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Dynamic analysis of the recurrent epidemic model

  • In this work, an SIRS model with age structure is proposed for recurrent infectious disease by incorporating temporary immunity and delay. We formulate the model as an abstract non-densely defined Cauchy problem and derive the conditions for the global stability of disease free equilibrium, the local stability of endemic equilibrium, and the existence of Hopf bifurcation. Both non-periodic and periodic behaviors are possible when the disease persists in population, where time delay plays an important role. Numerical examples are provided to illustrate our theoretical results.

    Citation: Hui Cao, Dongxue Yan, Ao Li. Dynamic analysis of the recurrent epidemic model[J]. Mathematical Biosciences and Engineering, 2019, 16(5): 5972-5990. doi: 10.3934/mbe.2019299

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  • In this work, an SIRS model with age structure is proposed for recurrent infectious disease by incorporating temporary immunity and delay. We formulate the model as an abstract non-densely defined Cauchy problem and derive the conditions for the global stability of disease free equilibrium, the local stability of endemic equilibrium, and the existence of Hopf bifurcation. Both non-periodic and periodic behaviors are possible when the disease persists in population, where time delay plays an important role. Numerical examples are provided to illustrate our theoretical results.


    In the real world, many diseases, such as Influenza, hand-foot-mouth-disease, rotavirus, and so on, can occur the secondary infection after recovery [1,2,3]. We can classify such diseases as recurrent epidemics. The study of recurrent epidemics which has been attracting great attention for decades, is currently one of the hottest topics in the field of epidemiology. A great deal of significant progress has been achieved so far (for examples, see [4,5,6,7,8,9,10,11,12]), including derivation of the threshold for outbreak and persistence of recurrent infectious disease, and the dynamic analysis of the seasonal and non-seasonal behaviors.

    At present, most of the existing deterministic models present periodic behaviors of recurrent infectious diseases by selecting seasonal parameters. Whether there are the deterministic models with non-seasonal parameters which can describe the possible periodic behaviors of recurrent infectious disease is worth exploring. Since the most important feature of recurrent infectious diseases is that the recovered individuals' immunity are temporary, the immunity age of the recovered individuals and the time required for loss of immunity must be characterized in the model. That is, the model should be built by combining immunity age and delayed immune loss.

    We assume that recovered individuals lose their immunity after a period of recovery, and then, they become susceptible again. Let m(a) be the immunity loss rate function of the recovered individual with immunity age a, and τ>0 be the minimal time that a recovered individual has immunity. If the immunity age a is less than τ, then the recovered individuals remain in the recovered class, which means m(a)=0. If the immunity age a is great than τ, then the recovered individuals may lose their immunity and enter into the susceptible class at the rate m(a)=m>0. Therefore, m(a) follows the following function:

    m(a)={m,aτ0,a<τ (1.1)

    Apparently, m(a)L+((0,+),R).

    In this paper, we mainly consider the recurrent infectious diseases with temporary immunity. Therefore, we incorporate loss of immunity into epidemic model by establishing an SIRS model with age structure and delay. Denote S(t) and I(t) respectively as the number of susceptible and infectious individuals, and denote R(t,a) as the number of recovered individuals with immunity age a at time t. The model is given as follows:

    {dS(t)dt=ΛdS(t)βS(t)I(t)1+αI(t)++0m(a)R(t,a)da,dI(t)dt=βS(t)I(t)1+αI(t)(d+μ+γ)I(t),t0,R(t,a)t+R(t,a)a=(d+m(a))R(t,a),t0,a0,R(t,0)=γI(t),t0, (1.2)

    with the initial condition

    S(0)=S00,I(0)=I00,R(0,a)=P0(a)L1+(0,+).

    where Λ is the recruitment rate of susceptible individuals, β is the transmission rate, 1α is the half-saturation constant of infectious individuals, d is the natural death rate, μ is the mortality rate due to disease, and γ is the recovery rate. All parameters are positive and constant.

    This paper is organized as follows. Some preliminary results and the well-posedness of system (1.2) are presented in Section 2. In Section 3, we prove the existence of equilibria, especially the existence and uniqueness of positive equilibrium, and linearize system (1.2) around the equilibrium E. In Section 4, we discuss the stability of both equilibrium, and analyze the existence of Hopf bifurcations when the stability of E changes. We conclude and discuss our findings in Section 5 with some numerical examples given to illustrate our theoretical results.

