vaccinated–Exposed–Infectious–Recovered

Introduction

Mathematical modeling enjoys popularity in both preventing and controlling infectious diseases such as severe acute respiratory syndrome (SARS) [1], human immunodeficiency virus infection/acquired immune deficiency syndrome (HIV/AIDS) [2], H5N1 (avian flu) [3] and H1N1 (swine flu)[4]. In recent years, a lot of efforts have been made to develop realistic diseases and further study the asymptotic behavior of such epidemic models [5]. In the field of studying epidemic model behavior, one of the most important parts is to analyze steady states together with their stability [6]. In general, there are two distinct techniques named Lyapunov’s direct method and Li–Muldowney’s geometric approach to give sufficient conditions of global stability for the equilibrium states (see, for example, [714]). We would like to mention some related work concerned with the existence of positive solutions for the discrete fractional boundary value problem [15], the sensitivity analysis for optimal control problems governed by nonlinear evolution inclusions [16] and the nonexistence of global in time solution of the mixed problem for the nonlinear evolution equation with memory generalizing the Voigt–Kelvin rheological model [17].

It is well known that the rate of incidence plays the main part in modeling infectious diseases. The rise and fall of epidemics can be influenced by some factors, such as density of population and life style [18, 19]. Many researchers have adopted different nonlinear incidence rates in their works. For more details, we refer the reader to [814, 2034] and the references therein. When it comes to control of a disease, it is generally known that the spread of many diseases can be prevented by vaccinating. When massive vaccination is impossible, the second stage of defensive mechanism could be medical treatment. Individuals need to bear in mind that the treatment is an indispensable way to take precautions for some diseases (for instance, measles, phthisis and influenza). In recent years, many treatment functions have been introduced by several authors to study some epidemic models under different conditions (see, for instance, [12, 14, 27, 31, 3538]).

Recently, Dénes and Röst [27] investigated the following SI model:

{dSdt=μf(S,I)μS,dIdt=f(S,I)g(I),1=S+I+R, 1.1

where a population of constant size (assumed to be equal to 1) is divided into three compartments: susceptible (denoted by S), infected (denoted by I) and recovered (denoted by R). The transmission of the infection is governed by the incidence rate f(S,I) and μ is birth rate as well as the death rate of the susceptible class. The nonlinear function g(I) denotes the sum of the death rate and the recovery rate for the infected individuals satisfying g(0)=0 and g(I)>0 for I>0. Using a Dulac function approach, which aims at eliminating the existence of the periodic solution and proving the global stability by the Poincaré-Bendixson theorem (see [39], p. 54), they obtained the global stability of the disease-free equilibrium and the endemic equilibrium for system (1.1).

Very recently, Upadhyay et al.[12] considered the following e-epidemic model:

{dSdt=Aδ0SαSIS+I+c+ηVμS,dEdt=αSIS+I+c(δ0+δ1)E,dIdt=δ1E(δ0+δ2+δ3)IβII+a,dRdt=δ2Iδ0R+βII+a,dVdt=μS(δ0+η)V. 1.2

with initial conditions: S(0)=S0>0, E(0)=E00, I(0)=I00, R(0)=R00 and V(0)=V00. All the parameters in model (1.2) are positive and are defined as follows: S, E, I, R and V represent the number of susceptible nodes, exposed nodes, infectious nodes, recovered nodes and vaccinated nodes at time t, respectively; A is the recruitment rate of new nodes, c is the half saturation constant for susceptible nodes S, α is the contact rate or the rate of transfer of virus from an infectious node to the susceptible node, η is rate at which the vaccinated nodes lose their immunity and join the susceptible class, β is the maximal treatment capacity of a network, δ0 is the natural crashing rate of nodes all classes, a is the half saturation constant for an infected node I, μ is the vaccination rate coefficient, δ3 is the virus induced crashing rate and δ1, δ2 are the state transition rates. Using a Lyapunov function and a geometric approach, they obtained the global stability of virus-free equilibrium and endemic equilibrium for system (1.2).

As pointed out by Liu and Yang [11], due to the high similarity between computer virus and biological virus, it is acceptable to establish dynamical models describing biological virus among a population by modifying an e-epidemic model. Thus, it is interesting and important to extend model (1.2) to study the biological virus in the infectious disease.

