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Hopf bifurcation of the age-structured SIRS model with the varying population sizes


  • The purpose of this paper is to investigate the impact of the varying population sizes on the dynamic behavior of the age-structured epidemic model. A age-structured SIRS epidemic model with the varying population sizes is established and investigated to take into account time delay. The non-negativity of the solution, the existence and stability of the steady states, and the existence of the Hopf bifurcation are discussed. The numerical simulations show that the varying population sizes can cause the age-structured SIRS model to produce multiple stability switches.

    Citation: Hui Cao, Mengmeng Han, Yunxiao Bai, Suxia Zhang. Hopf bifurcation of the age-structured SIRS model with the varying population sizes[J]. Electronic Research Archive, 2022, 30(10): 3811-3824. doi: 10.3934/era.2022194

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  • The purpose of this paper is to investigate the impact of the varying population sizes on the dynamic behavior of the age-structured epidemic model. A age-structured SIRS epidemic model with the varying population sizes is established and investigated to take into account time delay. The non-negativity of the solution, the existence and stability of the steady states, and the existence of the Hopf bifurcation are discussed. The numerical simulations show that the varying population sizes can cause the age-structured SIRS model to produce multiple stability switches.



    The recurrent epidemics refers to that the recovered individuals don't have the permanent immunity, and may be infected due to contact with the infectious individuals again[1,2]. For epidemics without the permanent immunity and obvious latent infection period, we can structure the SIRS model on the basis of the SIR epidemic model established earlier by Kermack and McKendrick in 1927 to describe it[3]. In fact, many papers have established and studied the dynamic behavior of SIRS epidemic model based on the above ideas[4,5,6,7,8,9,10,11,12]. However, even if the acquired immunity is temporary, it also doesn't disappear immediately, and it still ensure that the recovered individuals have immunity for a certain period of time, and then the immunity will gradually disappear with time[13,14,15,16]. Therefore, the model with immune age structure can well describe the disappearance of temporary acquired immunity over time[17,18,19].

    At present, most SIRS models with immune age structure assume that epidemics spread in populations with constant population complement or fixed size[17,18,19]. However, it is unreasonable to assume that the population size is constant if the population growth or decrease is significant, or if the disease causes enough deaths to affect the population size[5]. Size structure is considered to explore the effect of maturity size on the insect population [20].

    In this paper, our purpose is to investigate the effect of the varying population sizes on the dynamical behavior of the age-structured SIRS model. For this reason, we structure a age-structured SIRS model with the varying population sizes as follows:

    {dS(t)dt=bS(t)βS(t)I(t)dS(t)++0k(a)R(t,a)da,dI(t)dt=βS(t)I(t)(d+μ+δ)I(t),R(t,a)t+R(t,a)a=(d+k(a))R(t,a),R(t,0)=δI(t),S(0)=S00,I(0)=I00,R(0,)=R0()L1+(0,+). (1.1)

    Here, we use S(t) and I(t) to represent the number of the suspectable and infectious individuals at time t, respectively, and R(t,a) represents the density of the recovered individuals whose age of acquired immunity is a at time t.

    In particular, k(a) represents the acquired immunity loss function of the recovered individuals with the acquired immunity age a, which interprets the recovered individuals leaving the recovered class and entering the susceptible class again because the recovered individuals lose their acquired immunity. In fact, the acquired immunity of the recovered individuals gradually disappear, Therefore, k(a) follows the function:

    k(a)={k(a),a>τ,0,aτ, (1.2)

    and k(a)L+((0,+),R), where τ>0 is the longest time for the recovered individuals to maintain the acquired immunity.

    In addition, b represents the birth rate of susceptible individuals, d represents the natural mortality, β represents the transmission rate, μ represents the disease-related mortality of infectious individuals, and δ represents the recovery rate.

    Next, we will discuss the non-negativity of the solution and the boundedness of the system (1.1) in Section 2. The existence and stability of all the feasible equilibria in Sections 3 and 4, respectively, including the population extinction equilibrium P0, the disease free equilibrium P1, and the endemic equilibrium P. The conditions for the system (1.1) experiences Hopf bifurcation are given in Section 5. The numerical simulations and conclusions are presented in Section 6.