    In this section, we will rewrite system (1.2) into an abstract equation on a suitable Banach lattice, establish the well-posedness result for the system and prove the nonnegativity and boundedness of solutions. At first, we collect some preliminaries on linear operators and C0-semigroup theory and some notations to be used in this paper.

    Let L:D(L)XX be a linear operator on a Banach space X. Denote the resolvent set of L as ρ(L). The spectrum of L is σ(L)=Cnρ(L). The point spectrum of L is the set

    σp(L):={λC:N(λIL){0}}.

    Definition 2.1. Let L:D(L)XX be a linear operator. If there exist real constants M1 and ωR, such that (ω,+)ρ(L), and

    (λL)nM(λω)n,fornN+,andallλ>ω.

    Then the linear operator (L,D(L)) is called a Hille-Yosida operator.

    For a Hille-Yosida operator one has the following perturbation result.

    Lemma 2.1 (see [13,14]). Let (A,D(A)) be a Hille-Yosida operator on a Banach space X and BL(X), L(X) denotes the set of all bounded linear operators on X, then the sum C=A+B is a Hille-Yosida operator as well.

    If (L,D(L)) is a Hille-Yosida operator on the Banach space X and set

    X0=(¯D(L),),D(L0)={xD(L):LxX0},L0x=Lx,forxD(L0),

    then the operator (L0,D(L0)) is called the part of L in X0 and we have that:

    Lemma 2.2 (see [13,14]). If (L,D(L)) is a Hille-Yosida operator, then its part (L0,D(L0)) generates a C0-semigroup (T0(t))t0 on X0.

    Now we set about to rewrite system (1.2) into an abstract evolution equation. Let

    X=R3×L1((0,+),R).

    Define the linear operator A:D(A)XX by

    A(xy0z)=(dx(d+μ+γ)yz(0)z(d+m(a))z),

    with D(A)=R2×{0}×W1,1((0,+),R). Then ¯D(A)=R2×{0}×L1((0,+),R), which shows D(A) is not dense in X. We also introduce a nonlinear map F:¯D(A)X given by

    F(xy0z)=(Λβxy1+αy++0m(a)z(a)daβxy1+αyγy0),

    and let

    u(t)=(S(t),I(t),0,R(t,))T.

    Then we can reformulate system (1.2) as the following abstract Cauchy problem:

    {ddt(u(t))=Au(t)+F(u(t)),t0,u(0)=u0, (2.1)

    where u0=(S0,I0,0,R0(a))T.

    In general, it is difficult to find a strong solution for an abstract differential equation like (2.1). So, we solve (2.1) in integrated form

    u(t)=u0+At0u(s)ds+t0F(u(s))ds. (2.2)

    Set

    X0=¯D(A)=R2×{0}×L1((0,+),R),X0+=R2+×{0}×L1+((0,+),R).

    We will show in Theorem 3.2 in the next section that (A,D(A)) is a Hille-Yosida operator and hence from Lemma 2.2 it generates a C0-semigroup on the closure of its domain. As a result, we have the following well-posedness theorem for system (2.1).

    Theorem 2.1. For any u0X0+, the system (1.2) represented by the integral equation (2.2) has a unique continuous solution with values in X0+. Moreover, the map Φ:[0,+)×X0+X0+ defined by Φ(t,u0)=u(t,u0) is a continuous semi-flow, i.e. the map is continuous and satisfies that Φ(0,)=I and Φ(t,Φ(s,))=Φ(t+s,).

    Due to the biological interpretation of system (1.2), only non-negative solutions are meaningful to be considered. The following result reveals that the solutions (S(t),I(t),R(t,a)) of system (1.2) with non-negative initial value remain non-negative and bounded ultimately.

    Theorem 2.2. All solutions of system (1.2) with non-negative initial value remain non-negative for all t0 and are ultimately bounded.

    Proof. By using the second equation of system (1.2), we have

    I(t)=I0et0[βS(θ)1+αI(θ)(d+μ+γ)]dθ>0.

    Integrating the third equation of system (1.2) along the characteristic line yields that

    R(t,a)={R(ta,0)ea0(d+m(θ))dθ,at,R0(at)eaat(d+m(θ))dθ,a>t. (2.3)

    It is clear that R(t,a) remains nonnegative for all nonnegative initial values.

