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. 2019 Mar 14;267(3):1859–1898. doi: 10.1016/j.jde.2019.03.005

Bifurcation analysis of an SIRS epidemic model with a generalized nonmonotone and saturated incidence rate

Min Lu a, Jicai Huang a, Shigui Ruan a,b,, Pei Yu c
PMCID: PMC7094459  PMID: 32226129

Abstract

In this paper, we study a susceptible-infectious-recovered (SIRS) epidemic model with a generalized nonmonotone and saturated incidence rate kI2S1+βI+αI2, in which the infection function first increases to a maximum when a new infectious disease emerges, then decreases due to psychological effect, and eventually tends to a saturation level due to crowding effect. It is shown that there are a weak focus of multiplicity at most two and a cusp of codimension at most two for various parameter values, and the model undergoes saddle-node bifurcation, Bogdanov-Takens bifurcation of codimension two, Hopf bifurcation, and degenerate Hopf bifurcation of codimension two as the parameters vary. It is shown that there exists a critical value α=α0 for the psychological effect, and two critical values k=k0,k1(k0<k1) for the infection rate such that: (i) when α>α0, or αα0 and kk0, the disease will die out for all positive initial populations; (ii) when α=α0 and k0<kk1, the disease will die out for almost all positive initial populations; (iii) when α=α0 and k>k1, the disease will persist in the form of a positive coexistent steady state for some positive initial populations; and (iv) when α<α0 and k>k0, the disease will persist in the form of multiple positive periodic coexistent oscillations and coexistent steady states for some positive initial populations. Numerical simulations, including the existence of one or two limit cycles and data-fitting of the influenza data in Mainland China, are presented to illustrate the theoretical results.

Keywords: SIRS epidemic model, Saddle-node bifurcation, Bogdanov-Takens bifurcation, Hopf bifurcation, Degenerate Hopf bifurcation

1. Introduction

In the classical infectious disease transmission models (Kermack and McKendrick [16], Hethcote [12]), the population is divided into three classes labeled by S(t), I(t) and R(t), representing the numbers of susceptible, infective, and recovered or removed individuals at time t, respectively. Assuming the recovered individuals have temporary immunity, the classical susceptible-infectious-recovered (SIRS) model can be written as follows:

dSdt=bdSg(I)S+δR,dIdt=g(I)S(d+μ)I,dRdt=μI(d+δ)R, (1.1)

where b is the recruitment rate of the population, d is the natural death rate of the population, μ is the natural recovery rate of the infective individuals, δ is the rate at which recovered individuals lose immunity and return to the susceptible class. g(I)S is called the incidence rate, and g(I) is a function to measure the infection force of a disease.

The incidence rate g(I)S plays a very important role in describing the evolution of infectious disease. In [16] Kermack and McKendrick assumed that the incidence rate is bilinear, i.e.,

g(I)S=kIS, (1.2)

where g(I)=kI is unbounded when I0. The bilinear incidence rate (1.2) might be true when the number of the infective individuals I(t) is small, but it becomes unrealistic when I(t) is getting larger. Studying the data on the cholera epidemic spread in Bari, Italy, in 1973, Capasso et al. [5] and Capasso and Serio [6] proposed two types of nonlinear incidence rates, namely a saturated incidence rate and an incidence rate taking psychological effect into account (see Fig. 1.1 ).

Fig. 1.1.

Fig. 1.1

Two types of nonlinear incidence function g(I). (a) A saturated incidence function; (b) An incidence function with psychological effect.

(a) Saturated Incidence Rates. To compare with the bilinear incidence rate (1.2), Capasso and Serio [6] proposed a saturated incidence rate of the following form:

g(I)S=kIS1+αI, (1.3)

where kI measures the infection force of the disease and 11+αI measures the inhibition effect from the behavioral change of the susceptible individuals when their number increases or from the crowding effect of the infective individuals (Ruan and Wang [25]). Notice that the nonlinear incidence function g(I) eventually tends to a saturation level kα when I is getting larger.

The general incidence rate

g(I)S=kIpS1+αIq (1.4)

was proposed by Liu et al. [20] (q=p1) and Hethcote and van den Driessche [13] (pq), and used by a number of authors, see, for example, Alexander and Moghadas [1], [2], Derrick and van den Driessche [9], [10], Li et al. [17], Liu et al. [19], Lizana and Rivero [21], Moghadas and Alexande [22], and Wang [28]. According to Tang et al. [27] and Hu et al. [14], the incidence function g(I)=kIp1+αIq includes three types: (i) unbounded incidence function: p>q; (ii) saturated incidence function: p=q; and (iii) nonmonotone incidence function: p<q. In order to better understand the generic bifurcations in SIRS models with saturated incidence rates, Ruan and Wang [25] studied model (1.1) with a specific nonlinear incidence rate,

g(I)S=kI2S1+αI2, (1.5)

and presented a detailed qualitative and bifurcation analysis of the model.

(b) Nonmonotone Incidence Rates with Psychological Effect. Though Capasso and Serio [6] described incidence functions taking into account psychological effect, but they did not give any specific function to describe such incidence. To model the effects of psychological factor, protection measures and intervention policies when a serious disease emerges, Xiao and Ruan [29] proposed the following specific incidence rate:

g(I)S=kIS1+αI2, (1.6)

where the incidence function g(I)=kI1+αI2 is nonmonotone when I0 (see Fig. 1.1(b)). This implies that the contact rate and the infection probability are increasing when a new infectious disease emerges, since people have very little knowledge about the disease. However, when I is large and the disease becomes more serious, psychological factor leads people to implementing measures to control the spread of the disease. For example, in the outbreak of severe acute respiratory syndrome (SARS), the aggressive measures and policies, such as border screening, mask wearing, quarantine, isolation, etc. were proved to be very effective in reducing the transmission. So the infection force decreases when the number of infected individuals becomes larger. Liu et al. [18] used (1.6) to describe the psychological effect toward avian influenza in the human population. In [29], Xiao and Ruan presented a global analysis for model (1.1) with nonmonotone incidence rate (1.6), and showed that either the number of infective individuals tends to zero as time evolves or the disease persists. Hence, model (1.1) with nonmonotone incidence rate (1.6) cannot exhibit complicated dynamics and bifurcations.

Xiao and Zhou [30] considered a complete form of the nonmonotone incidence rate (1.6) as follows:

g(I)S=kIS1+βI+αI2, (1.7)

where β is a parameter such that 1+βI+αI2>0 for all I0, hence, β>2α. They presented qualitative analysis of model (1.1) with nonmonotone incidence rate (1.7) and showed the existence of bistable phenomenon and periodic oscillation. Zhou et al. [32] further studied the existence of different kinds of bifurcations, such as Hopf and Bogdanov-Takens bifurcations.

(c) Nonmonotone and Saturated Incidence Rates. Note that both nonmonotone incidence functions kI1+αI2 and kI1+βI+αI2, given in (1.6) and (1.7), tend to zero when I goes to infinite, which indicates that the psychological or inhibitory effect from the behavioral change of the susceptible individuals or from the crowding effect of the infective individuals is too strong, which may be unreasonable for some specific infectious diseases, such as influenza. Thus, a more reasonable incidence function g(I) may be one that first increases to a maximum when a new infectious disease emerges or an old infectious disease reemerges, then decreases due to psychological effect, and eventually tends to a saturation level due to crowding effect. On the other hand, in some specific infectious diseases, the incidence rate may not be monotonic or non-monotonic alone, a more general incidence rate may have a combination of monotonicity, nonmonotonicity and saturation properties.

Based on the above discussions, in this paper, we propose the following general nonmonotone and saturated incidence rate:

g(I)S=kI2S1+βI+αI2, (1.8)

where α>0 is a parameter which measures the psychological or inhibitory effect, and k is the infection rate. β is a parameter such that 1+βI+αI2>0 for all I0, hence, β>2α. When β0, g(I)=kI21+βI+αI2 is monotonic, always increases and then tends to a saturated level kα as I goes to infinite. When 2α<β<0, g(I) is nonmonotonic, increases when I is small and decreases when I is large, and finally tends to a saturated level kα as I goes to infinite (see Fig. 1.2 ). It can be seen from Fig. 1.2 that when α and k are fixed, g(I) increases faster for smaller β when I is small, and then decreases to the same fixed value kα for any β.

Fig. 1.2.

Fig. 1.2

Properties of function g(I) in (1.8) for α = 1, k = 1 with β = −1,−0.5,0,1.

When β=0, the general incidence rate (1.8) becomes the saturated incidence rate (1.5). Ruan and Wang [25] studied model (1.1) with incidence rate (1.5) and presented a detailed qualitative and bifurcation analysis of the model. They showed that the system undergoes Bogdanov-Takens bifurcation of codimension two and Hopf bifurcation of codimension one, but the exact codimension of Hopf bifurcation remains unknown. In [27], Tang et al. proved that the maximal multiplicity of the weak focus is two by complex algebraic calculations but did not give the explicit conditions for degenerate Hopf bifurcation. Moreover, they claimed the existence of Bogdanov-Takens bifurcation of codimension three. They also conjectured that model (1.1) with nonmonotone incidence rate would not exhibit complicated dynamics and bifurcations.