    Theorem 2.1. Any solution (S(t),I(t),R(t,a)) of system (1.1) starting from any non-negative initial value (S0,I0,R0()) is non-negative when t0, where R0()L1+(0,+).

    Proof. Firstly, we prove the non-negativity of R(t,a) for t0. For this purpose, we use the characteristic line method to integrate the third equation of system (1.1), then

    R(t,a)={R(ta,0)ea0(μ+k(θ))dθ,at,R0(at)eaat(μ+k(θ))dθ,a>t. (2.1)

    It implies that R(t,a) is non-negative for t0.

    Secondly, we prove the non-negativity of S(t) for t0. Without loss of generality, for the positive initial value, we assume that there exists T1>0, such that S(T1)=0, and S(t)>0 when t(0,T1). Then, the first equation in system (1.1) means that dS(T1)dt=+0k(a)R(t,a)da>0. It contradicts S(T1)=0. Namely, S(t) is non-negative for t0.

    Finally, we prove the non-negativity of I(t) for t0. By directly solving the second equation in system (1.1), we have

    I(t)=I0et0[βS(s)(d+μ+δ)]ds. (2.2)

    Obviously, I(t) is non-negative for t0 when I00.

    Summing up the above discussion, we know any solution of system (1.1) starting from any non-negative initial value is non-negative.

    At the end of this subsection, we discuss the boundedness of the system (1.1). To this end, we denote ˉR(t)=+0R(t,a)da, and assume that lima+R(t,a)=0 since the age of an individual is limited in the real world. Then,

    d(S(t)+I(t)+ˉR(t))dt=bS(t)d(S(t)+I(t)+ˉR(t))μI(t)(bd)(S(t)+I(t)+ˉR(t)).

    That is, S(t)+I(t)+ˉR(t)N0e(bd)t with N0=S(0)+I(0)+ˉR(0). It implies that the total population exponentially decays to 0 when b<d, is constant N0 when b=d, and gradually tends to positive infinity when b>d.

    It is obvious that system (1.1) always has a population extinction equilibrium P0(0,0,0). When b=d, system (1.1) only exists the disease free equilibrium P1(S0,0,0), where S0 is any positive constant. To discuss the existence of the endemic equilibrium P(S,I,R(a)), we need to solve the following equations:

    {bSβSIdS++0k(a)R(a)da=0,βSI(d+μ+δ)I=0,dR(a)da=(d+k(a))R(a),R(0)=δI. (3.1)

    The second equations of (3.1) implies that

    S=d+μ+δβ.

    By direct calculation, the third and the last equation of (3.1) implies that

    R(a)=δIea0(d+k(θ))dθ.

    Substituting the expression of S and R(a) into the first equation of (3.1), we have

    I=bdβ(1δd+μ+δ+0k(a)ea0(d+k(θ))dθda).

    Denote

    M=δd+μ+δ+0k(a)ea0(d+k(θ))dθda,

    then, the expression of I can be rewritten as I=bdβ(1M). It implies that b>d and M<1 together can guarantee I>0. Therefore, we give the conclusion of the existence of the equilibria of system (1.1):

    Theorem 3.1. (i) System (1.1) always exists a population extinction equilibrium P0=(0,0,0).

    (ii) If b=d, system (1.1) exists a disease free equilibrium P1=(S0,0,0), where S0 is any positive constant;

    (iii) If b>d and M<1, system (1.1) exists a endemic equilibrium P=(S,I,R(a)) with

    S=d+μ+δβ,I=bdβ(1M),R(a)=δIea0(d+k(θ))dθ.

    We will mainly discuss the stability of equilibria in this section, including the global stability of the population extinction equilibrium P0 and disease free equilibrium P1, and the local stability of the endemic equilibrium P when τ=0.

    According to the discussion in Section 2, we know the total population will decrease exponentially and approach 0 when b<d. Furthermore, the following result holds.

    Theorem 4.1. If b<d, the population extinction equilibrium P0 of system (1.1) is globally asymptotically stable.