    In the following, we prove that S(t) is nonnegative for t0. In fact, if there exists t1>0 such that S(t1)=0, and S(t)>0 for t(0,t1), then by the first equation of system (1.2), we have S(t1)=Λ++0m(a)R(t1,a)da>0. It implies that S(t)0 for all t0.

    Summarizing the above analysis, we know that any solution of system (1.2) with non-negative initial data remains nonnegative for all t0.

    Next, we will show that the solutions of system (1.2) are ultimately bounded. Let ˉR(t)=+0R(t,a)da, which represents the total number of recovered individuals at time t. Biologically, there exists a finite maximum age, so it is reasonable to assume that lima+R(t,a)=0. Then from system (1.2), we have

    (S(t)+I(t)+ˉR(t))=ΛdS(t)(d+μ+γ)I(t)++0m(a)R(t,a)da++0(R(t,a)a(d+m(a))R(t,a))da=ΛdS(t)(d+μ)I(t)dˉR(t)Λd(S(t)+I(t)+ˉR(t)).

    Therefore,

    lim supt+(S(t)+I(t)+ˉR(t))Λd.

    It follows that the omega limit set of system (1.2) is contained in the following bounded feasible region:

    Γ={(S,I,R()):S,I,R()0,S+I++0R(t,a)daΛd}.

    Obviously, this region is positively invariant with respect to system (1.2). It implies that the system (1.2) is ultimately bounded.

    In this section, we devote to linearizing the nonlinear system (1.2) around the equilibrium solutions. For this purpose, we firstly discuss the existence of equilibria of system (1.2).

    It is clear that system (1.2) always has a disease free equilibrium E0=(S(0),0,0) with S(0)=Λd. In order to find the positive equilibrium E=(S,I,R(a)) of system (1.2), we have

    {ΛβSI1+αIdS++0m(a)R(a)da=0,βSI1+αI(d+μ+γ)I=0,dR(a)da=(d+m(a))R(a),R(0)=γI. (3.1)

    Solving the third equation of (3.1), we get

    R(a)=R(0)ea0(d+m(θ))dθ=γIea0(d+m(θ))dθ. (3.2)

    By using the second equation of (3.1), we have

    S=d+μ+γβ(1+αI).

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

    I=Λβ(1d(d+μ+γ)Λβ)(β+dα)(d+μ+γ)βγ+0m(a)ea0(d+m(θ))dθda.

    Let R0=βS(0)d+μ+γ=Λβd(d+μ+γ). Then, I can be rewritten as

    I=Λβ(11R0)(β+dα)(d+μ+γ)βγ+0m(a)ea0(d+m(θ))dθda>0,

    which is positive if R0>1. Hence, system (1.2) has a unique positive equilibrium when R0>1.

    Summarizing the above analysis, we have the following result.

    Theorem 3.1. System (1.2) always has a disease free equilibrium E0=(S(0),0,0). If R0>1, there also exists a unique endemic equilibrium E=(S,I,R(a)) for fixed a.

    In fact, each term in R0 has clear epidemiological interpretation. 1d+μ+γ is the average infection period. β denotes the transmission rate of an infectious individual. S(0) is the total number of susceptible individuals. Therefore, R0 represents average new cases generated by a typical infectious member in the entire infection period. That is, R0 is the basic reproduction number of system (1.2).

    Let S(t)=x(t)+¯S, I(t)=y(t)+¯I, R(t,a)=z(t,a)+¯R(a), where ¯E=(¯S,¯I,¯R(a)) is a steady state of system (1.2), and let ˜u(t)=(x(t),y(t),0,z(t,a)), ˉu=(¯S,¯I,0,¯R(a)). Then, system (2.1) is equivalent to the following Cauchy problem

    {ddt˜u(t)=A˜u(t)+F(˜u(t)+ˉu)F(ˉu(t)),t0,˜u(0)=u(0)ˉu.

    By conducting direct computations one can obtain readily the linearized system of (2.1) around ˉu as the following form

    {ddt˜u(t)=A˜u(t)+DF(ˉu)(˜u(t)),t0,˜u(0)=u(0)ˉu, (3.3)

    in which

    DF(ˉu)(x(t)y(t)0z(t,a))=(β¯I1+α¯Ix(t)β¯S(1+α¯I)2y(t)++0m(a)z(t,a)daβ¯I1+α¯Ix(t)+β¯S(1+α¯I)2y(t)γy(t)0).

    Clearly, DF(ˉu) is a compact bounded linear operator on X.