In this paper, for the case β>2α we find that model (1.1) with general incidence rate (1.8) can exhibit complicated dynamical behaviors and bifurcation phenomena. More precisely, we will show that there are a weak focus of multiplicity at most two and a cusp of codimension at most two for various parameter values, and the model undergoes saddle-node bifurcation, Bogdanov-Takens bifurcation of codimension two, Hopf bifurcation, and degenerate Hopf bifurcation of codimension two as the parameters vary. By considering a more general model, our results show that Bogdanov-Takens bifurcation of codimension higher than two cannot occur, which clarifies and corrects the corresponding results obtained by Tang et al. [27], who claimed the existence of Bogdanov-Takens bifurcation of codimension three. Moreover, our results about degenerate Hopf bifurcation of codimension two can be seen as a complement of the results obtained by Ruan and Wang [25], who only discussed the Hopf bifurcation of codimension one. Furthermore, it is shown that there exists a critical value α=α0 for the psychological or inhibitory effect, and two critical values k=k0,k1(k0<k1) for the infection rate such that: (i) when α>α0, or αα0 and kk0, the disease will die out for all positive initial populations; (ii) when α=α0 and k0<kk1, the disease will die out for almost all positive initial populations; (iii) when α=α0 and k>k1, the disease will persist in the form of a positive coexistent steady state for some positive initial populations; and (iv) when α<α0 and k>k0, the disease will persist in the form of multiple positive periodic coexistent oscillations and coexistent steady states for some positive initial populations.

The rest of the paper is organized as follows. In section 2, we carry out a qualitative analysis to give the types and stability of equilibria of model (1.1) with general incidence rate (1.8). In section 3, we show that the model undergoes saddle-node bifurcation, Bogdanov-Takens bifurcation of codimension at most two, Hopf bifurcation, and degenerate Hopf bifurcation of codimension at most two as parameters vary. In section 4 we use the model to simulate the influenza data in Mainland China from 2004 to 2017. Conclusion and discussion are given in section 5.

2. Types and stability of equilibria

We consider an SIRS epidemic model in the following form

dSdt=bdSkSI21+βI+αI2+δR,dIdt=kSI21+βI+αI2(d+μ)I,dRdt=μI(d+δ)R, (2.1)

under the initial conditions S(0)0, I(0)0, R(0)0, where S(t), I(t) and R(t) denote the numbers of susceptible, infective, and recovered individuals at time t, respectively, b>0 is the recruitment rate of the population, d>0 is the natural death rate of the population, k>0 is the infection rate, μ>0 is the natural recovery rate of the infective individuals, δ>0 is the rate at which recovered individuals lose immunity and return to the susceptible class, α>0 is a parameter which measures the psychological or inhibitory effect, and β>2α such that 1+βI+αI2>0 for all I0.

To study the dynamics of model (2.1), we first present a lemma.

Lemma 2.1

The plane S+I+R=bd is an invariant manifold of system (2.1) , which is attracting in the first octant.

Proof

Summing up the three equations in (2.1) and denoting N(t)=S(t)+I(t)+R(t), we have

dNdt=bdN.

It is clear that N(t)=bd is a solution and for any N(t0)0, the general solution is

N(t)=1d[b(bdN(t0))ed(tt0)].

Thus,

limtN(t)=bd,

which implies the conclusion. □

It is clear that the limit set of system (2.1) is on the plane S+I+R=bd. Thus, we focus on the reduced system

dIdt=kI21+βI+αI2(bdIR)(d+μ)I,dRdt=μI(d+δ)R. (2.2)

We know that the positively invariant set of system (2.2) is

D={(I,R)|I0,R0,I+Rbd}.

System (2.2) always has an equilibrium E0=(0,0) which corresponds to the disease-free equilibrium (bd,0,0) of system (2.1). To find the endemic equilibria, we rescale (2.2) by using

I=d+δkx,R=d+δky,t=1d+δτ.

Then we obtain (for simplicity we still denote τ by t)

dxdt=x21+mx+nx2(Axy)px,dydt=qxy, (2.3)

where

m=βd+δk,n=αd+δk,A=bdkd+δ,p=d+μd+δ,q=μd+δ.

It can be seen that

A,p,q,n>0,m>2α(d+δ)k=2n,p>q, (2.4)

and the positively invariant region of system (2.3) is

D˜={(x,y)|x0,y0,x+yA}

since x=0 is an invariant line, and when y=0, we have dydt>0.

To find the positive equilibria of system (2.3), we set

x21+mx+nx2(Axy)px=0,qxy=0, (2.5)

which yield

(np+q+1)x2+(mpA)x+p=0. (2.6)

We can see from (2.5) and (2.6) that system (2.3) has at most two positive equilibria E1(x1,y1) and E2(x2,y2), which may coalesce into a unique positive equilibrium E(x,y), where

x1=Amp(Amp)24(np+q+1)p2(np+q+1),y1=qx1;
x2=Amp+(Amp)24(np+q+1)p2(np+q+1),y2=qx2;
x=Amp2(np+q+1),y=qx.

The discriminant of (2.6) is

Δ=(Amp)24(np+q+1)p,

and we have

x1x2=pnp+q+1>0,x1+x2=Ampnp+q+1.

Note that Δ0 is equivalent to n(Amp)24(q+1)p4p2. Let

n=(Amp)24(q+1)p4p2. (2.7)

Then we have the following existence conditions of equilibria in system (2.3).

Theorem 2.2

Model (2.3) always has an equilibrium E0(0,0) . Moreover,

  • (I)
    System (2.3) has no positive equilibria if and only if one of the following conditions holds:
    • (I.1)
      n>n ,
    • (I.2)
      nn and Amp .
  • (II)

    System (2.3) has a unique positive equilibrium E(x,y) if and only if n=n and A>mp , where 0<x1 .

  • (III)

    System (2.3) has two positive equilibria E1(x1,y1) and E2(x2,y2) if and only if n<n and A>mp , where 0<x1<x<x2<2x .

Next we study local stability of equilibria of system (2.3). We first study the disease-free equilibrium E0(0,0). The Jacobian matrix of system (2.3) at E0(0,0) is

J(E0)=(p0q1),

which has two eigenvalues λ1=1,λ2=p. We obtain the following result.

Theorem 2.3

The disease-free equilibrium E0(0,0) of system (2.3) is a stable hyperbolic node. A phase portrait is shown in Fig. 2.1 .

Fig. 2.1.

Fig. 2.1

The phase portrait of system (2.3) with no positive equilibria for A = 2, m = −5, p = 2, q = 1.4, n = 9.

To discuss whether the disease can invade the population, we study the global stability of the equilibrium (0,0). Since x=0 is an invariant line and D˜ is positively invariant, by index theory, we can conclude that system (2.3) does not have nontrivial periodic orbits in R+2 when system (2.3) has no positive equilibria.

Theorem 2.4

The disease-free equilibrium (db,0,0) of (2.1) is globally asymptotical stable in the interior R+3 and the disease cannot invade the population if n>n , or nn and Amp .

Remark 2.1

From Theorem 2.4 and system (2.3), we can see that n>n is equivalent to α>α0, where

α0(bkβd(d+μ))2(d+δ)4kd2(μ+d)(μ+d+δ)4d2(d+δ)(μ+d)2, (2.8)

while nn and Amp are equivalent to αα0 and kk0, where

k0βdb(d+μ). (2.9)

These indicate that the disease will die out for all positive initial populations when the psychological or inhibitory effect α is greater than a critical value α0, or the psychological effect α is smaller than the critical value α0 and the infection rate k is also smaller than a critical value k0.

Now we consider the positive equilibria of system (2.3). The positive equilibria with coordinates (x,y) satisfy

y=qx,x(Axy)p(1+mx+nx2)=0,

and the Jacobian matrix of system (2.3) at a positive equilibrium E(x,y) is given by

J(E)=[x2px(m+2nx)+x(Axqx)1+mx+nx2x21+mx+nx2q1].

Then the determinant of J(E) is

det(J(E))=x[2(np+q+1)x+(mpA)]1+mx+nx2

and its sign is determined by

SD=2(np+q+1)x+(mpA). (2.10)

The trace of J(E) is

tr(J(E))=(2np+n+q+2)x2+(Ampm)x11+mx+nx2

and its sign is determined by

ST=(2np+n+q+2)x2+(Ampm)x1. (2.11)

To discuss the topological type of the positive equilibria of system (2.3), we let

q1=A22pAmp2p(1+p), (2.12)

which will be used in the following theorem.

Theorem 2.5

When n=n , A>mp and conditions (2.4) are satisfied, system (2.3) has a unique positive equilibrium E(x,y) . Moreover,

  • (I)

    if qq1 , then E(x,y) is a saddle-node, which is attracting (or repelling) if q<q1 (or q>q1 );

  • (II)

    if q=q1 , then E(x,y) is a cusp of codimension two.

The phase portraits are shown in Fig. 2.2 .

Fig. 2.2.

Fig. 2.2

The phase portraits of system (2.3) with a unique positive equilibrium: (a) an attracting saddle-node for A = 2, m = −5, p = 2, q = 1, n = 8; (b) a repelling saddle-node for A = 2, m = −5, p = 2, q = 3, n = 7; (c) a cusp of codimension two for A=2,m=5,p=2,q=53,n=233.