    Proof. In order to discuss the global stability of P0, we construct the following Lyapunov function:

    V0(t)=S(t)+I(t)++0φ(a)R(t,a)da,

    where φ(a)=+ak(ξ)eξa(d+m(θ))dθdξ] is a differential function of a on [0,), and φ(0)<1. Then

    V0(t)dt=(bd)S(t)βS(t)I(t)++0k(a)R(t,a)da+βS(t)I(t)(d+μ+δ)I(t)++0φ(a)R(t,a)tda=(bd)S(t)βS(t)I(t)++0k(a)R(t,a)da+βS(t)I(t)(d+μ+δ)I(t)+0φ(a)(d+k(a))R(t,a)da+0φ(a)R(t,a)ada.=(bd)S(t)++0k(a)R(t,a)da(d+μ+δ)I(t)φ(a)R(t,a)|a=++φ(0)R(t,0)+0k(a)R(t,a)da=(bd)S(t)(d+μ)I(t)φ(a)R(t,a)|a=+δ(1φ(0))I(t). (4.1)

    Obviously, b<d can ensure that dV0(t)dt<0. Therefore, the Lyapunov stability theorem means that P0 is globally asymptotically stable when b<d.

    The conclusion of Theorem 4.1 is easy to understand. It means that once the birth rate b of the population is less than the natural mortality d, the total population will inevitably decay to extinction as t tends to +.

    When b=d, the total population always keep constant N0. In this case, we study the stability of the disease free equilibrium P1, and give the following stability conclusion.

    Theorem 4.2. If b=d and S0<d+μ+δβ, then the disease free equilibrium P1 of system (1.1) is globally asymptotically stable.

    Proof. Let

    V1(t)=S(t)S0S0lnS(t)S0+I(t)++0φ(a)R(t,a)da. (4.2)

    Then, we have

    V1(t)dt=(1S0S(t))dS(t)dt+dI(t)dt++0φ(a)R(t,a)tda=(1S0S(t))[+0k(a)R(t,a)da+(bd)S(t)βS(t)I(t)]+βS(t)I(t)(d+μ+δ)I(t)+0φ(a)R(t,a)ada+0φ(a)(d+k(a))R(t,a)da=S0S(t)+0k(a)R(t,a)da(S0S(t))(bd)+(βS0dμδ+δφ(0))I(t)φ(a)R(t,a)|a=+.

    Because of 0S(t)N0=S0, we have V1(t)0, and dV1(t)dt<0 when S0<d+μ+δβ. Therefore, the Lyapunov stability theorem means that P1 is globally asymptotically stable.

    Theorem 4.2 shows when the total population remains unchanged, if the number of susceptible people is small, the disease will not spread within the population and eventually die out.

    When b>d, Theorem 3.1(iii) shows that system (1.1) has unique endemic equilibrium P. In this case, we denote k(a)=k, k>0. It implies that M=kδedτ(d+k)(d+μ+δ)M(τ), and satisfies 0<M(τ)<1. And then, we give the following conclusion.

    Theorem 4.3. If b>d, then the endemic equilibrium P=(S,I,R(a)) of system (1.1) is locally asymptotically stable for τ=0.

    Proof. Let x(t)=S(t)S, y(t)=I(t)I, and z(t,a)=R(t,a)R(a), then system (1.1) can be reorganized as

    {dx(t)dt=bx(t)βx(t)Iβy(t)Sdx(t)++0k(a)z(t,a)da,dy(t)dt=βx(t)I+βy(t)S(d+μ+δ)y(t),dz(t,a)dt+z(t,a)da=(d+k(a))z(t,a),z(t,0)=δy(t). (4.3)

    Suppose that system (4.3) has the solution in the form of x(t)=x0eλt, y(t)=y0eλt, and z(t,a)=z0(a)eλt. Then, we obtain the following equations:

    {λx0=bx0βx0Iβy0Sdx0++0k(a)z0(a)da,λy0=βx0I+βy0S(d+μ+δ)y0,λz0+dz0(a)da=(d+k(a))z0(a),z0(0)=δy0. (4.4)

    Direct calculation allows us to obtain the following characteristic equation

    g(λ,τ)=λ3+A2(τ)λ2+A1(τ)λ+A0(τ)+B0(τ)eλτ=0, (4.5)

    with

    A2(τ)=(bd)M(τ)1M(τ)+d+k,A1(τ)=bd1M(τ)[(d+k)M(τ)+(d+μ+δ)],A0(τ)=(bd)(d+k)(d+μ+δ)1M(τ),B0(τ)=k(bd)δ1M(τ)edτ.