    Denote Ω={λC:Re(λ)>d}. We claim then prove the following statement.

    Theorem 3.2. The operator (A,D(A)) is a Hille-Yosida operator.

    Proof. For (ϕ,φ,ψ,ω)X, (˜ϕ,˜φ,0,˜ω)D(A), λΩ, we have

    (λA)1(ϕφωψ)=(g1g20h){(λ+d)g1=ϕ,(λ+d+μ+γ)g2=φ,h(0)=ω,h+(λ+d+m(a))h=ψ.

    It then follows that

    {g1=ϕλ+d,g2=φλ+d+μ+γ,h=ea0(λ+d+m(θ))dθω+a0esa(λ+d+m(θ))dθψ(s)ds. (3.4)

    Integrating the last equation of (3.4) with regard to the age variable a and adding all the equations, we obtain that

    |g1|+|g2|+hL11λ+d(|ϕ|+|φ|+|ω|+ψL1).

    Thus, we have

    (λA)11λ+d,forallλΩ,

    which shows that (A,D(A)) is a Hille-Yosida operator.

    By Lemma 2.1 and Theorem 3.2, it follows that

    Theorem 3.3. The operator A+DF(ˉu) is a Hille-Yosida operator.

    Using Lemma 2.2, we further derive that

    heorem 3.4. The part of (A,D(A)) and (A+DF(ˉu),D(A+DF(ˉu))) generate C0-semigroups (S(t))t0 and (T(t))t0, respectively, on space X0.

    In order to establish the stability results for system (1.2), we will analyze the compactness of the generated C0-semigroups. Firstly, we introduce the definition of quasi-compactness for a semigroup below.

    Definition 3.1 (cf. [15]). A C0-semigroup (T(t))t0 is called quasi-compact if T(t)=T1(t)+T2(t) with the operator families T1(t) and T2(t) satisfying that

    (i) T1(t)0, as t+,

    (ii) T2(t) is eventually compact, that is, there is t0>0, such that T2(t) is compact for all t>t0.

    For a quasi-compact C0-semigroup, one has that

    Lemma 3.1 (cf. [15]). Let (T(t))t0 be a quasi-compact C0-semigroup and (B,D(B)) its infinitesimal generator. Then eδtT(t)0, as t+ for δ>0 if and only if all eigenvalues of B have strictly negative real part.

    By the Hille-Yosida estimate in the proof of Theorem 3.2, we have S(t))eξt. Furthermore, DF(ˉu)S(t):X0X is compact for every t>0. Since

    T(t)=eDF(ˉu)tS(t)=S(t)++k=1(DF(ˉu)t)kk!S(t),

    it is seen that (T(t))t0 is quasi-compact. Then by Lemma 3.1 we deduce that, for some η>0, eηtT(t)0 as t+ whenever all the eigenvalues of (A+DF(ˉu)) have negative real part.

    From the above arguments we can now make the following conclusion.

    Theorem 3.5. The solution semi-flow Φ(t,u0) of system (1.2), defined as in Theorem 2.1, satisfies the following properties.

    (i) If all the eigenvalues of (A+DF(ˉu)) have strictly negative real part, then the steady state ˉu is locally asymptotically stable.

    (ii) If, however, at least one eigenvalue of (A+DF(ˉu)) has strictly positive part, then the steady state ˉu is unstable.

    Based on the preceding analysis, in this section, we will firstly discuss the global stability of the disease free equilibrium E0=(S(0),0,0). Then, we study the stability of the endemic equilibrium E=(S,I,R(a)). At last, we analyze the existence of the Hopf bifurcation when E is unstable.

    Theorem 4.1. If R0<1, then disease free equilibrium E0=(S(0),0,0) of system (1.2) is globally asymptotically stable. While if R0>1, E0 is unstable.

    Proof. Let x(t)=S(t)S(0), y(t)=I(t), z(t,a)=R(t,a). Linearizing system (3.3) at E0 turns out to be the following system:

    {x(t)=dx(t)βS(0)y(t)++0m(a)z(t,a)da,y(t)=βS(0)y(t)(d+μ+γ)y(t),z(t,a)t+z(t,a)a=(d+m(a))z(t,a),z(t,0)=γy(t). (4.1)

    Solving the second and the third equations of (4.1), we obtain

    z(t,a)={R0(at)eaat(d+m(θ))dθ,a>t,γy(ta)et0(d+m(θ))dθ,a<t,y(t)=y(0)e(βS(0)(d+μ+γ))t. (4.2)

    The second equation of (4.2) implies that limt+y(t)=0 when R0<1. Furthermore, we have limt+z(t,a)=0. Substituting limt+y(t)=0 and limt+z(t,a)=0 into the first equation of (4.1) and solving for x(t), we obtain that limt+x(t)=0 as well. It implies that E0 is locally asymptotically stable when R0<1. In addition, when R0>1, we have y(t) as t+, which implies that E0 is unstable when R0>1.