Proof

Substituting x and n into SD and ST, we deduce that SD(x)=0 and

ST(x)=2[A2+Amp+2p+2p(1+p)q](Amp)2.

Letting ST(x)=0, we have

q=A22pAmp2p(1+p).

Then, using Theorem 7.1 in Zhang et al. [33], we obtain the conclusion in (I).

To show that the assertion (II) holds, let X=xx, Y=yy, n=n and q=q1. Then using Taylor expansions, we can rewrite system (2.3) as follows (for simplicity, we still denote X, Y by x, y, respectively)

dxdt=a1x+a2y+a3x2+a4xy+o(|(x,y)|2),dydt=q1xy, (2.13)

where

a1=1,a2=1q1,a3=(Amp)2((Amp)p2A)8p3q1,a4=A(Amp)24p3q12.

Next let X=x, Y=x1q1y. Then system (2.13) is transformed into (we still denote X, Y by x, y, respectively)

dxdt=y+(a3+q1a4)x2q1a4xy+o(|(x,y)|2),dydt=(a3+q1a4)x2q1a4xy+o(|(x,y)|2). (2.14)

By Remark 1 of section 2.13 in [24] (see also [15]), we obtain an equivalent system of (2.14) in the small neighborhood of (0,0) as follows:

dxdτ=y,dydτ=(a3+q1a4)x2+(2a3+q1a4)xy+o(|(x,y)|2), (2.15)

where

a3+q1a4=(Amp)38p2q1,2a3+q1a4=(Amp)2((Amp)pA)4p3q1.

It is seen that a3+q1a4<0 because A>mp. We next prove 2a3+q1a40 (i.e., mA(p1)p2) by contradiction. Supposing m=A(p1)p2 and substituting it into n=n and q=q1, we obtain

n=4p4+A2(p1)4p4(1+p),q=A22p22p2(1+p). (2.16)

Further, since n>0, p>q>0 and m>2n, it follows from (2.16) that

0<p<1,4p21p<A2<2p2(1+p+p2).

However, 4p21p>2p2(1+p+p2) if 0<p<1, which results in a contradiction. Thus mA(p1)p2 (i.e., 2a3+qa40). By the results in [15], E(x,y) is a cusp of codimension two. □

Remark 2.2

When m=0 (i.e., β=0), our system (2.2) is reduced to system (1.3) in [27], our Theorem 2.5 (II) indicates that Bogdanov-Takens bifurcation of codimension higher than two cannot occur around E, which clarifies and corrects the corresponding results in [27], where the authors claimed the existence of Bogdanov-Takens bifurcation of codimension three.

Remark 2.3

When the psychological effect α equals the critical value α0 given by (2.8), Theorem 2.5 implies that whether the disease persists or dies out will depend on the infection rate and the initial population. More precisely, when the psychological effect α equals the critical value α0 and the infection rate k is greater than the first critical value k0 given by (2.9), i.e., n=n and A>mp, then system (2.1) has two equilibria, a disease-free equilibrium and an endemic equilibrium. Moreover, from Fig. 2.2 (b) and (c), we can see that the disease will die out for almost all positive initial populations if the infection rate k is less than another larger critical value

k1βdb(d+μ)+2d2(d+μ)((d+δ)2+μ(μ+δ+2d))b2(d+δ)2(kk1, i.e.qq1), (2.17)

and the disease will persist to a positive coexistent steady state for some positive initial population if the infection rate k is greater than the second critical value k1 (k>k1, i.e. q<q1), as shown in Fig. 2.2 (a).

Theorem 2.6

When n<n , A>mp and conditions (2.4) are satisfied, then system (2.3) has two positive equilibria E1(x1,y1) and E2(x2,y2) . Moreover, E1 is always a hyperbolic saddle and E2 is

  • (i)

    a stable hyperbolic focus (or node) if ST(x2)<0 ; or

  • (ii)

    a weak focus (or a center) if ST(x2)=0 ; or

  • (iii)

    an unstable hyperbolic focus (or node) if ST(x2)>0 ,

where ST is given in (2.11) .

Proof

To determine the types of E1 and E2, it is suffice to consider the signs of SD(x1), SD(x2) and ST(x2), where SD and ST are given in (2.10) and (2.11), respectively, from which we have

SD(x1)=2(np+q+1)x1+(mpA),
SD(x2)=2(np+q+1)x2+(mpA).

On the other hand, since x1 and x2 are two different positive roots of (2.6), we have

(np+q+1)x12+(mpA)x1+p=0,2(np+q+1)x1+(mpA)<0, (2.18)
(np+q+1)x22+(mpA)x2+p=0,2(np+q+1)x2+(mpA)>0, (2.19)

yielding SD(x1)<0 and SD(x2)>0. Hence we obtain the types of E1 and E2. □

Remark 2.4

It is seen from Theorem 2.6 that when the psychological effect α is smaller than the critical value α0 but the infection rate k is greater than the first critical value k0, i.e., n<n and A>mp, then the disease will become more severe because of the existence of multiple positive coexistent steady states.

3. Bifurcation analysis

From Theorem 2.2, Theorem 2.5, Theorem 2.6, we know that system (2.3) may exhibit saddle-node bifurcation, Bogdanov-Takens bifurcation around the equilibrium E(x,y), and Hopf bifurcation around the equilibrium E2(x2,y2). In this section, we investigate various possible bifurcations in system (2.3).

3.1. Saddle-node bifurcation

From Theorem 2.2, Theorem 2.5, Theorem 2.6, we know that the surface

SN={(A,m,n,p,q):n=n,qq1,2n<m<Ap,p>q,A,n,p,q>0}

is the saddle-node bifurcation surface. When the parameters are varied to cross the surface from one side to the other side, the number of positive equilibria of system (2.3) changes from zero to two, the saddle-node bifurcation yields two positive equilibria. This implies that there exists a critical psychological effect value α0 such that the disease cannot invade the population when α>α0 (i.e., n>n), and the disease will persist for some positive initial populations when αα0 (i.e., nn).

3.2. Bogdanov-Takens bifurcation

In this subsection, we discuss if system (2.3) undergoes Bogdanov-Takens Bifurcation of codimension two under a small parameter perturbation if the bifurcation parameters are chosen suitably. Actually, we have the following theorem.

Theorem 3.1

When n=n , q=q1 , A>mp and conditions (2.4) hold, system (2.3) has a cusp E(x,y) of codimension two (i.e., Bogdanov-Takens singularity). If we choose A and q as bifurcation parameters, then (2.3) undergoes Bogdanov-Takens bifurcation of codimension two in a small neighborhood of the unique positive equilibrium E(x,y) . Hence, there exist some parameter values such that system (2.3) has an unstable limit cycle, and there exist some other parameter values such that system (2.3) has an unstable homoclinic loop.

Proof

Consider

dxdt=x21+mx+nx2(A+λ1xy)px,dydt=(q1+λ2)xy, (3.1)

where λ1 and λ2 are parameters in a small neighborhood of (0,0). We are interested only in the phase portraits of system (3.1) when x and y lie in a small neighborhood of the interior equilibrium E(x,y).

Let X=xx, Y=yy. Then system (3.1) can be rewritten as (for simplicity, we still denote X, Y by x, y, respectively)

dxdt=b1+b2x1q1y+b3x2+b4xy+P1(x,y,λ1,λ2),dydt=b5+b6xy, (3.2)

where P1(x,y,λ1,λ2) is a C function at least of third order with respect to (x,y), whose coefficients depend smoothly on λ1 and λ2, and

b1=λ11q1,b2=1+λ1A(Amp)24p3q12,b3=(Amp)232p6q13{4p3q12[(Amp)p2A]+λ1(Amp)[A3A(2Am+6(1+q1))p+m(Am+2(1+q1))p2]},b4=A(Amp)24p3q12,b5=λ22pAmp,b6=q1+λ2.

Let

X=x,Y=b1+b2x1q1y+b3x2+b4xy+P1(x,y,λ1,λ2),

and rewrite X, Y as x, y, respectively. Then system (3.2) becomes

dxdt=y,dydt=c1+c2x+c3y+c4x2+c5xy+c6y2+Q1(x,y,λ1,λ2), (3.3)

where Q1(x,y,λ1,λ2) is a C function at least of third order with respect to (x,y), whose coefficients depend smoothly on λ1 and λ2, and

c1=q1b1b5q1,c2=q1b2+q1b4b5+q13b12b42b6q1,c3=0,c4=b3+b4b6+q1b1b3b4+q12b1b3b42,c5=2b3+q1b2b4q12b1b42,c6=q1b4.

Next let dt=(1c6x)dτ, under which system (3.3) becomes (still denote τ by t)

dxdt=y(1c6x),dydt=(1c6x)(c1+c2x+c3y+c4x2+c5xy+c6y2+Q1(x,y,λ1,λ2)). (3.4)

Letting X=x, Y=y(1c6x), and rewriting X, Y as x, y, respectively, we obtain

dxdt=y,dydt=d1+d2x+d3x2+d4xy+Q2(x,y,λ1,λ2), (3.5)

where Q2(x,y,λ1,λ2) is a C function at least of third order with respect to (x,y), whose coefficients depend smoothly on λ1 and λ2, and

d1=c1,d2=c22c1c6,d3=c42c2c6+c1c62,d4=c5.