    In the case where τ=0, Ai(0)>0, i=2,1,0, B0(0)>0, and

    A2(0)A1(0)(A0(0)+B0(0))=(bd)2M(0)(1M(0))2[(d+k)M(0)+d+μ+δ]+(bd)1M(0)[(d+k)2M(0)+kδedτ]>0.

    Then, according to the Routh-Hurwitz criterion, we can see that the real parts of all roots of g(λ,0)=0 are negative. It implies that P is locally asymptotically stable when b>d and τ=0.

    If b>d, the total population gradually tends to + as t tends to +. In this case, Theorem 4.3 implies that system (1.1) does not exist the disease-free equilibrium, and the disease will certainly spread within the population. In addition, since the roots of g(λ,τ)=0 also depend on τ continuously, the roots of g(λ,τ)=0 may pass through the imaginary axis and enter the right side as τ increases, which may lead to the change in the stability of P. For this reason, we will study the stability of P when τ>0 in the following.

    In the case where b>d, k(a)=k, and τ>0, since the coefficients Ai(τ)(i=0,1,2) and B0(τ) of the characteristic equation g(λ,τ)=0 are functions of τ, we can use the method in [21] to study the stability of endemic equibrium P and the conditions under which Hopf bifurcation occurs. To this end, the characteristic equation g(λ,τ)=0 can be rewritten as

    g(λ,τ)=P3(λ,τ)+Q0(λ,τ)eλτ=0, (5.1)

    with

    P3(λ,τ)=λ3+A2(τ)λ2+A1(τ)λ+A0(τ),Q0(λ,τ)=B0(τ).

    It is clear that Ai(τ)(i=0,1,2) and B0(τ) are all continuous and differentiable respect to τ, and satisfy

    P3(0,τ)+Q0(0,τ)=(bd)1M(τ)[(d+k)(d+μ+δ)kδedτ]>0.

    In addition, since P3(λ,τ) and Q0(λ,τ) are both differentiable in τ and analytic functions in λ, we can get

    P3(iω,τ)+Q0(iω,τ)=A2(τ)ω2A0(τ)B0(τ)+i(ω3A1(τ)ω)0,lim|λ||Q0(λ,τ)P3(λ,τ)|=lim|λ||B0(τ)λ3+A2(τ)λ2+A1(τ)λ+A0(τ)|=0,

    and

    G(ω,τ)=|P3(iω,τ)|2|Q0(iω,τ)|2=ω6+(A22(τ)2A1(τ))ω4+(A21(τ)2A2(τ)A0(τ))ω2+A20(τ)B20(τ). (5.2)

    It implies that these assumptions (i)–(iv) in [21] hold.

    Suppose λ=iω(τ), ω(τ)>0 is the root of the characteristic of g(λ,τ)=0, then we know

    cosωτ=A2(τ)ω2A0(τ)B0(τ),sinωτ=ω3+A1(τ)ωB0(τ).

    Put Θ=ω2, then (5.2) can be rewrite as

    Q(Θ):=Θ3+q2(τ)Θ2+q1(τ)Θ+q0(τ), (5.3)

    where q2(τ)=A22(τ)2A1(τ), q1(τ)=A21(τ)2A2A0(τ), and q0(τ)=A20(τ)B20(τ)>0. Let Θ=q2(τ)+q22(τ)3q1(τ)3 be the roots of Q(Θ)=0 when q22(τ)3q1(τ)0, we give the results of the positive root of the equation Q(Θ)=0 in the following Lemma 5.1.

    Lemma 5.1.