    In the following, we construct the Lyapunov function to investigate the global stability of the disease free equilibrium E0 of system (1.2). Define a Lyapunov function

    V(t)=S(t)S(0)S(0)lnS(t)S(0)+I(t)+θ+0α(a)R(t,a)da,

    where θ>0 is constant, which will be determined later, and α(a)=+am(ξ)eξa(d+m(η))dηdξ is a differential function of a on [0,), then the derivative of V(t) along the solution of system is given by

    dV(t)dt=(1S(0)S)dSdt+dIdt+θ+0α(a)tR(t,a)da.

    By using of Λ=dS(0), we obtain

    dVdt=d(SS(0))2S(1S(0)S)βSI1+αI+(1S(0)S)+0m(a)R(t,a)da+βSI1+αI(d+μ+γ)Iθ+0α(a)[aR(t,a)+(d+m(a))R(t,a)]da=d(SS(0))2S+βS(0)I1+αI+SS(0)S+0m(a)R(t,a)da(d+μ+γ)Iθ+0α(a)aR(t,a)daθ+0α(a)(d+m(a))R(t,a)da.

    Because of

    +0α(a)aR(t,a)da=α(a)R(t,a)|+a=0+0α(a)R(t,a)da=α(0)R(t,0)+α(a)R(t,a)|a=++0[(d+m(a))α(a)m(a)]R(t,a)da,

    we have

    dVdt=d(SS(0))2S+βS(0)I1+αI+SΛdS+0m(a)R(t,a)da(d+μ+γ)I+θα(0)γIθα(a)R(t,a)|a=+θ+0m(a)R(t,a)dad(SS(0))2S+SΛdS+0m(a)R(t,a)daθα(a)R(t,a)|a=+θ+0m(a)R(t,a)da+βS(0)I(d+μ+γ)I+θα(0)γI=d(SS(0))2S+SΛdS+0m(a)R(t,a)daθα(a)R(t,a)|a=+θ+0m(a)R(t,a)da((d+μ+γ)(1R0)θα(0)γ)I.

    It is clear that SΛd0. If R0<1, assuming that there exists ε>0 such that θα(0)=(d+μ+γ)(1R0)γε>0, we obtain

    dVdtd(SS(0))2S+SΛdS+0m(a)R(t,a)daθα(a)R(t,a)|a=+θ+0m(a)R(t,a)daεγI0.

    Therefore, R0<1 ensures that the positive-definite function V(t) has negative derivative dV(t)dt. Moreover, the strict equality dV(t)dt=0 holds if and only if S(t)=Λd, I(t)=0 and R(t,a)=0. Thus, the singleton E0 is the largest invariant subset of dV(t)dt=0. By the LaSalle's invariant principle, the disease free equilibrium E0 is globally attractive. Therefore, E0 is globally asymptotically stable when R0<1.

    Next, we are interested in the stability of endemic equilibrium E=(S,I,R(a)) and the existence of Hopf bifurcations around E when its stability changes. In order to show the local stability of E, we linearize system (1.2) around E and put it as follows:

    {x(t)=(d+βI1+αI)x(t)βS(1+αI)2y(t)++0m(a)z(t,a)da,y(t)=βI1+αIx(t)+βS(1+αI)2y(t)(d+μ+γ)y(t),z(t,a)t+z(t,a)a=(d+m(a))z(t,a),z(t,0)=γy(t).