Note that when λ1=λ2=0,

d1=0,d2=0,d3=a3+q1a4=(Amp)38p2q1<0,
d4=2a3+q1a4=(Amp)2((Amp)pA)4p3q1<0.

Further, let

X=x+d22d3,Y=y.

Then system (3.5) can be rewritten as (still denote X, Y by x, y, respectively)

dxdt=y,dydt=e1+e2y+e3x2+e4xy+Q3(x,y,λ1,λ2), (3.6)

where Q3(x,y,λ1,λ2) is a C function at least of third order with respect to (x,y), whose coefficients depend smoothly on λ1 and λ2, and

e1=d1d224d3,e2=d2d42d3,e3=d3,e4=d4.

Making the final change of variables by setting

X=e42e3x,Y=e43e32y,τ=e3e4t,

then we finally obtain (still denote X, Y and τ by x, y and t, respectively)

dxdt=y,dydt=μ1+μ2y+x2+xy+Q4(x,y,λ1,λ2), (3.7)

where Q4(x,y,λ1,λ2) is a C function at least of third order with respect to (x,y), whose coefficients depend smoothly on λ1 and λ2, and

μ1=e1e44e33,μ2=e2e4e3.

We can express μ1 and μ2 in terms of λ1 and λ2 as follows:

μ1=s1λ1+s2λ2+s3λ12+s4λ1λ2+s5λ22+o(|(λ1,λ2)|),μ2=t1λ1+t2λ2+t3λ12+t4λ1λ2+t5λ22+o(|(λ1,λ2|), (3.8)

where

s1=2(AAp+mp2)4p6(Amp)q12,s2=4(AAp+mp2)4p5(Amp)2q12,s3=(AAp+mp2)34p10(Amp)q14{4m2p4(1+q1)+2Amp2[m2p2+3m2p38p(1+q1)6(1+q1)]+A2p[5m2p218m2p3+6p(2m2+2q1)+36(1+q1)]+A3mp(23+4p+18p2)A4(17+p+6p2)},s4=(AAp+mp2)3p9(Amp)2q14{2m2p4(1+q1)+Amp2[3m2p3+p2(m214q1)8p(1+q1)6(1+q1)]+A2p[9m2p3+p2(3m2+14q1)+p(63m28q1)+18(1+q1)]+A3mp(179p+9p2)+A4(14+5p3p2)},s5=(AAp+mp2)4p8(Amp)4q14[11A4+22A3mpA2p2(11m2+28q1)+28Amp2+4p4q12],t1=A[A(1+p)mp2]22p5q12,t2=(AAp+mp2)2(A2+Amp+2p2q1)p4(Amp)2q12,t3=A24p9q14[A(1+p)mp2]{A2mp(8+2p3p2)+A3(6p+p2)+mp2[4(1+q1)m2p3]+Ap[m2p(2p+3p2)12(1+q1)]},t4=A[A(1+p)mp2]2p8(Amp)2q14{A4mp(11+9p4p2)+A5(53p+p2)+A2mp2[8m2p(13p+4p2)+(8+4p+4p2+6p3)q1]+2mp4q1[m2p32(1+q1)]+A3p[m2p(79p+6p2)2(3+(3+p+p2+p3)q1)]+Ap3[m4p3+12q1(1+q1)2m2(1+(1+p+p2+3p3)q1)]},t5=4A(AAp+mp2)2(A2Amp+2p2q1)(A2+Amp+2p2q1)p7(Amp)3q14.

Since

|(μ1,μ2)(λ1,λ2)|λ=0=4(AAp+mp2)6p8(Amp)3q130

for mA(p1)p2, p>0, q1>0 and A>mp, the parameter transformation (3.8) is a homeomorphism in a small neighborhood of the origin, and μ1 and μ2 are independent parameters.

The results in Bogdanov [3], [4] and Takens [26] now imply that system (3.7) (i.e., (3.1) or (2.3)) undergoes Bogdanov-Takens bifurcation when (λ1,λ2) changes in a small neighborhood of (0,0). □

By the results of Perko [24], we obtain the following local representations of the bifurcation curves up to second-order approximations:

(i) The saddle-node bifurcation curve is

SN={(μ1,μ2)|μ1=0,μ20}={(λ1,λ2)|2(AAp+mp2)4p6(Amp)q12λ1+4(AAp+mp2)4p5(Amp)2q12λ2(AAp+mp2)34p10(Amp)q14{4m2p4(1+q1)+2Amp2[m2p2+3m2p38p(1+q1)6(1+q1)]+A2p[5m2p218m2p3+6p(2m2+2q1)+36(1+q1)]+A3mp(23+4p+18p2)A4(17+p+6p2)}λ12+(AAp+mp2)3p9(Amp)2q14{2m2p4(1+q1)+Amp2[3m2p3+p2(m214q1)8p(1+q1)6(1+q1)]+A2p[9m2p3+p2(3m2+14q1)+p(63m28q1)+18(1+q1)]+A3mp(179p+9p2)+A4(14+5p3p2)}λ1λ2(AAp+mp2)4p8(Amp)4q14[11A4+22A3mpA2p2(11m2+28q1)+28Amp2+4p4q12]λ22=0,μ20}.

(ii) The Hopf bifurcation curve is

H={(μ1,μ2)|μ2=μ1,μ1<0}={(λ1,λ2)|2(AAp+mp2)4p6(Amp)q12λ1+4(AAp+mp2)4p5(Amp)2q12λ2(AAp+mp2)32p10(Amp)q14{2m2p4(1+q1)+Amp2[m2p2+3m2p38p(1+q1)6(1+q1)]+A2p[2m2p29m2p3+p(63m2+6q1)+18(1+q1)]+A3mp(12+p+9p2)3A4(3+p2)}λ12+(AAp+mp2)3p9(Amp)2q14{2m2p4(1+q1)+Amp2[3m2p3+p2(m212q1)8p(1+q1)6(1+q1)]+A2p[9m2p3+4p2(m2+3q1)3p(2+m2+2q1)+18(1+q1)]+A3mp(1811p+9p2)3A4(52p+p2)}λ1λ2+12A(AAp+mp2)4(A2Amp+2p2q)p8(Amp)3q14λ22=0,μ1<0}.

(iii) The homoclinic bifurcation curve is

HL={(μ1,μ2)|μ2=57μ1,μ1<0}={(λ1,λ2)|50(AAp+mp2)449p6(Amp)q12λ1+100(AAp+mp2)449p5(Amp)2q12λ2(AAp+mp2)398p10(Amp)q14{50m2p4(1+q1)+25Amp2[m2p2+3m2p38p(1+q1)6(1+q1)]+A2p[38m2p2225m2p375p(2+m22q1)+450(1+q1)]+A3mp(312+p+225p2)3A4(794p+25p2)}λ12+(AAp+mp2)349p9(Amp)2q14{50m2p4(1+q1)+Amp2[75m2p3+p2(25m2252q1)200p(1+q1)150(1+q1)]+A2p[225m2p3+4p2(31m2+63q1)3p(50+25m2+34q1)+450(1+q1)]+A3mp(474323p+225p2)3A4(13358p+25p2)}λ1λ2+12(AAp+mp2)449p8(Amp)3q14[27A454A3mp42Amp3+8p4q12+3A2p2(9m2+16q1)]λ22=0,μ1<0}.

The Bogdanov-Takens bifurcation diagram and corresponding phase portraits of system (3.1) are given in Fig. 3.1 , where we fix A=2, m=1, p=2, q=1/3 and n=1/3, which satisfy n=n, q=q1, A>mp and conditions (2.4), and then perturb A and q. The bifurcation curves H,HL and SN divide the small neighborhood of the origin in the parameter (λ1,λ2)-plane into four regions (see Fig. 3.1(a)).

Fig. 3.1.

Fig. 3.1

The bifurcation diagram and phase portraits of system (3.1) for A = 2, m = −1, p = 2, q = 1/3, n = 1/3. (a) Bifurcation diagram; (b) No positive equilibria when (λ1,λ2)=(0.1,0.11) lies in the region I; (c) An unstable focus when (λ1,λ2)=(0.1,0.1005) lies in the region II; (d) An unstable limit cycle when (λ1,λ2)=(0.1,0.0996) lies in the region III; (e) An unstable homoclinic loop when (λ1,λ2)=(0.1,0.09905427) lies on the curve HL; (f) A stable focus when (λ1,λ2)=(0.1,0.0983) lies in the region IV.

(a) When (λ1,λ2)=(0,0), the unique positive equilibrium is a cusp of codimension two (see Fig. 2.2(c)).

(b) There are no equilibria when the parameters lie in region I (see Fig. 3.1(b)), implying that the disease dies out.

(c) When the parameters lie on the curve SN, there is a unique positive equilibrium E, which is a saddle-node.

(d) Two positive equilibria, one is an unstable focus E2 and the other is a saddle E1, will occur through the saddle-node bifurcation when the parameters cross the SN curve into region II (see Fig. 3.1(c)).

(e) An unstable limit cycle will appear through the subcritical Hopf bifurcation around E2 when the parameters are varied to cross the H curve into region III (see Fig. 3.1(d)), where the focus E2 is stable, whereas the focus E2 is an unstable one with multiplicity one when the parameters lie on the curve H.