Inspired by these research results above, in this paper, we consider the following system with five compartments:

{dSdt=Aδ0Sf(S,I)+ηVμS,dEdt=f(S,I)(δ0+δ1)E,dIdt=δ1E(δ0+δ2+δ3)Ig(I),dRdt=δ2Iδ0R+g(I),dVdt=μS(δ0+η)V, 1.3

where S(t), E(t), I(t), R(t), V(t) are the number of susceptible population, exposed population, infective population, recovered population, vaccinated population, respectively. The two-variable function f(S,I) represents incidence rate and the nonlinear function g(I) denotes the removal rate of infective individuals because of the treatment of infective. The initial conditions for system (1.3) are as follows:

S(0)=S00,E(0)=E00,I(0)=I00,R(0)=R00,V(0)=V00. 1.4

Clearly, N=S(t)+E(t)+I(t)+R(t)+V(t) denotes the total number of high-risk human population at time t.

The model parameters of system (1.3) are described as follows:

A:

the rate at which new individuals (including newborns and immigrants) enter the susceptible population,

δ0:

natural death rate of population all classes,

η:

the rate at which the vaccinated population lose their immunity and join the susceptible class,

μ:

vaccination rate coefficient,

δ1:

the rate at which exposed population become infective,

δ2:

natural recovery rate of infective population,

δ3:

disease-related death rate of infective population.

Model (1.3) involves certain assumptions which consist of the following:

  • (i)

    The new individuals enter the population with a constant rate and all the new individuals are susceptible.

  • (ii)

    Susceptible individuals move to exposed class by adequate contact with infective individuals and after some time (i.e., latency period), they become infectious and move to infectious class.

  • (iii)

    The infectious individuals are assumed to leave the infectious class as a result of natural death and disease-related death as well as recovery of infected individuals.

  • (iv)

    After recovery the individuals become immunized and hence they are no longer susceptible to it.

  • (v)

    It is assumed that a fraction of susceptible individuals get vaccinated and join the vaccinated class. A part of vaccinated individuals may lose their immunity and rejoin the susceptible class.

It is easy to see that system (1.3) includes (1.1) and (1.2) as special cases and so model (1.3) provides a uniform setting for the computer virus and biological virus studies. Following the classical assumptions [27, 40], it is reasonable to suppose that the transmission of the infection is governed by an incidence rate f(S,I) in model (1.3). Moreover, as pointed out by Wang [31], the recovery rate is naturally dependent on the number of infected individuals provided the health care resources are constrained and so it is natural to use the nonlinear function g(I) as the treatment function in model (1.3).

The main purpose of this paper is to derive the expression for the basic reproduction number and further show the global stability of disease-free as well as endemic equilibria by the aid of Lyapunov function and Li–Muldowney geometric approach applied to four dimensional systems. This paper is organized as follows. In Sect. 2, some elementary assumptions on the functions f and g will be given, and the basic reproduction number R0 is provided. Also the equilibrium points are discussed. The global stability of disease-free equilibrium and endemic equilibrium are analyzed in Sects. 3 and 4, respectively. All our important analytical findings are numerically verified with the help of Mathlab in Sect. 5. Finally, a brief conclusion is given in Sect. 6.

Basic reproduction number and equilibrium

To define the basic reproduction number R0 and indicate the existence of equilibrium, we give some hypotheses.

  1. f:R+2R+ is differentiable such that
    • f(S,0)=f(0,I)=0 for all S,I0;
    • f(S,I)>0 for all S,I>0;
    • f(S,I)S>0 for all S0 and I>0;
    • f(S,I)I0 for all S,I0;
    • If(S,I)If(S,I)0 for all S,I0.
  2. g:R+R+ is differentiable such that g(0)=0, g(I)>0 and g(I)0 for I0.

  3. ddI(logg(I)fS(I))0 holds for all S,I>0, where fS(I):=f(S,I) for S,I>0.

Remark 2.1

  1. It is easy to check that the classes of f(S,I) satisfying (H1) include incidence rates such as
    f(S,I)=βSI1+aIq,f(S,I)=βSI1+aS+bI,f(S,I)=βSI1+aS+bI+abSI,
    for β,a,b>0 and 0q1.
  2. It is straightforward to show that the classes of g(I) satisfying (H2) include removal rates such as
    g(I)=rI1+bI,g(I)=rII+a,g(I)=rarctanI,
    for r>0, a>0, b>0.
  3. By hypothesis (H2), we know that Φ(I)=g(I)I is a monotone decreasing function on I>0.

  4. The assumption (H3) is equivalent to the following inequality:
    If(S,I)g(I)f(S,I)ddIg(I),
    which can be found in [27].
  5. By the assumptions, it is easy to find that system (1.3) always has a disease-free equilibrium point P0=(S0,0,0,0,V0), where
    S0=(δ0+η)Aδ02+(μ+η)δ0,V0=Aμδ02+(μ+η)δ0.