    (i) If q1(τ)<0, the equation Q(Θ)=0 has the positive real root when Q(Θ)0, andhas no positive root when Q(Θ)>0;

    (ii) If q1(τ)0, q2(τ)<0 and q22(τ)3q1(τ)0, the equation Q(Θ)=0 has the positive real root when Q(Θ)0, and has no positive root when Q(Θ)>0;

    (iii) If q1(τ)0 and q2(τ)0, the equation Q(Θ)=0 has no positive root.

    If there is no positive real root for equation Q(Θ)=0, the stability of the endemic equilibrium P will not change with the increase of τ. It implies that the following conclusions are true.

    Theorem 5.1. Suppose that b>d and M(τ)<1.

    (i) If q1(τ)<0, the endemic equilibrium P of system (1.1) is locally asymptotically stable for any τ>0 when Q(Θ)>0;

    (ii) If q1(τ)0 and q2(τ)<0, the endemic equilibrium P of system (1.1) is locally asymptotically stable for any τ>0 when Q(Θ)>0;

    (iii) If q1(τ)0 and q2(τ)0, the endemic equilibrium P of system (1.1) is locally asymptotically stable for any τ>0.

    Theorem 5.1 implies that the stability of the endemic equilibrium P does not change as τ increases when b>d, M(τ)<1, and the conditions in (i), (ii), and (iii) of Theorem 5.1 hold. Next, let's discuss the case where the equation Q(Θ)=0 has the positive real root. Without loss of generality, we assume that Θ is the root of Q(Θ)=0. That is, ω(τ)=Θ is the positive real root of G(ω,τ)=0. Thus, by Lemma 5.1, we can define a set

    Γ=Γ1Γ2,

    with

    Γ1={τ>0:q1(τ)<0,Q(Θ)0},Γ2={τ>0:q1(τ)0,q2(τ)<0,Q(Θ)0}.

    Namely, there exists ω=ω(τ)>0 such that G(ω,τ)=0 when τΓ.

    Define θ(τ)[0,2π], τΓ as

    cosθ(τ)=A2(τ)ω2A0(τ)B0(τ),sinθ(τ)=ω3+A1(τ)ωB0(τ). (5.4)

    The relation between ω(τ)τ and θ(τ) implies that ω(τ)τ=θ(τ)+2lπ, τΓ, lN. And then, we define Sl(τ) as

    Sl(τ)=τθ(τ)+2lπω(τ),τΓ,lN, (5.5)

    where ω>0 with ω=ω(τ) is the positive root of (5.2) if and only if Sl(τ) = 0 for some τΓ, lN. Then, Theorem 2.2 in [21] guarantees that the characteristic equation (5.1) has a pair of simple conjugate pure imaginary roots when τ=τ, which are λ+(τ)=iω(τ), and λ(τ)=iω(τ), respectively. Furthermore, it crosses the imaginary axis from left to right if F(τ)>0 and crosses the imaginary axis from right to left if F(τ)<0, where

    F(τ)=sign{dRe(λ)dτ|λ=iω(τ)}=sign{Q(Θ)}sign{dSl(τ)dτ|τ=τ}.

    Based on the Hopf bifurcation theory of functional differential equations in [22], we know the following conclusion is true.

    Theorem 5.2. Suppose that b>d, Q(Θ)0, and Q(Θ)0.

    (i) If q1(τ)<0, the endemic equilibrium P of system (1.1) is locally asymptotically stable for τ[0,τ), and system (1.1) experiences the Hopf bifurcation at τ=τ;

    (ii) If q1(τ)0, and q2(τ)<0, the endemic equilibrium P of system (1.1) is locally asymptotically stable for τ[0,τ), and system (1.1) experiences the Hopf bifurcation at τ=τ.

    We have established and discussed a age-structured SIRS epidemic model with the varying population sizes in this paper. The purpose is to investigate the impact of the varying population sizes on the dynamic behavior of the age-structured epidemic model. In theoretical analysis, we study the boundedness and non-negativity of the solution of system (1.1), the existence and stability of the equilibria of system (1.1), including the population extinction equilibrium P0, the disease free equilibrium P1 and the endemic equilibrium P, and give the conditions that system (1.1) undergoes Hopf bifurcation.