    To analyze the asymptotic behavior of E, we look for solutions of the form x(t)=x0eλt, y(t)=y0eλt, z(t,a)=z0(a)eλt. Thus, we have the following eigenvalue problem:

    {λx0=(d+βI1+αI)x0βS(1+αI)2y0++0m(a)z0(a)da,λy0=βI1+αIx0+βS(1+αI)2y0(d+μ+γ)y0,dz0(a)da=(λ+d+m(a))z0(a),z0(0)=γy0. (4.3)

    Solving the second and the third equation in (4.3), we obtain

    z0(a)=γy0ea0(λ+d+m(θ))dθ,x0=λ+d+μ+γβS(1+αI)2βI1+αIy0. (4.4)

    Substituting z0(a) and x0 into the first equation of (4.3), we get the following characteristic equation:

    Δ1(λ,τ)=b3λ3+b2λ2+b1λ+b0+a0eλτλ+d+m=f(λ,τ)g(λ)=0,

    where

    b3=1+αIβI,b2=1+2d+m+αI(3d+μ+γ+m)βI,b1=(1+α(2d+m)β)(d+μ+γ)+(d+m)(d+βI1+αI)1+αIβI,b0=(d+m)(1+αdβ)(d+μ+γ),a0=γmedτ.

    It is easy to see that

    {λΩ:det(Δ1(λ,τ))=0}={λΩ:f(λ,τ)=0}.

    In addition, if τ=0, then

    f(λ,0)=˜b3λ3+˜b2λ2+˜b1λ+˜b0+˜a0=0, (4.5)

    where ˜bi=bi|τ=0,i=0,1,2,3,˜a0=a0|τ=0. It is easy to check that ˜bi>0 for i=0,1,2,3, and ˜a0+˜b0>0. Therefore, by using of the Routh-Hurwitz criterion, we know if

    ˜b1˜b2>˜b3(˜a0+˜b0), (4.6)

    then all roots of (4.5) have negative real parts, which implies that the endemic equilibrium E is locally asymptotically stable. That is, the following result holds:

    Theorem 4.2. If R0>1, τ=0, and ˜b1˜b2>˜b3(˜a0+˜b0), then the endemic equilibrium E of system (1.2) is locally asymptotically stable.

    In fact, the roots of f(λ,τ)=0 depend on τ continuously, and the roots may pass through the imaginary axis and enter the right side as τ increasing. In the following, we discuss the case where τ>0.

    Let λ=iω(ω>0) be purely imaginary roots of f(λ,τ)=0. By submitting λ=iω into f(λ,τ)=0 and separating the real and imaginary parts, we have

    {b3ω3+b1ω=a0sinωτ,b2ω2+b0=a0cosωτ, (4.7)

    which yields that

    p3ω6+p2ω4+p1ω2+p0=0, (4.8)

    where p3=b23,p2=b222b1b3,p1=b212b0b2,p0=b20a20. It is clear that p3>0, and p0>0.

    Put Θ=ω2, (4.8) turns out to be

    Q(Θ)=p3Θ3+p2Θ2+p1Θ+p0=0. (4.9)

    Let F(Θ)=3p3Θ2+2p2Θ+p1. When p223p1p3<0, we know F(Θ)=0 has no real roots. When p223p1p30, we know F(Θ)=0 has two real roots, which are Θ1=p2p223p1p33p3, and Θ2=p2+p223p1p33p3, respectively. The following lemma gives the results on the positive root of the equation Q(Θ)=0.

    Lemma 4.1.

    (i) If p223p1p3<0, then Q(Θ)=0 has no positive root;

    (ii) If p223p1p30 and Θ20, then Q(Θ)=0 has no positive root;

    (iii) If p223p1p30, Θ2>0, and Q(Θ2)>0, then Q(Θ)=0 has no positive root;

    (iv) If p223p1p30, then Q(Θ)=0 has positive roots if and only if Θ2>0 and Q(Θ2)0.

    If Q(Θ)=0 does not have a positive root, then the stability of E will not change as τ increasing. Therefore, the following result holds:

    Theorem 4.3. Assume that R0>1, τ>0, and ˜b1˜b2>˜b3(˜a0+˜b0).

    (i) If p223p1p3<0, then the endemic equilibrium E of system (1.2) is locally asymptotically stable;

    (ii) If p223p1p30 and Θ20, then the endemic equilibrium E of system (1.2) is locally asymptotically stable;

    (iii) If p223p1p30, Θ2>0, and Q(Θ2)>0, then the endemic equilibrium E of system (1.2) is locally asymptotically stable.

    While if Q(Θ)=0 has positive root, then the stability of E may change when τ passes through some specific values. Let Θ be the positive real root of (4.9). Then ω=Θ is the only one positive real root of (4.8), so f(λ,τ)=0 with τ=τk, k=0,1,2,, has a pair of purely imaginary roots ±iω, where

    τk={1ω(arccosb2ω2b0a0+2kπ),c0,1ω(arccosb2ω2b0a0+2(k+1)π),c<0, (4.10)

    for k=0,1,2,, and c=b3ω3+b1ωa0.