We shall assume that (H1), (H2) and (H3) hold in the rest of this paper.

Now we define the basic reproduction number R0 for model (1.3) as follows:

R0=δ1m2(m3+g(0))fI(Am1μηm4,0),

where

m1=δ0+μ,m2=δ0+δ1,m3=δ0+δ2+δ3,m4=δ0+η.

In order to find the positive equilibria of model (1.3), set

{Af(S,I)m1S+ηV=0,f(S,I)m2E=0,δ1Em3Ig(I)=0,δ2Iδ0R+g(I)=0,μSm4V=0. 2.1

It follows that Am1S+ηV=m2E=m2m3I+g(I)δ1 and V=μSm4.

Substituting the above equalities into the second equation in (2.1), one has

f(Am2m3I+m2g(I)δ1m1μηm4,I)=m2m3I+g(I)δ1.

Let

F(I)=f(Am2m3I+m2g(I)δ1m1μηm4,I)m2m3I+g(I)δ1. 2.2

Then it is easy to see that the positive equilibrium points of system (2.1) are given by zeros of F in the interval (0,Aδ1m3m2].

We denote G(I)=m3I+g(I)Aδ1m2 for convenience. Then it is easy to see

G(0)=Aδ1m2<0,G(Aδ1m3m2)=g(Aδ1m3m2)>0.

Therefore, we conclude that G(I) has at least one root named Ĩ in the interval (0,Aδ1m3m2]. That is, m3I˜+g(I˜)=Aδ1m2 and so

F(I˜)=f(Am2m3I˜+m2g(I˜)δ1m1μηm4,I˜)m2m3I˜+g(I˜)δ1=m2Aδ1m2δ1=A<0.

Since f(S,0)=0, we know that fS(Am1μηm4,0)=0 and so

F(0)=fI(Am1μηm4,0)m2δ1(m3+g(0))=m2δ1(m3+g(0))(R01).

If R0>1, then system (2.1) has a positive equilibrium point P=(S,E,I,R,V), where

S=Am2m3I+m2g(I)δ1m1μηm4,E=m3I+g(I)δ1,R=δ2I+g(I)δ0,V=μSm4.

In the following, we show that P is the unique positive equilibrium point of system (2.1). For any positive equilibrium point P, by (2.2) and hypotheses (H1) and (H2), we have

F(I)=f(S,I)S(m2)(m3+g(I))δ1(m1μηm4)+f(S,I)Im2(m3+g(I))δ1. 2.3

Since m1m4=(δ0+μ)(δ0+η)>μη and hypotheses (H1) and (H2) hold, we have

f(S,I)S1m1μηm4(1δ1)(m2m3+m2g(I))<0. 2.4

Since g(0)=0 and g is differentiable on R+, there exists ξ(0,I) such that g(I)I=g(ξ). By using hypotheses (H2) and (H3), one has

f(S,I)Im2δ1(m3+g(I))=f(S,I)If(S,I)m3I+g(I)(m3+g(I))<f(S,I)g(I)g(I)f(S,I)(m3+g(I))m3I+g(I)=f(S,I)[g(I)g(I)m3+g(I)m3I+g(I)]=f(S,I)m3Ig(I)m3g(I)g(I)[m3I+g(I)]=f(S,I)m3I[g(I)g(I)I]g(I)[m3I+g(I)]=f(S,I)m3I[g(I)g(ξ)]g(I)[m3I+g(I)]<0. 2.5

Thus, it follows from (2.3), (2.4) and (2.5) that F(I)<0.

Suppose that there exists another positive equilibrium point P1=(S1,E1,I1,R1,V1). Then F(I1)0 due to the property of continuous function. This is a contradiction. Therefore, system (2.1) has a unique endemic equilibrium P when R0>1. It can be stated as follows.

Theorem 2.1

System (1.3) has a disease-free equilibrium P0 as follows:

P0=((δ0+η)Aδ02+(μ+η)δ0,0,0,0,Aμδ02+(μ+η)δ0),

which exists for all parameter values. For R0>1, the endemic equilibrium P admits the unique positive equilibrium point for system (1.3).

Remark 2.2

From the proof of the existence of endemic equilibrium P, it is not difficult to arrive at such a conclusion that the nonlinear treatment function g(I) has an upper bound Aδ1m2, which is reasonable for limited medical resources in our daily life.