    In order to use the numerical simulations to illustrate the complex dynamical behaviors of system (1.1), let the maximum infection age be 500. Firstly, we demonstrate the stability of P in the case where b>d and τ0. Taking τ=0, b=0.0852, d=0.001, μ=0.01, β=0.0011, δ=0.01, and k=0.06, Figure 1(a) shows that P is stable focus. Choosing τ=180,200,220, respectively, and choosing b=0.0155, β=0.001, δ=0.005, d=0.0001, μ=0.001, k=0.01, then we have q1(τ)>0, q2(τ)>0, and Figure 1(b) displays P is stable focus. When we fix b=0.0852, β=0.001, δ=0.01, d=0.001, μ=0.01, k=0.01, and τ=180,200,220, respectively, then q1(τ)>0, q2(τ)<0, and Q(Θ)>0, Theorem 5.1(ii) implies that P is stable focus, see Figure 1(c). In addition, we take b=0.0155, β=0.001, δ=0.005, d=0.002, μ=0.005, k=0.01, and the value of τ is consistent with these in Figure 1(c), then q1(τ)<0, and Q(Θ)>0. In this case, Figure 1(d) shows that P is still stable focus, which is consistent with Theorem 5.1(i).

    Figure 1.  The stability of P of system (1.1) when τ0.

    And then, we demonstrate that system (1.1) experiences the Hopf bifurcation as τ changes when q1(τ)0, q2(τ)<0, and Q(Θ)<0. Fixing b=0.00852, d=0.001, μ=0.03, β=0.002, δ=0.005, k=0.009, and taking τ=180,200,220, respectively, we have q1(τ)>0, q2(τ)<0, Q(Θ)<0, and τ=163. Figure 2 displays system (1.1) undergoes the Hopf bifurcation, where Figure 2(a) is the time series diagram, and Figure 2(b) is the phase diagrams.

    Figure 2.  System (1.1) experiences the Hopf bifurcation when q1(τ)0, q2(τ)<0.

    Similarly, we also demonstrate that system (1.1) experiences the Hopf bifurcation when q1(τ)<0 and Q(Θ)<0. For this purpose, we chose b=0.00852, d=0.002, μ=0.01, β=0.001, δ=0.005, k=0.015, and τ=280,290,300, respectively, then we have q1(τ)<0, Q(Θ)<0, and τ=273. Figure 3 displays that system (1.1) experiences the Hopf bifurcation when q1(τ)<0 and Q(Θ)<0, where Figure 3(a) is the time series diagram, and Figure 3(b) is the phase diagrams.

    Figure 3.  System (1.1) experiences the Hopf bifurcation when q1(τ)<0.

    Finally, we take k(a)=0.1669e1.319a+0.0119e0.000152a to numerically study the complex dynamic behavior of system (1.1). Let b=0.00852, d=0.001, μ=0.03, β=0.002, δ=0.005, and choose τ=180,200,220, respectively, Then, Figure 4 displays system (1.1) still undergoes the Hopf bifurcation.

    Figure 4.  System (1.1) experiences the Hopf bifurcation when k(a) is an exponential function.

    In particular, fixing b=0.0155, d=0.001, μ=0.1, β=0.001, δ=0.05, and using τ as the bifurcation parameter, we demonstrates system (1.1) may happen multiple stability switches (see Figure 5(a)). That is, the varying population sizes can lead to the age-structured SIRS epidemic model happens the complex dynamical behavior.

    Figure 5.  The dynamics behavior changes of system (1.1) as τ changes.

    It is clear that τ cannot reach to the infinite since the coefficient of the characteristic equation g(λ,τ)=0 is related to τ. The numerical simulation shows that the system (1.1) is ultimately stable when τ=250, see Figure 5(b), where the parameter values are the same as those in Figure 5(a).

    This work is supported by National Natural Science Foundation of China 12071268 and 11971281, and by Natural Science Basic Research Plan in Shaanxi Province of China Grant 2022JM-038.

    The authors declare there is no conflict of interest.



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