    Differentiating both sides of f(λ,τ)=0 with respect to τ yields

    (dλdτ)1=(3b3λ2+2b2λ+b1)eλτλa0τλ. (4.11)

    From (4.7) and the fact that sign{Re[(dλdτ)1|λ=iω]}=sign{dRe(λ)dτ|τ=τk}, we have

    sign{dRe(λ)dτ|τ=τk}=sign{Re[((3b3λ2+2b2λ+b1)eλτλa0τλ)|λ=iω]}=sign{3b23ω6+2(b222b1b2)ω4+(b212b0b2)ω2(b3ω4b1ω2)2+(b0ωb2ω3)2}=sign{Q(ω2)(b3ω3b1ω)2+(b0b2ω2)2}=sign{Q(ω2)}=sign{Q(Θ)}.

    The transversality condition holds and a Hopf bifurcation occurs at τ=τk, k=0,1,2, when Q(Θ)0. According to the Hopf bifurcation theorem for functional differential equations [17], we have the following result.

    Theorem 4.4. Assume R0>1.

    (i) If p223p1p30, Θ2>0, and Q(Θ2)0, then the endemic equilibrium E of system (1.2) is asymptotically stable for all τ[0,τ0) under condition (4.6);

    (ii) If p223p1p30, Θ2>0, Q(Θ2)0, and Q(Θ)0, then system (1.2) undergoes Hopf bifurcation at E when τ=τk, k=0,1,2,.

    In this paper, we have proposed and analyzed an SIRS model with age structure for recurrent infectious disease by incorporating temporary immunity. A delayed differential equation system can be derived from this model and the delay corresponds to the time that recovery individuals lose their immunity. The purpose of this article is to explore the conditions switching between periodic and non-periodic behavior of recurrent infectious diseases which have the temporary immunity.

    On the dynamic behavior analysis of system (1.2), we showed the well-posedness, gave the basic reproduction number R0, and proved that R0=1 is the threshold that determines whether the epidemic persists or not by studying the stability of both disease free equilibrium E0 and the endemic equilibrium E. The disease free equilibrium E0 is globally asymptotically stable if R0<1 and is unstable if R0>1. Moreover, the disease persists in the later case, in the sense that infected individuals survive above a certain number for any initial infection numbers. We also proved the existence of Hopf bifurcation around the endemic equilibrium E when E is unstable.

    In order to display our conclusions more intuitively, we will use Matlab to demonstrate the nonlinear dynamics behavior of system (1.2). We denote the numbers of recovery individuals at time t as R(t)=+0R(t,a)da. Numerically, we set the maximum immunity age as 100.

    Firstly, we illustrate that the disease free equilibrium E0 is globally asymptotically stable when R0<1. The parameter values are chosen as Λ=1, d=0.007, μ=0.0025, α=0.1, γ=0.9, m=0.1, and β=0.005. Accordingly, we obtain R0<1. Since R0 is independent of τ, R0 does not change with time delay τ. When τ=0, the solutions of system (1.2) with three different initial values all approach to E0 as t trends to infinity(see Figure 1(a)). When τ=10, something similar happens(see Figure 1(b)). It means if we control the basic regeneration number R0 to be less than unity, the disease will die out in population. In this case, we don't need to worry about the recurrence of the epidemic disease.

    Figure 1.  The disease free equilibrium E0 of system (1.2) is globally asymptotically stable for any τ0 when R0<1.

    Secondly, we illustrate that the stability of the endemic equilibrium E when R0>1. Here, we only change the values of γ and β, and keep all other parameter values same as theses in Figure 1. In the case where τ=0, we take γ=0.9 and β=0.01, then, R0>1, and ˜b1˜b2>˜b3(˜a0+˜b0). Figure 2(a) shows that the solutions of system (1.2) with three different initial values all approach to E as t trends to infinity. In the case where τ=10>0, we take three different pairs of value for β and γ, which are (β,γ)=(0.05,0.9), (β,γ)=(0.03,0.1), and (β,γ)=(0.03,1), respectively. Accordingly, we have (ⅰ) p223p1p3<0, (ⅱ) p223p1p3>0 and Θ2<0, (ⅲ) p223p1p3>0, Θ2>0, and Q(Θ2)>0. Theorem 4.3 indicates that the endemic equilibrium E of system (1.2) is asymptotically stable under these conditions, which is consistent with the results shown in Figure 2(b). That is, under these conditions of Theorem 4.2 and Theorem 4.3, no matter how the delay τ changes, the system (1.2) doesn't have the periodic behavior even if the disease persists in the population. Accordingly, the distribution of recovery individuals with respect to immunity age at the endemic equilibrium E, R(a) is shown in Figure 3(a), which corresponding to the second solution line in Figure 2(a), and the distributions with both immunity age and time, R(t,a) is shown in Figure 3(b).