Proposition 2.1

The set

Ω={(S,E,I,R,V)R+5,0<S,E,I,R,V,S+E+I+R+VAδ0}

is a positively invariant and attracting region for the disease transmission model given by system (1.3) with initial conditions (1.4).

Proof

Summing up the five equations in system (1.3) and denoting

N(t)=S(t)+E(t)+I(t)+R(t)+V(t),

we get

dN(t)dt=Aδ0Nδ3IAδ0N,

i.e.,

dN(t)dt+δ0NA.

Now integrating both sides of the above inequality and using the theory of differential inequality [41], we obtain

0<N(N(0)eδ0t+Aδ0(1eδ0t)).

Clearly, 0<NAδ0 as t. If N(0)Aδ0, then N(t)Aδ0. Thus, the set Ω is positive-invariant, that is, all initial solutions belong to Ω remain in Ω for all t>0. □

Global stability of the disease-free equilibrium by means of Lyapunov function

In this section, we investigate the global stability of the disease-free equilibrium P0 for system (1.3).

Theorem 3.1

If R0<1Ag(0)δ0g(Aδ0)A(m3+g(0)), then the disease-free equilibrium P0 of system (1.3) is globally asymptotically stable in the feasible region Ω. If R0>1, then P0 is unstable.

Proof

The Jacobian matrix of system (1.3) at P0 is

J(P0)=(m10fI((δ0+η)Aδ02+(μ+η)δ0,0)0η0m2fI((δ0+η)Aδ02+(μ+η)δ0,0)000δ1m3g(0)0000δ2+g(0)δ00μ000m4).

Obviously, λ1=δ0 is an eigenvalue of J(P0). The other eigenvalues of J(P0) are determined by the equations

λ2+(m1+m4)λ+(m1m4μ)=0

and

λ2+(m2+m3+g(0))λ+m2(m3+g(0))(1R0)=0,

respectively. If R0>1, then one eigenvalue is positive. Thus, P0 is unstable.

When R0<1Ag(0)δ0g(Aδ0)A(m3+g(0)), to prove the disease-free equilibrium P0 is globally asymptotically stable, we consider the Lyapunov function V(E,I)=δ1E+m2I. The derivative of V(E,I) along system (1.3) satisfies

dV(E,I)dt=δ1(f(S,I)m2E)+m2(δ1Em3Ig(I))=δ1f(S,I)m2(m3I+g(I))=I(δ1f(S,I)Im2m3I+g(I)I)I(δ1f(Am1μηm4,I)Im2(m3+g(I)I))I(δ1limI0+f(Am1μηm4,I)Im2(m3+g(I)I))=I[δ1f(Am1μηm4,0)Im2(m3+g(I)I)]=I[m2(m3+g(0))R0m2(m3+g(I)I)]=Im2(m3+g(0))[R0m2(m3+g(I)I)m2(m3+g(0))]=Im2(m3+g(0))[R01+m3+g(0)m3g(I)Im3+g(0)]Im2(m3+g(0))[R01+Ag(0)δ0g(Aδ0)A(m3+g(0))]0.

Furthermore, dV(E,I)dt=0 iff I=0. Thus, the largest compact invariant set in {(S,E,I,R,V)|V˙(E,I)=0}, when R0<1Ag(0)δ0g(Aδ0)A(m3+g(0)), is the singleton P0. By the LaSalle invariance principle theorem ([42], p. 30), the disease-free equilibrium P0 is globally asymptotically stable if R0<1Ag(0)δ0g(Aδ0)A(m3+g(0)). This completes the proof. □

Global stability of the endemic equilibrium by means of geometric approach

In this section, we analyze the stability of the endemic equilibrium P. First, we show the local stability of the endemic equilibrium of system (1.3) around the endemic equilibrium P.

Theorem 4.1

If R0>1, then the endemic equilibrium P exists and is locally asymptotically stable if the following conditions hold:

  • (i)

    η<a11m4μ;

  • (ii)

    a13<min{a11m4+(a11+m4)(a33+m2)+a33m2μηδ1,a11(a33+m2)m4+a33(a11+m4)m2μη(a33+m2)(m1+m4)δ1,a11a33m2m4μηa33m2(m1m4μη)δ1};

  • (iii)

    0<hza33m4+(a33+m4)m2 and a11>(a33μm2ηa21a13m4δ1)h2a13δ1h(μηh+z)+a33hz(m2+m4)+hz(m2m4μη)z2h[a33m2m4ha13m4δ1h(a33+m2+m4)z]. Here all the parameters a11, a13, a21, a33, a43 are defined in (4.1). The values of h and z equal to B1 and B3, respectively.