(f) An unstable homoclinic orbit will occur through the homoclinic bifurcation around E1 when the parameters pass region III and lie on the curve HL (see Fig. 3.1(e)).

(g) The relative location of one stable and one unstable manifold of the saddle E1 will be reversed when the parameters are varied to cross the HL curve into region IV (compare Fig. 3.1(c) and Fig. 3.1(f)).

3.3. Hopf bifurcation

In this subsection we discuss Hopf bifurcation around the equilibrium E2(x2,y2). Let

a=p1npn+m+1,q2=c0+c1m+c2m2d0+d1m+d2m2,m1=(p1np)2p(n+1)p,m2=2n,m3=n(1+(3+n)p)n2(1+(3+n)p)24p(3n1)(1+2np)2p,m4=n(1+(3+n)p)+n2(1+(3+n)p)24p(3n1)(1+2np)2p,c0=3n1+(34n+9n2)p+2n(32n+3n2)p2,c1=n+(3+3n+2n2)p+(n+1)3p2,c2=2p(1+np),d0=(3n1)(1+2np),d1=n(1+(3+n)p),d2=p,p=32nn+512n1/2+6n+4n3/23n22(n1)2, (3.9)

which will be used in the following subsection.

To simplify the computation, by following the technique in [11], we reduce system (2.3) to an equivalent polynomial differential system by using the following state variable scaling and time rescaling:

x=xx2,y=yy2,τ=x22t, (3.10)

under which system (2.3) is transformed into (we still denote τ by t)

dxdt=x21+mx2x+nx22x2(Ax2xqy)px22x,dydt=1x22(xy). (3.11)

Then taking the parameter scaling,

A=Ax2,m=mx2,n=nx22,p=px22,q=q,a=1x22,

into system (3.11) and dropping the bars, we obtain

dxdt=x21+mx+nx2(Axqy)px,dydt=a(xy). (3.12)

Since system (3.12) has an equilibrium E˜2(1,1) (i.e., E2(x2,y2) of system (2.3)), we have

A=p(1+m+n)+q+1.

Note that x1x2=pnp+q+1 for system (2.3), which becomes x1x2=pnp+q+1 under the parameter scaling (3.10), dropping the bars, so we have np+q+1p>0 because x1x2<1. Regarding the above parameter scaling, the condition (2.4), n<n and A>mp become

p,q,n,a>0,p1np<q<pa,m>2n. (3.13)

Since the transformation (3.10) is a linear sign-reserving transformation, system (3.12) and system (2.3) have the same qualitative property.

Next letting dt=(1+mx+nx2)dτ and substituting A=p(1+m+n)+q+1 into (3.12), we obtain (still denote τ by t)

dxdt=x2[p(1+m+n)+q+1xqy]p(1+mx+nx2)x,dydt=a(xy)(1+mx+nx2), (3.14)

where m, p, q, n, a satisfy (3.13). Obviously system (3.14) has the same topological structure as that of system (3.12), since we consider system (3.12) in R2+={(x,y):x0,y0}, and 1+mx+nx2>0 holds for all x0. In the following, we study the Hopf bifurcation around E˜2(1,1) in system (3.14), which corresponds to the Hopf bifurcation around E2(x2,y2) in system (2.3).

Theorem 3.2

When conditions in (3.13) hold, system (3.14) has an equilibrium at E˜2(1,1) . Moreover,

  • (I)

    when a<a , E˜2(1,1) is an unstable hyperbolic node or focus;

  • (II)

    when a>a , E˜2(1,1) is a locally asymptotically stable hyperbolic node or focus;

  • (III)

    when a=a , E˜2(1,1) is a fine focus or center.

Proof

The Jacobian matrix of system (3.14) at E˜2(1,1) is

J(E˜2(1,1))=[p1npqa(m+n+1)a(m+n+1)].

Then the determinant of J(E˜2(1,1)) is

det(J(E˜2))=a(m+n+1)(np+q+1p),

and the trace of J(E˜2(1,1)) is

tr(J(E˜2))=p1npa(m+n+1).

By conditions in (3.13), we can see that det(J(E˜2))>0 and tr(J(E˜2))=0 (>0 or <0) if a=a (a<a or a>a), so the conclusions follow. □

Next we continue to consider the case (III) of Theorem 3.1 and study Hopf bifurcation around E˜2(1,1) in system (3.14). We have the following necessary conditions for Hopf bifurcation:

a=a,0<n<1,p>11n,m>2n,p1np<q<pa. (3.15)

Firstly we can check the transversality condition

dda(trJ(E˜2))|a=a=(m+n+1)<0.

We investigate the nondegenerate condition and stability of the bifurcating periodic orbit from the positive equilibrium E˜2(1,1) of system (3.14) by calculating the first Lyapunov coefficient.

Let X=x1, Y=y1, and a=a. Then system (3.14) can be written as (still denote X, Y,τ by x, y,t, respectively)

dxdt=b˜xqy+(p22np)x22qxy(1+np)x3qx2y,dydt=b˜xb˜y+a(m+2n)x2a(m+2n)xy+anx3anx2y, (3.16)

where b˜=p1np. Let ω=b˜qb˜2, and make a transformation of x=X, y=1q(b˜XωY) and dt=1ωdτ, then system (3.16) becomes (we still denote X, Y by x, y, respectively)

dxdt=y+f(x,y),dydt=x+g(x,y), (3.17)

where

f(x,y)=a20x2+a11xy+a02y2+a30x3+a21x2y+a12xy2+a03y3,
g(x,y)=b20x2+b11xy+b02y2+b30x3+b21x2y+b12xy2+b03y3,

and

a20=pω,a11=2,a02=0,a30=pω,a21=1,a12=0,a03=0,
b20=1ω2(b˜p+a(m+2n)(b˜q)),b11=1ω(2b˜a(m+2n)),b02=0,
b30=1ω2(b˜p+an(qb˜)),b21=b˜anω,b12=0,b03=0.

Using the formula in [33] and calculating first Lyapunov coefficient with the aid of MATLAB, we obtain

σ1=(c0+c1m+c2m2)+(d0+d1m+d2m2)q4(1+m+n)2(np+q+1p)3/2(p1np)1/2, (3.18)

where c0, c1, c2, d0, d1 and d2 are given in (3.9). By conditions in (3.15), the sign of σ1 is the same as that of

σ11=(c0+c1m+c2m2)+(d0+d1m+d2m2)q. (3.19)

Now we investigate the sign of σ11 (i.e., σ1) and will see that there exist some values of parameters such that σ11=0 (i.e., σ1=0) when conditions (3.15) are satisfied. We first give the following Lemma.

Lemma 3.3

When conditions (3.15) are satisfied, then c0+c1m+c2m2>0 , where ci (i=0,1,2) are given in (3.9) .

Proof

By conditions (3.15), it is easy to show that ci>0 (i=0,1,2) and

m>2n,p1np<q<pa=p(m+n+1)p1np.

Then we have

m>max{m1,m2},

where m1 and m2 are given in (3.9).

(I) Firstly, we consider the discriminant of c0+c1m+c2m2=0, which is given by

Δ(p)=c124c0c2=Δ0+Δ1p+Δ2p2+Δ3p3+Δ4p4,

where

Δ0=n2>0,Δ1=818n+6n2+4n3,Δ2=15+60n69n2+18n3+6n4,
Δ3=648n+104n284n3+18n4+4n5,Δ4=1+6n33n2+52n333n4+6n5+n6.

We consider the third derivative of Δ(p) with respect to p, which is given by

Δ(3)(p)=6Δ3+24Δ4p.

Because Δ(3)(11n)=60(1n)3(1+n)>0, we can show that Δ4>0 when 0<n<1. Thus

Δ(3)(p)>0forp>11n.

On the other hand, we have Δp(11n)=18(n1)2>0, and so

Δp(p)>0forp>11n.

Similarly, we have Δp(11n)=0 and Δ(11n)=0, which yield

Δ(p)>0forp>11n.

(II) Secondly, we analyze the sign of m1m2, which is same as

m12(p)=1+(2n+n3)p+(n1)2p2.

By noticing 0<n<1 and using a simple analysis, we have

2n+n3<0,2n+n32(n1)211n=(n1)22(n1)>0,m12(11n)=n1n+1<0.

Thus, we can see that m12(p)>0, m12(p)=0 and m12(p)<0 if and only if p>p, p=p and 11n<p<p, respectively, where p=32nn+512n1/2+6n+4n3/23n22(n1)2 (>11n).

(III) Thirdly, we analyze the relationship between c12c2 and m1, m2. The sign of c12c2m1 is the same as that of

ms1(p)=4n+(911n2n2)p+(5+17n11n2n3)p24n(n1)2p3.

The first derivative of ms1 with respect to p is

ms1(p)=911n2n2+2(5+17n11n2n3)p12n(n1)2p2.

Since 0<n<1 and p>11n, one can prove that ms1(p)<0. Moreover, we have ms1(11n)=0. Thus we have ms1(p)<0, i.e., m1>c12c2, when conditions (3.15) are satisfied.

The sign of c12c2m2 is the same as that of

ms2(p)=n+(3+8n1/23n2n2)p+(13n+8n3/23n2n3)p2.