    Figure 2.  The endemic equilibrium E of system (1.2) is asymptotically stable when R0>1 and Q(Θ)=0 does not have positive roots.
    Figure 3.  The distributions of recovery individuals when E is asymptotically stable under R0>1 and τ=0.

    Thirdly, we demonstrate the case when R0>1 and Q(Θ)=0 has the positive root. According to Theorem 4.4, the endemic equilibrium E is asymptotically stable for τ[0,τ0), and periodic solutions occur as the stability of E changes, which means that Hopf bifurcation appears. Setting Λ=1, d=0.0006, μ=0.00003, γ=3, α=0.000001, β=0.02, and m=0.0085, the conditions R0>1, p223p1p3>0, Θ2>0 and Q(Θ2)<0 are satisfied. The critical time value is τ0=10.

    When time delay is small, say τ=0,2,4,6,8,10, the solutions shown in Figure 4 all approaches to the endemic equilibrium E through damped oscillations. While if we choose τ=12,14,16,18,20, Figure 5 displays periodic solutions with different periods and amplitudes. That is, with increasing of time delay, the stable endemic equilibrium is replaced by stable periodic orbits. Accordingly, when τ=12, we displays the distributions R(t,a) with both immunity age and time in Figure 6.

    Figure 4.  The endemic equilibrium E of system (1.2) is asymptotically stable for τ[0,10] when R0>1, and Q(Θ)=0 has the positive root.
    Figure 5.  Periodic solutions occur via Hopf bifurcation when E loses its stability.
    Figure 6.  Periodic solutions of system (1.2) when E loses its stability.

    In fact, when Hopf bifurcation exists, it is global continuation. That is, Hopf bifurcation always exits for any τ[τk,τk+1]. We show this numerically by the following Figure 7, where τ=12.2,12.4,12.6,12.8,13, and other parameter values are the same as those of Figure 5. The system presents periodic behaviors for all these chosen time delays.

    Figure 7.  Hopf bifurcation around endemic equilibrium E exits for any τ[tk,tk+1].

    Based on our analysis, we know that both non-periodic and periodic behaviors are possible when the disease persists in population. These findings are consistent with the results in [7,11]. It means that the dynamical behaviors of recurrent epidemics is dependent on the parameters of system (1.2). In particular, immune age and time delay is an important effects on the transmission of recurrent epidemics. Once R0>1, we can control how disease spreads through controlling the conditions theorem 4.3 and theorem 4.4. If the parameters of system (1.2) satisfy these conditions of theorem 4.3, or the conditions of theorem 4.4(ⅰ), the recurrent infectious disease is going to be a steady state as t goes to infinity. While if the parameters of system (1.2) satisfy these conditions of theorem 4.4(ⅱ), the recurrent infectious disease will persist in the population in the form of periodic oscillations.

    Although the simple delay differential equations model may show the switching between periodic and non-periodic behavior, it cannot express the immunity age of the recovery individual. In fact, the immunity age of the individual is important since the immunity age of the individual can be used to describe whether the recovered individual has the immunity or not. The model (1.2) may more accurately describe how the recurrent infectious disease spreads. In addition, our results also implies that model (1.2) may be closer to the transmission mechanism of the recurrent infectious disease. We suspect that the seasonality of recurrent epidemics is also related to age structure and the delay.

    We would like to thank the referees very much for the careful review and the valuable comments to this manuscript which improve it greatly.

    This work is supported by National Natural Science Foundation of China(grant 11301314, 11671142, and 11371087), by Natural Science Basic Research Plan in Shaanxi Province of China grant 2019JM-081, and by Natural Science Foundation of Shaanxi Provincial Department of Education in China grant 18JK0092.

    The authors have declared that no competing interests exist.



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