Proof

The Jacobian matrix of system (1.3) at P is given by

J(P)=(a110a130ηa21m2a13000δ1a330000a43δ00μ000m4),

where

a11=f(S,I)S+m1,a13=f(S,I)I,a21=f(S,I)S,a33=m3+g(I),a43=δ2+g(I). 4.1

Clearly, one of the roots of J(P) is negative, i.e. δ0. The remaining roots can be determined from the following equation:

λ4+B1λ3+B2λ2+B3λ+B4=0,

where

B1=a11+a33+m2+m4>0,B2=a11m4+(a11+m4)(a33+m2)+a33m2μηδ1a13,B3=a11(a33+m2)m4+a33(a11+m4)m2μη(a33+m2)δ1a13(m1+m4),B4=a11a33m2m4a33μηm2δ1a13m1m4+δ1a13μη.

Using assumptions (i) and (ii), by a direct calculation, we have Bi>0 for i=1,2,3,4. It follows from the Routh–Hurwitz criteria [43] that all the eigenvalues associated to J(P) have negative real parts iff Bi>0 for i=1,2,3,4 and B1B2B3>B32+B12B4.

Now,

B1B2B3B32B12B4=B3(B1B2B3)B12B4=[a11(a33+m2)m4+a33(a11+m4)m2μη(a33+m2)δ1a13(m1+m4)]{a11(a11+m4)m4+(a11+m4)2(a33+m2)+(a11+m4)(a33+m2)2+a33(a33+m2)m2(a11+m4)μηδ1a13(a21+a33+m2)}B4h2=B4h2+h[a11m4+(a11+m4)(a33+m2)+a33m2μηδ1a13]z[a11(a33+m2)m4+m2a33(a11+m4)μη(a33+m2)δ1a13(m1+m4)]z=B4h2+h[a33m4+(a33+m4)m2+a11(a33+m2+m4)μηδ1a13]z[a11a33m4+a33m2m4+a11(a33+m4)m2(a33+m2)μηδ1a13(m1+m4)]z=B4h2+h[a33m4+(a33+m4)m2+a11(a33+m2+m4)μηδ1a13]z[a11a33m4+a33m2m4+a11(a33+m4)m2(a33+m2)μηδ1a13(m1+m4)]2>0,

if (iii) holds. This ends the proof. □

To find the global stability of system (1.3), it is necessary to reduce system (1.3) first. Since recovered class R does not have any effect on the dynamics of S, V, E and I class, we shall investigate the following system:

{dSdt=Aδ0Sf(S,I)+ηVμS,dEdt=f(S,I)(δ0+δ1)E,dIdt=δ1E(δ0+δ2+δ3)Ig(I),dVdt=μS(δ0+η)V. 4.2

The solutions of (4.2) corresponding to nonnegative initial values remain nonnegative for all time. Moreover, we observe that the total population size of (4.2) denoted by X(t) satisfies X˙=Aδ0Xδ2Iδ3Ig(I), so that we can study the model in the region:

Θ={(S,E,I,V)R+4:S+E+I+VAδ0}.

Here we follow the approach used in [8] for a SVEIR model of SARS epidemic spread.

Let us consider the following autonomous dynamical system:

x˙=f(x), 4.3

where f:DRn, DRn which is an open set, simply connected and fC1(D). Suppose that x is an equilibrium point of (4.3), i.e. f(x)=0. Therefore, x is said to be globally stable in D if it is locally stable and all trajectories in D converge to x.

Let Q(x) be a matrix-valued function of order (n2)×(n2) that is C1 on D. We also consider the matrix A which is defined as

A=QfQ1+QMQ1,

where the matrix Qf is

(qij(x))f=(qij(x)x)Tf(x)=qijf(x),

and the matrix M is the second additive compound matrix of the Jacobian matrix J. Further the Lozinskiĭ measure μ̄ of A with respect to a vector norm can be defined in R(n2) as follows:

μ¯(A)=limh0+I+hAh.

We will apply the following theorem according to [44].

Lemma 4.1

If D1 is a compact absorbing subset in the interior of D, and there exist γ>0 and a Lozinskiĭ measure μ¯(A)γ for all xD1, then every omega limit point of system (4.2) in the interior of D is an equilibrium in D1.