Since 0<n<1, by a direct computation, we can show that

13n+8n3/23n2n3<0,
3+8n1/23n2n22(13n+8n3/23n2n3)11n=5+2n+5n2(n21)(1+2n+6n+2n3/2+n2)<0,

and

ms2(11n)=4(1+n)2<0.

It then follows that ms2(p)<0, i.e., m2>c12c2, when conditions (3.15) are satisfied.

(IV) Finally, we show that c(m)=c0+c1m+c2m2>0 when conditions (3.15) are satisfied. When pp (>11n), we have m1m2 by the step (II), then m>max{m1,m2}=m1 and c(m)>c(m1) by the step (III). Moreover, we can show that c(m1)>0. In fact, the sign of c(m1) is the same as that of

cm1(p)=2+n+(6+7n+n2)p+(39n+5n2+n3)p2+2n(n1)2p3.

By a direct computation with conditions in (3.15), we have

cm1(11n)=n1<0,cm1(p)=c12(1n)(1+n)4,

where

c1=7+(3+3n+5n+3n3/2+2n2)(1n)3(5+3n)n(3+2n+4n)n2(5+n+2n).

We can see that c1 is monotonic decreasing for 0<n<1. Moreover, since c1(0)=7 and c1(1)=0, we have c1>0 (i.e., cm1(p)>0) when 0<n<1, and thus c(m1)(p)>0, i.e., c(m1)>0, when p>p.

When 11n<p<p, we have m1<m2 by the step (II), then m>max{m1,m2}=m2 and c(m)>c(m2) by the step (III). Moreover, we can show that c(m2)>0. In fact, the sign of c(m2) is same as

cm2(p)=12n+(3+n4n3/2)p2n(1+n)2(1+n+n)p2.

By direct computation, we have cm2(11n)=2(1+n)2>0 and cm2(p)=cm1(p)>0. Then c(m2)(p)>0, i.e., c(m2)>0, when 11n<p<p.

Summarizing the above results, we have shown that c0+c1m+c2m2>0 when conditions (3.15) are satisfied. □

Lemma 3.4

When the conditions in (3.15) are satisfied, d0+d1m+d2m2<0 if and only if m3<m<m4 , where di (i=0,1,2) and mj (j=3,4) are given in (3.9) .

Proof

Let

d(m)=d0+d1m+d2m2,

where

d0=(3n1)(1+2np)d1=n(1+(3+n)p)>0,d2=p>0.

We then show that

d124d0d2=n2+2(n3+3n26n+2)p+n(n3+6n215n+8)p2>0.

In fact, let

h(p)=n2+2(n3+3n26n+2)p+n(n3+6n215n+8)p2.

By the conditions in (3.15), we obtain

n(n3+6n215n+8)>0,

and

h(n3+3n26n+2n(n3+6n215n+8))=4(1n)(3n1)n(8+n).

Then when 13<n<1, we have

h(p)>0;

when 0<n13, we have

2(n3+3n26n+2)>0,

and

h(0)=n2>0,

thus

h(p)>0.

From the above analysis, we have d124d0d2>0 when conditions (3.15) are satisfied, implying that the equation d(m)=0 has two positive roots:

m3=n(1+(3+n)p)n2(1+(3+n)p)24p(3n1)(1+2np)2p,
m4=n(1+(3+n)p)+n2(1+(3+n)p)24p(3n1)(1+2np)2p,

and d(m)<0 if and only if m3<m<m4. □

Theorem 3.5

When the conditions in (3.15) are satisfied, the following statements hold.

  • (I)

    If mm3 or mm4 (i.e., σ11>0 or σ1>0 ), then system (3.14) exhibits subcritical Hopf bifurcation and an unstable limit cycle appears around E˜2(1,1) .

  • (II)
    If m3<m<m4 and
    • (II.1)
      q>q2 (i.e., σ11<0 or σ1<0 ), then system (3.14) exhibits supercritical Hopf bifurcation and a stable limit cycle appears around E˜2(1,1) ;
    • (II.2)
      q<q2 (i.e., σ11>0 or σ1>0 ), then system (3.14) exhibits subcritical Hopf bifurcation and an unstable limit cycle appears around E˜2(1,1) ;
    • (II.3)
      q=q2 (i.e., σ11=0 or σ1=0 ), then system (3.14) may exhibits degenerate Hopf bifurcation and multiple limit cycles may appears around E˜2(1,1) .

Here, m3 , m4 and q2 are given in (3.9) .

One stable (or unstable) limit cycle arising from supercritical (or subcritical) Hopf bifurcation around the equilibrium E˜2(1,1) of system (3.14) is given in Fig. 3.2 . In Fig. 3.2(a), we fix n=0.1, p=1.2, m=0.6 and q=2, and get a=0.16 from tr(J(E˜2))=0, and further obtain σ1=3.24949. Finally, we perturb a such that a decreases to 0.12, then E˜2(1,1) becomes an unstable hyperbolic focus, leading to a stable limit cycle to appear around E˜2(1,1). In Fig. 3.2(b), we fix n=0.1, p=1.2, m=0.6 and q=0.6, and get a=0.16 from tr(J(E˜2))=0, and further get σ1=2.62886. Finally, we perturb a such that a increases to 0.18, and so E˜2(1,1) becomes a stable hyperbolic focus, yielding an unstable limit cycle to appear around E˜2(1,1).

Fig. 3.2.

Fig. 3.2

(a) A stable limit cycle created by the supercritical Hopf bifurcation of the system (3.14) with n = 0.1, p = 1.2, m = −0.6, q = 2 and a = 0.12. (b) An unstable limit cycle created by the subcritical Hopf bifurcation of the system (3.14) with n = 0.1, p = 1.2, m = −0.6, q = 0.6 and a = 0.18.

Remark 3.1

In Fig. 3.2(a), the model has three equilibria, a disease-free equilibrium which is a stable hyperbolic node, two endemic equilibria (one is a hyperbolic saddle and the other is an unstable focus) and a stable limit cycle. If the initial population lies on the right side of the two stable manifolds of the saddle, then the disease will tend to a periodic coexistent oscillation. If the initial population lies on the left side of the two stable manifolds of the saddle, then the disease will die out.

Remark 3.2

In Fig. 3.2(b), the model has three equilibria, a disease-free equilibrium which is a stable hyperbolic node, two endemic equilibria (one is a hyperbolic saddle and the other is a stable focus) and an unstable limit cycle. If the initial population lies on the limit cycle, then the disease will persist in the form of a periodic coexistent oscillation. If the initial population lies inside the limit cycle, then the disease will tend to a stable steady state. If the initial population lies outside the limit cycle, the disease will die out for almost all positive initial populations.

3.4. Degenerate Hopf bifurcation of codimension two

From (II.3) of Theorem 3.5, we know that system (3.14) may exhibit degenerate Hopf bifurcation (i.e., Hopf bifurcation of codimension two) when q=q2, m3<m<m4 and conditions (3.15) are satisfied. Using the formal series method in [33] and MATLAB software, we obtain the second Lyapunov coefficient

σ2=e0+e1m+e2m2+e3m324(m+n+1)3(2+4np+m(np+p+1))(m+n+1)p(p1np)(2+4np+m(np+p+1))(d0+d1m+d2m2), (3.20)

where

e0=3(1n2)(1+2np)2,e1=n29n+4+(3n331n2+21n1)p+2n(n313n2+13n1)p2,e2=4n(3+5n2)p+n(1n2)p2,e3=n2(n22n+2)p+(14n+4n2n3)p2.

Next we investigate the sign of σ2 and first give the following lemma.

Lemma 3.6

When conditions in (3.15) are satisfied, the inequality 2+4np+m(np+p+1)>0 holds.

Proof

Let

h(m)=2+4np+m(np+p+1).

When pp (>11n), we have m1m2 by the step (II) of Lemma 3.3. Then m>max{m1,m2}=m1 and h(m)>h(m1). Moreover, we can show that h(m1)>0. In fact, the sign of h(m1) is the same as that of

h(m1)(p)=1+2np+2(n21)p2+(n1)2(n+1)p3.

By a direct calculation, we have

h(m1)(p)=2n+4(n21)p+3(n1)2(n+1)p2.

It follows that h(m1)(p)>0 when p>p. Further, by a direct calculation, we have

h(m1)(p)=3+3n+2n3/2+(1n)3(5+3n)(1+n)4>0,

so h(m1)(p)>0 (i.e., h(m1)>0) when p>p.

When 11n<p<p, we have m1<m2 by the step (II) in the proof of Lemma 3.3. Then m>max{m1,m2}=m2 and h(m)>h(m2). Moreover, we can show that h(m2)>0. In fact

h(m2)=2(1n)[1n(1n)p].

By a direct calculation, we have

h(m2)(11n)=2(1n)1+n,
h(m2)(p)=2nn3/2n(1n)3(5+3n)(1+n)2.

It follows that h(m2)(11n)>0 and h(m2)(p)>0 for 0<n<1. Thus, h(m2)>0 when 11n<p<p.