Theorem 2.1 states that R0>1 implies the existence and uniqueness of the endemic equilibrium P. Further, we know that the disease-free equilibrium P0 is unstable when R0>1. The instability of P0, together with P0Θ, which implies the uniform persistence of the state variables (see [45]). Thus, there exists a constant a>0 such that any solution (S(t),E(t),I(t),V(t)) with (S(0),E(0),I(0),V(0)) in the orbit of system (4.2) satisfies

min{limtinfS(t),limtinfE(t),limtinfI(t),limtinfV(t)}a.

The uniform persistence of system (4.2), incorporating the boundedness of Θ, suggests that the compact absorbing set in the interior of Θ; see [46]. Hence, Lemma 4.1 may be applied, with D=Θ.

According to [47], the Lozinskiĭ measure in Lemma 4.1 can be evaluated as:

μ¯(A)=inf{k¯:D+zk¯z,for all solutions of z=Az},

where D+ is the right-hand derivative. The endemic equilibrium is locally asymptotically stable, provided R0>1. Hence, to get the global asymptotic stability, according to Lemma 4.1, the trick of the proof is to find a norm such that μ¯(A)<0 for all x in the interior of Θ.

Starting with the Jacobian matrix J of (4.2),

J=(a11a12a13a14a21a22a23a24a31a32a33a34a41a42a43a44),

the second additive compound matrix is given by

(a11+a22a23a24a13a140a32a11+a33a34a120a14a42a43a11+a440a12a13a31a210a22+a33a34a24a410a21a43a22+a44a230a41a31a42a32a33+a44).

Hence, the second additive compound matrix of J is given as follows:

M=(M11M120M14M150M21M22000M2600M3300M360M420M4400M510M530M55M560M6200M65M66),

where

M11=2δ0f(S,I)S(μ+δ1),M12=f(S,I)I,M14=f(S,I)I,M15=η;M21=δ1,M22=2δ0f(S,I)Sμ(δ2+δ3)g(I),M26=η;M33=2δ0f(S,I)S(μ+η),M36=f(S,I)I;M42=f(S,I)S,M44=2δ0(δ1+δ2+δ3)g(I);M51=μ,M53=f(S,I)S,M55=2δ0(δ1+η),M56=f(S,I)I,M62=μ,M65=δ1;M66=2δ0(δ2+δ3+η)g(I).

Now we consider the following matrix:

Q=(1I0000001I00000001I00001V00000001V0000001V). 4.4

Then we obtain the matrix A=QfQ1+QMQ1, where Qf is the derivative of Q in the direction of the vector field f. More accurately, we have

QfQ1=diag{I˙I,I˙I,I˙I,V˙V,V˙V,V˙V}.

Hence, in view of the fact that

I˙I=δ1EI(δ0+δ2+δ3)g(I)I,V˙V=μSV(δ0+η),

we obtain

A=(A11A12A130A150A21A22000A260A32A33000000A440A46A5100A54A55A560A6200A65A66),

where

A11=g(I)I+δ2+δ3δ0δ1δ1EIf(S,I)Sμ,A12=f(S,I)I,A13=f(S,I)I,A15=ηVI;A21=δ1,A22=δ0f(S,I)Sμg(I)+g(I)Iδ1EI,A26=ηVI;A32=f(S,I)S,A33=g(I)I(δ0+δ1)g(I)δ1EI;A44=δ0f(S,I)SμμSV,A46=f(S,I)I;A51=μIV,A54=f(S,I)S,A55=μSV(δ0+δ1),A56=f(S,I)I;A62=μIV,A65=δ1,A66=(δ0+δ2+δ3)g(I)μSV.

As in [8], we consider the following norm on R6:

z=max{U1,U2}, 4.5

where zR6, with components zi, i=1,2,,6, and U1(z1,z2,z3) is defined as:

U1(z1,z2,z3)={max{|z1|,|z2|+|z3|},if sgn(z1)=sgn(z2)=sgn(z3),max{|z2|,|z1|+|z3|},if sgn(z1)=sgn(z2)=sgn(z3),max{|z1|,|z2|,|z3|},if sgn(z1)=sgn(z2)=sgn(z3),max{|z1|+|z3|,|z2|+|z3|},if sgn(z1)=sgn(z2)=sgn(z3),

and U2(z4,z5,z6) is defined as

U2(z4,z5,z6)={|z4|+|z5|+|z6|if sgn(z4)=sgn(z5)=sgn(z6),max{|z4|+|z5|,|z4|+|z6|},if sgn(z4)=sgn(z5)=sgn(z6),max{|z5|,|z4|+|z6|},if sgn(z4)=sgn(z5)=sgn(z6),max{|z4|+|z6|,|z5|+|z6|},if sgn(z4)=sgn(z5)=sgn(z6).

In the next, we will use the following inequalities:

|z1|,|z2|,|z3|,|z2+z3|U1

and

|zi|,|zi+zj|,|z4+z5+z6|U2(z),i=4,5,6;ij.

Furthermore, we assume that

δ2+δ3>δ1. 4.6

We will use the inequalities mentioned above to get the estimates on D+z.

Theorem 4.2

For R0>1, system (4.2) admits an unique endemic equilibrium which is globally asymptotically stable in the interior of Θ, provided that inequality (4.6) is satisfied and that

max{δ2+δ3+,δ1δ0+}<ω 4.7

for some positive constant ω, where

=supt(0,)g(I)Isupt(0,)δ1EI+supt(0,)ηVI+supt(0,){f(S,I)S,f(S,I)I},=supt(0,)2μIVsupt(0,)μSV+supt(0,)f(S,I)I.

Proof

The basic idea of the proof is to obtain the estimate of the right derivate D+z of the norm (4.5). For this purpose, we need to discuss sixteen cases according to the different orthants and the definition of the norm (4.5) within each orthant.

Case 1:

U1>U2 and z1,z2,z3>0 with |z1|>|z2|+|z3|. Then,z=|z1|. 4.8

This shows that

D+z=z1=A11z1+A12z2+A13z3+A15z5[g(I)I+δ2+δ3δ0δ1δ1EIf(S,I)Sμ]|z1|+f(S,I)I(|z2|+|z3|)+ηVI|Z5|.

By using |z5|<U2<|z1| and |z2|+|z3|<|z1|, it follows from (4.8) that

D+z[g(I)I+δ2+δ3δ0δ1δ1EIf(S,I)Sμ+f(S,I)I+ηVI]z.

Case 2:

U1>U2 and z1,z2,z3>0 with |z1|<|z2|+|z3|. Then,z=|z2|+|z3|. 4.9

Thus, we have

D+z=z2+z3=A21z1+A22z2+A26z6+A32z2+A33z3δ1|z1|+(g(I)Ig(I)δ1EI)(|z2|+|z3|)+ηVI|z6|.

Using |z6|<U2<|z2|+|z3| and |z1|<|z2|+|z3|, in view of (4.9), one has

D+z[δ1+g(I)Ig(I)δ1EI+ηVI]z.

The discussion for the other fourteen cases are similar to the ones discussed in [7] and so we omit it here. Thus, we can get the following estimate:

D+zmax{δ2+δ3+,δ1δ0+}z,

where

=supt(0,)g(I)Isupt(0,)δ1EI+supt(0,)ηVI+supt(0,){f(S,I)S,f(S,I)I},=supt(0,)2μIVsupt(0,)μSV+supt(0,)f(S,I)I.

Now the global stability follows from Lemma 4.1. □

Remark 4.1

As pointed out by Buonomo and Lacitignola [7], in some real situations, different choices of the matrix Q and of the vector norm may lead to better sufficient conditions than those we presented here, in the sense that the assumptions on the parameters may be weakened. Thus, it is worth to note that sufficient conditions (4.6) and (4.7) in Theorem 4.2 are derived from the application of the method and numerical simulations suggest that they may be not necessary (see Example 5.1).

Numerical simulations

The aim of this section is to give a numerical example to illustrate our main results.

Example 5.1

Consider the system

{dSdt=Aδ0SmSI1+nI+ηVμS,dEdt=mSI1+nI(δ0+δ1)E,dIdt=δ1E(δ0+δ2+δ3)IγII+a,dRdt=δ2Iδ0R+γII+a,dVdt=μS(δ0+η)V, 5.1

which is a particular case of system (1.3) by letting f(S,I)=mSI1+nI and g(I)=γII+a, where m, n, γ, a are positive and na>1. The other parameters in (5.1) have the same biological meanings as in model (1.3).

We first consider the case when

R0=0.571429<1Ag(0)δ0g(Aδ0)A(m3+g(0))=0.910714

by using the parameter values given in Table 1. Using these parameter values, for different initial conditions the dynamics of model (5.1) is presented in Figs. 15. It shows that system (5.1) has a disease-free equilibrium and it is globally asymptotically stable. This numerical verification supports the result stated in Theorem 3.1.

Figure 2.

Figure 2

Time series plot of the exposed population for R0=0.571429<0.910714 with various initial conditions, parameter values are given in Table 1

Figure 3.

Figure 3

Time series plot of the infective population for R0=0.571429<0.910714 with various initial conditions, parameter values are given in Table 1

Figure 4.