Summarizing the above results, we have shown that h(m)>0 (i.e., 2+4np+m(np+p+1)>0) when conditions (3.15) are satisfied. □

When m>2n, 0<n<1, p>11n, m3<m<m4, and by Lemma 3.6, we know that the sign of σ2 in (3.20) is the same as that of

e0+e1m+e2m2+e3m3σ21. (3.21)

Based on extensive numerical calculations, we conjecture that E˜2(1,1) is an unstable multiple focus with multiplicity two, i.e., σ21>0 (or σ2>0) when q=q2, m3<m<m4 and conditions in (3.15) are satisfied. However, it is very difficult to pursue a pure algebraic proof. Next we combine geometric (graphic) and algebraic methods to show that E˜2(1,1) is actually an unstable multiple focus with multiplicity at most two.

Actually, we have the following result.

Theorem 3.7

The equilibrium E˜2(1,1) in system (3.14) (i.e., E2(x2,y2) in system (2.3) ) is an unstable multiple focus with multiplicity at most two, system (2.3) can exhibit degenerate Hopf bifurcation of codimension two around E2(x2,y2) , and the outer bifurcating limit cycles is unstable.

Proof

The Jacobian of the linearized system of (3.14) shows that Hopf bifurcation occurs at the critical point:

a=aH=p(1n)11+m+n.

Setting a=aH yields the eigenvalues at the critical point as λ±=±ωci, where

ωc=[p(1n)1][q(p(1n)1)].

In order to have ωc>0, it needs

0<p(1n)1<q, (3.22)

which in turn yields 1+m+n>0 from aH>0. It is obvious that we need the following condition:

0<n<1. (3.23)

To simplify the analysis, we introduce two new parameters:

P=p(1n)1,Q=qPp=1+P1n,q=P+Q,(0<n<1). (3.24)

Thus, the conditions 0<p(1n)1<q are equivalent to P>0,Q>0. Then, aH=P1+m+n>0 and ωc is reduced to ωc=PQ. Note that the condition q<pa=paH becomes

P+Q<(1+P)(1+m+n)(1n)P0<Q<(1+P)(1+m+n)(1n)P2(1n)P.

Therefore, the conditions in (3.15) are equivalent to the following conditions:

0<n<1,1+m+n>0,P>0,(1+P)(1+m+n)(1n)P2>0,0<Q<(1+P)(1+m+n)(1n)P2(1n)PQmax. (3.25)

Now, introducing the transformation,

x=1(P+Q)u,y=1Pu+ωcv,

and the time rescaling τ1=ωcτ into (3.14), we obtain

dudτ1=v+(P+Q)(1+P)(1n)PQu22(P+Q)uv(P+Q)2(1+P)(1n)PQu3+(P+Q)2u2v,dvdτ1=u+(P+Q)[(1+P)(1+m+n)Q(mn+2n22nm)](1+m+n)(1n)Qu2(P+Q)(2+m)PQ(1+m+n)Quv(P+Q)2[(1+P)(1+m+n)+Qn(1n)](1+m+n)(1n)Qu3+(P+Q)2(1+m)PQ1+m+n)Qu2v. (3.26)

Next, applying the Maple program [31] we obtain the following focus values:

v1=(P+Q)28(1n)2(1+m+n)2QPQF1,v2=(P+Q)4288(1n)4(1+m+n)4Q3PQF2,v3=(P+Q)6663552(1n)6(1+m+n)6P2Q5PQF3,

where

F1=P2(1+m+n)(mn+m+4n)+PQ(1n)(mn2+m2+3mn+6n22n)+P(1+m+n)(mn+3m+6n+2)+Q(1n)(1+m+n)(m+3n1)+2(1+m+n)2,F2=(1+m+n)4(1+P)[P(1+n)+Q(1n)+2][20P3+P2Q(5n2+8n+7)13PQ2(1n)2+40P2+2PQ(9n+11)+20(P+Q)](1+m+n)3(1n)2[20P5+P4Q(15n2+49n+58)+P3Q2(5n3+38n2+39n+20)+P2Q3(1n)(19n12)(n+2)+60P4+P3Q(15n2+128n+203)+P2Q2(48n2+125n+71)+3PQ3(15n8)(1n)+60P3+P2Q(79n+247)+91PQ2(1+n)+20P2+102PQ+40Q2]+(1+m+n)2PQ(1n)4[3P3(5n+12)+P2Q(15n2+97n+62)+PQ2(18n2+58n+11)+3P2(5n+29)+3PQ(39n+53)+6Q2(9n+4)+51(P+2Q)](1+m+n)PQ(1n)6[5P3+P2Q(15n+41)+3PQ2(19n+14)+5P2+51PQ+40Q2]+5P2Q2(1n)8(P+4Q),F3=,

where F3 is a lengthy polynomial, which is omitted here for brevity.

In the following, we prove that when v1=0, v2>0 for the parameters satisfying the conditions in (3.25). Since v1 and v2 have the same sign of F1 and F2, respectively, we consider the polynomials F1 and F2.

First, suppose that the two polynomial equations F1=F2=0 have solutions for P and Q and we study if the solutions satisfy the conditions in (3.25). Note that F1 is linear in Q, we solve Q from F1=0 to obtain

Q=(1+m+n)(1+P)[P(mn+m+4n)+2(1+m+n)](n1)[P(mn2+m2+3mn+6n22n)+m2+4mn+3n2+2n1], (3.27)

and then substitute it into F2 to get

F2=6(n1)(1+m+n)4(1+P)3P[P(mn+m+4n)+2(1+m+n)]2[P(mn2+m2+3mn+6n22n)+m2+4mn+3n2+2n1]3(A0P2A1P+A2),

where

A0=m3n23m3n+m2n22mn3+m3+m2n+24mn2+12n32mn+12n2,A1=(1+m+n)(2m2n+mn2+2m26mn12n2+m12n),A2=3(1+nm)(1+m+n)2.

Note that the solutions of F2=0 come from the quadratic polynomial equation A0P2A1P+A2=0. Solving this polynomial equation yields two solutions:

P±=12A0(A1±Δ),Δ=A124A0A2,

and then we have

Q±=(1+m+n)(1+P±)[P±(mn+m+4n)+2(1+m+n)](n1)[P±(mn2+m2+3mn+6n22n)+m2+4mn+3n2+2n1].

To have real solutions for P± and Q±, it requires Δ>0. Summarizing the above results shows that if the two sets of solutions satisfy v1=v2=0, they must satisfy the conditions given in (3.25) as well as Δ>0. Define

Ω±={(m,n)|0<n<1,1+m+n>0,Δ>0,P±>0,Q±>0,(1+P±)(1+m+n)(1n)P±2>0}.

It is clear that the conditions given in (3.25) must be in Ω±. We will show that the obtained solutions P± and Q± do not belong to Ω±, then P± and Q± do not satisfy conditions in (3.25), thus there are no feasible parameter values for v1=v2=0, and the best possibility is v1=0 but v20, which implies that the maximal number of limit cycles bifurcating from the Hopf critical point is two.

To prove the result by combining geometric (graphic) and algebraic methods, first we consider the set Ω. Define the functions:

C1=P,C2=Q,C3=(1+P)(1+m+n)(1n)P2=0,

then plot the curves Δ=0 and Ck=0,k=1,2,3 on the m-n plane, and identify the regions on the boundary regime: 0<n<1,1+m+n>0, satisfying Δ>0 and Ck>0,k=1,2,3. If these regions do not overlap, then no solutions exist; if these regions do overlap, we need to further check the last condition in (3.25), Q<Qmax.

For the set Ω, we show the curves Δ=0 and Ck=0,k=1,2,3, in Fig. 3.3 (a) with the colors in red, blue, brown and green, respectively. Fig. 3.3(b) is a zoomed area near the m-axis. The region for Δ<0 is inside the red loop, and Δ>0 is outside the loop. Thus, we only need to consider the region outside the red loop. We use + or − to indicate Ck>0 or Ck<0. Fig. 3.3(c) is a zoomed area near the corner of (m,n)=(2,1), showing that all three curves are tangent to the line 1+m+n=0 at the corner. This can be rigorously proved using an algebraic argument. Figs. 3.3(a), (b) and (c) clearly show that there are no regions with Δ>0 and all three functions Ck>0,k=1,2,3. Thus, the set Ω does not have feasible solutions satisfying v1=v2=0.

Next, consider the set Ω+. We have a similar result, as shown in Fig. 3.4 . Again, this set also does not have feasible solutions satisfying v1=v2=0.

To this end, we have shown that under the restrictions on the parameters, as given in (3.25), it is not possible to have solutions such that v1=v2=0 and to have three limit cycles bifurcating from the equilibrium (x0,y0)=(1,1) due to Hopf bifurcation. Therefore, the next best choice is to have v1=0 and v20, and P can then be treated as a free parameter. The above proof implies that v2 must be kept the same sign for the feasible parameter values. Otherwise, if it can change sign, then it must have solutions for v2=0, which contradicts the above result. To determine whether the sign of v2 is positive or negative, we only need to choose a solution such that v1=0 and then calculate v2. For example, taking P=n=m=110, we obtain

Q=359487299<(1+P)(1+m+n)(1n)P2(1n)P=70374172990,

giving v1=0 and

v2=8175332680651336418386743659728845703491966184311975452303564800000>0,

implying that v2>0 for any parameter values which satisfy the conditions given in (3.25). Thus, the outer bifurcating limit cycle is always unstable and the inner one is stable, both enclose an unstable focus (1,1). The proof is complete. □

Fig. 3.3.

Fig. 3.3

Graphs of the regions on the m-n plane, divided by the curves Δ = Ck = 0, k = 1,2,3: (a) the boundary region 0 < n < 1, 1 + m + n > 0; (b) the zoomed area near the m-axis; and (c) the zoomed area near the corner (m,n)=(−2,1). (For interpretation of the colors in the figure(s), the reader is referred to the web version of this article.)

Fig. 3.4.

Fig. 3.4

Graphs of the regions on the m-n plane, divided by the curves Δ = Ck = 0, k = 1,2,3: (a) the boundary region 0 < n < 1, 1 + m + n > 0; (b) the zoomed area near the m-axis; and (c) the zoomed area near the corner (m,n)=(−2,1).

Remark 3.3

If m=0 (i.e., β=0), then σ21=e0>0 (i.e., σ2>0), thus E˜2(1,1) (i.e., E2(x2,y2)) is an unstable multiple focus with multiplicity two when q=q2, m3<m<m4 and conditions in (3.15) are satisfied. Moreover, when β=0 (i.e., m=0), our system (2.2) is reduced to system (1.2) in [25], where the authors only discussed the Hopf bifurcation of codimension one, thus our results about Hopf bifurcation of codimension two can be seen as a complement of [25] by considering a more general system. On the other hand, when β=0 (i.e., m=0), our system (2.2) also becomes system (1.3) in [27], where the authors showed the existence of degenerate Hopf bifurcation by complex algebraic calculations, our Theorem 3.5, Theorem 3.7 give more explicit conditions and our proofs are easier to follow.

Next we give some numerical simulations in Fig. 3.5 to show the existence of two limit cycles based on Theorem 3.5, Theorem 3.7. Firstly, we fix n=1/3, p=2 and m=1, then get q=2315 from σ1=0, and get a=1 from tr(J(E˜2))=0, finally get σ2=2.65719, i.e., E˜2(1,1) is an unstable multiple focus with multiplicity two for those fixed parameters. Next we first perturb q such that q increases to 2315+0.1, then E˜2(1,1) becomes a stable multiple focus with multiplicity one, an unstable limit cycle occurs around E˜2(1,1) which is the outer limit cycle in Fig. 3.5. Secondly, we perturb a such that a decreases to 10.003, then E˜2(1,1) becomes an unstable hyperbolic focus, another stable limit cycle occurs around E˜2(1,1), which is the inner limit cycle in Fig. 3.5.

Fig. 3.5.

Fig. 3.5

Two limit cycles enclosing an unstable hyperbolic focus in system (3.14) with n=13, p = 2, m = −1, q=2315+0.1 and a = 1 − 0.003.

Remark 3.4

From Fig. 3.5, we can see that the existence of multiple periodic coexistent oscillations and coexistent steady states when the psychological effect α is smaller than the critical value α0 but the infection rate k is greater than the first critical value k0, i.e., n<n and A>mp. The disease will die out for almost all initial populations outside the outer unstable periodic orbit, and will tend to periodic outbreaks for almost all initial populations on or inside the outer unstable periodic orbit, and will persist in the form of positive steady states when the initial population lies on the positive equilibria or their stable manifolds.

4. Simulations of the influenza data in Mainland China

In section 1 we mentioned that nonmonotone and saturated incidence rates may apply to some infectious diseases such as influenza. In this section, we use model (2.1) to simulate the reported human influenza data from China. From the Chinese Center for Disease Control and Prevention (CCDC) [8], we obtain the annual data on human influenza cases from 2004 to 2017 which are shown in Table 1 . Most parameter values can be obtained from the literature or by estimation. We estimate k, α, β, δ and R(0) by using the unconstrained optimization functions fminsearch, a part of the optimization toolbox in MATLAB, to fit I(ti) through discretizing the ordinary differential system (2.1) as follows

I(ti+Δt)=(kS(ti)I(ti)21+βI(ti)+αI(ti)2(d+μ)I(ti))Δt+I(ti).

The fitting is to minimize the objective function

J(θ)=i=1n(I(ti)Iˆ(ti))2I(ti),

where I(ti) is numerical solution of model (2.1) and Iˆ(ti) is the reported human influenza data from China.

Table 1.

The data on human influenza cases in China from 2004-2017 ([8]).

Year 2004 2005 2006 2007 2008 2009 2010
Cases 49496 45672 57557 36434 41692 198381 64502




Year 2011 2012 2013 2014 2015 2016 2017
Cases 66133 122140 129873 215533 195723 306682 456718

The parameter values are listed in Table 2 . From the data in 2004, we know that I(0)=49496; we make the data fitting to obtain that R(0)=13, then S(0)=1.29983×109; and assume that μ=3655 from Casagrandi et al. [7], data fitting gives δ=0.33042, k=2.8668×108, α=4.9077×106 and β=78.12.

Table 2.

Parameters of model (2.1).

Para Value Unit Interpretation Source
b 1.64 × 107 Year−1 human recruitment rate [23]
d 0.006988 Year−1 human natural mortality rate [23]
μ 3655 Year−1 human natural recovery rate [7]
δ 0.33042 Year−1 human loss rate of immunity fitting
k 2.8668 × 10−8 None the infection rate fitting
α 4.9077 × 10−6 None measures the psychological or inhibitory effect fitting
β 78.12 None none fitting

Based on the parameter values given in Table 2, we use model (2.1) to simulate the data from 2004 to 2017 and predict the trend of human influenza infections in China. Fig. 4.1 represents the simulation of our model with reasonable parameter values which provides a good match to the data on infected human influenza cases in China from 2004 to 2017. In Fig. 4.2 our model predicts that the number of human influenza infection will increase in the next a couple of years.

Fig. 4.1.

Fig. 4.1

Simulation of human influenza cases over time in China. The smooth curve represents the solution I(t) of model (2.1) and the dashed curve represents the reported human influenza cases from 2004 to 2017.

Fig. 4.2.

Fig. 4.2

Prediction of human influenza cases in China.

5. Conclusion and discussion

In most classic SIRS epidemic models, the incidence rate is either monotonic or non-monotonic, and the infection force g(I) usually tends to zero as I when the incidence rate is non-monotonic, which may be unreasonable for some specific infectious diseases. In this paper, we considered the SIRS epidemic model (1.1) with a generalized nonmonotone and saturated incidence function g(I)=kI21+βI+αI2, which exhibits three different properties: (i) when β0, g(I) is monotonic, which always increases and then tends to a saturated level kα as I intends to infinite. (ii) When 2α<β<0, g(I) is nonmonotonic, which increases when I is small and decreases when I is large, and finally tends to a saturated level kα as I tends to infinite (see Fig. 1.2), which can be used to describe the phenomenon that the infection force first increases to a maximum when a new infectious disease emerges, and then decreases due to psychological effect and eventually tends to a saturation level due to crowding effect. (iii) When β>2α, g(I) has both properties of (i) and (ii), i.e., g(I) is first nonmonotonic and then monotonic when β increases from negative to positive. In this paper, we performed qualitative and bifurcation analysis, and found that the model (1.1) with general incidence rate (1.8) has complicated dynamical behaviors and bifurcation phenomena. It has been shown that there exists a weak focus of multiplicity at most two and a cusp of codimension at most two for various parameter values, and the model undergoes saddle-node bifurcation, Bogdanov-Takens bifurcation of codimension two, Hopf bifurcation and degenerate Hopf bifurcation of codimension two as the parameter values vary. By considering a more general model, our results show that Bogdanov-Takens bifurcation of codimension higher than two cannot occur, which clarifies and corrects the corresponding results by Tang et al. [27]. Moreover, our results about degenerate Hopf bifurcation (i.e., Hopf bifurcation of codimension two) can also be seen as a complement of the results in Ruan and Wang [25]. We also used model (2.1) to simulate the reported human influenza data from 2004 to 2017 reported by the Chinese Center for Disease Control and Prevention.

In recent years, people realize the importance of the inhibition effect from the behavioral change of susceptible individuals when their number increases or from the crowding effect of the infective individuals, and the psychological effect or inhibition effect can cause people to adopt some aggressive measures and policies, such as border screening, mask wearing, quarantine, isolation and so on, which have been proved to be very effective in reducing the contact rate or the infection force. However, it is difficult to measure the psychological effect. So can we give a quantitative description about the psychological effect with respect to variation of the parameters involved in the infectious diseases? In this paper, we presented a concrete critical value to measure the psychological effect. More specifically, we have shown that there exists a critical value α=α0 for the psychological or inhibitory effect and two critical values k=k0,k1(k0<k1) for the infection rate such that: (i) when α>α0, or αα0 and kk0, the disease will die out for all positive initial populations; (ii) when α=α0 and k0<kk1, the disease will die out for almost all positive initial populations; (iii) when α=α0 and k>k1, the disease will persist in the form of a positive coexistent steady state for some positive initial populations; and (iv) when α<α0 and k>k0, the disease will persist in the form of multiple positive periodic coexistent oscillations and coexistent steady states for some positive initial populations.

Footnotes

Research was partially supported by NSFC (No. 11471133, No. 11871235, No. 11771168), NSF (DMS-1853622) and NSERC (No. R2686A02).

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