Figure 4

Time series plot of the recovered population for R0=0.571429<0.910714 with various initial conditions, parameter values are given in Table 1

Table 1.

Parameter for Figs. 15

Parameter Values
A 2
δ0 0.2
m 0.2
n 2
η 0.2
μ 0.4
δ1 0.8
δ2 0.5
δ3 0.55
γ 0.3
a 2

Figure 1.

Figure 1

Time series plot of the susceptible population for R0=0.571429<0.910714 with various initial conditions, parameter values are given in Table 1

Figure 5.

Figure 5

Time series plot of the vaccinated population for R0=0.571429<0.910714 with various initial conditions, parameter values are given in Table 1

Next, we consider the case when R0=2.211436>1 using the parameter values given in Table 2. Using these parameter values, for different initial conditions the dynamics of model (5.1) is presented in Figs. 610. It shows that system (5.1) has an endemic equilibrium and it is globally asymptotically stable with different initial values, which supports our analytical results stated in Theorem 4.2.

Figure 7.

Figure 7

Time series plot of the exposed population for R0=2.211436>1 with various initial conditions, parameter values are given in Table 2

Figure 8.

Figure 8

Time series plot of the infective population for R0=2.211436>1 with various initial conditions, parameter values are given in Table 2

Figure 9.

Figure 9

Time series plot of the recovered population for R0=2.211436>1 with various initial conditions, parameter values are given in Table 2

Table 2.

Parameter for Figs. 610

Parameter Values
A 6
δ0 0.5
m 0.8
n 2
η 0.2
μ 0.4
δ1 0.8
δ2 0.5
δ3 0.55
γ 0.3
a 2

Figure 6.

Figure 6

Time series plot of the susceptible population for R0=2.211436>1 with various initial conditions, parameter values are given in Table 2

Figure 10.

Figure 10

Time series plot of the vaccinated population for R0=2.211436>1 with various initial conditions, parameter values are given in Table 2

Conclusions

In this paper, we have considered an SVEIR epidemic model with general nonlinear incidence rate. In model (1.3), we have divided the total population into five compartments, namely susceptible, exposed, infective, recovered, vaccinated population and investigated the dynamical behavior of this model. Here, we have found that

R0=δ1m2(m3+g(0))fI(Am1μηm4,0)

is a basic reproduction number of system (1.3), which helps us to determine the dynamical behavior of the system. We have showed that system (1.3) to be globally asymptotically stable at disease-free equilibrium P0 when

R0<1Ag(0)δ0g(Aδ0)A(m3+g(0)).

When R0>1, the endemic equilibrium stable both locally and globally has been derived and analyzed under some conditions. The important mathematical findings for the dynamical behavior of model (1.3) have also numerically been verified for a special case of model (1.3). We would like to point out that the model considered in this paper is not a case study and so it is difficult to choose parameter values from quantitative estimation. We have used hypothetical sets of parameters to verify our analytical results. It is worth to mention that the results presented in this paper improve and extend some related results in [9, 10, 12, 13].

Finally, we remark that there are quite a few spaces to deserve further investigation. For example, we can continue the research in this line considering the vaccination rate μ in our model (1.3) as a continuous function, and, later, a discontinuous function. On the other hand, as is well known, epidemiological models which incorporate the control strategies can be useful to both control the spread of disease and minimize the intervention costs. For our model, it is natural to consider vaccination rate coefficient as a control to reduce the disease burden. Thus, it is important and interesting to prove the existence of optimal control, characterize the optimal control, prove the uniqueness of optimal control, compute the optimal control numerically and investigate how the optimal control depends on various parameters in the models. We will devote to these questions our future work.

Acknowledgments

Acknowledgements

We would like to thank the editors and referees for their valuable comments and suggestions to improve our paper.

Availability of data and materials

Not applicable.

Abbreviations

(SVEIR)

Susceptible–Vaccinated–Exposed–Infectious–Recovered

Authors’ contributions

All authors contributed equally to this work. All authors read and approved the final manuscript.

Funding

This work was supported by the National Natural Science Foundation of China (11371015, 11471230, 11671282) and the Natural Science Foundation of Sichuan Provincial Education Department (Grant Nos. 18ZB0581, 14ZB0142) and the Meritocracy Research Funds of China West Normal University (17YC373).

Ethics approval and consent to participate

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Not applicable.

Footnotes

Publisher’s Note

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

Contributor Information

Nan-jing Huang, Email: nanjinghuang@hotmail.com.

Cong Zhang, Email: congmike@163.com.

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