Processing math: 100%
 

The risk index for an SIR epidemic model and spatial spreading of the infectious disease

  • Received: 05 May 2016 Accepted: 19 September 2016 Published: 01 October 2017
  • MSC : Primary: 35K51, 35R35; Secondary: 35B40, 92D25

  • In this paper, a reaction-diffusion-advection SIR model for the transmission of the infectious disease is proposed and analyzed. The free boundaries are introduced to describe the spreading fronts of the disease. By exhibiting the basic reproduction number RDA0 for an associated model with Dirichlet boundary condition, we introduce the risk index RF0(t) for the free boundary problem, which depends on the advection coefficient and time. Sufficient conditions for the disease to prevail or not are obtained. Our results suggest that the disease must spread if RF0(t0)q1 for some t0 and the disease is vanishing if RF0()<1, while if RF0(0)<1, the spreading or vanishing of the disease depends on the initial state of infected individuals as well as the expanding capability of the free boundary. We also illustrate the impacts of the expanding capability on the spreading fronts via the numerical simulations.

    Citation: Min Zhu, Xiaofei Guo, Zhigui Lin. The risk index for an SIR epidemic model and spatial spreading of the infectious disease[J]. Mathematical Biosciences and Engineering, 2017, 14(5&6): 1565-1583. doi: 10.3934/mbe.2017081

    Related Papers:

    [1] Meng Zhao, Wan-Tong Li, Yang Zhang . Dynamics of an epidemic model with advection and free boundaries. Mathematical Biosciences and Engineering, 2019, 16(5): 5991-6014. doi: 10.3934/mbe.2019300
    [2] Zhen Jin, Zhien Ma . The stability of an SIR epidemic model with time delays. Mathematical Biosciences and Engineering, 2006, 3(1): 101-109. doi: 10.3934/mbe.2006.3.101
    [3] Qianqian Cui, Zhipeng Qiu, Ling Ding . An SIR epidemic model with vaccination in a patchy environment. Mathematical Biosciences and Engineering, 2017, 14(5&6): 1141-1157. doi: 10.3934/mbe.2017059
    [4] J. Amador, D. Armesto, A. Gómez-Corral . Extreme values in SIR epidemic models with two strains and cross-immunity. Mathematical Biosciences and Engineering, 2019, 16(4): 1992-2022. doi: 10.3934/mbe.2019098
    [5] Shuixian Yan, Sanling Yuan . Critical value in a SIR network model with heterogeneous infectiousness and susceptibility. Mathematical Biosciences and Engineering, 2020, 17(5): 5802-5811. doi: 10.3934/mbe.2020310
    [6] Andrei Korobeinikov, Elena Shchepakina, Vladimir Sobolev . A black swan and canard cascades in an SIR infectious disease model. Mathematical Biosciences and Engineering, 2020, 17(1): 725-736. doi: 10.3934/mbe.2020037
    [7] Toshikazu Kuniya, Yoshiaki Muroya, Yoichi Enatsu . Threshold dynamics of an SIR epidemic model with hybrid of multigroup and patch structures. Mathematical Biosciences and Engineering, 2014, 11(6): 1375-1393. doi: 10.3934/mbe.2014.11.1375
    [8] Chenxi Huang, Qianqian Zhang, Sanyi Tang . Non-smooth dynamics of a SIR model with nonlinear state-dependent impulsive control. Mathematical Biosciences and Engineering, 2023, 20(10): 18861-18887. doi: 10.3934/mbe.2023835
    [9] Andrey V. Melnik, Andrei Korobeinikov . Lyapunov functions and global stability for SIR and SEIR models withage-dependent susceptibility. Mathematical Biosciences and Engineering, 2013, 10(2): 369-378. doi: 10.3934/mbe.2013.10.369
    [10] Xia Wang, Shengqiang Liu . Global properties of a delayed SIR epidemic model with multiple parallel infectious stages. Mathematical Biosciences and Engineering, 2012, 9(3): 685-695. doi: 10.3934/mbe.2012.9.685
  • In this paper, a reaction-diffusion-advection SIR model for the transmission of the infectious disease is proposed and analyzed. The free boundaries are introduced to describe the spreading fronts of the disease. By exhibiting the basic reproduction number RDA0 for an associated model with Dirichlet boundary condition, we introduce the risk index RF0(t) for the free boundary problem, which depends on the advection coefficient and time. Sufficient conditions for the disease to prevail or not are obtained. Our results suggest that the disease must spread if RF0(t0)q1 for some t0 and the disease is vanishing if RF0()<1, while if RF0(0)<1, the spreading or vanishing of the disease depends on the initial state of infected individuals as well as the expanding capability of the free boundary. We also illustrate the impacts of the expanding capability on the spreading fronts via the numerical simulations.


    1. Introduction

    The 20th century is the period that human has made most brilliant achievements in the conquest of infectious diseases: raging smallpox for about a thousand years was finally eradicated; the day that people get rid of leprosy and poliomyelitis will be not far off; the occurrence rate of diphtheria, measles, whooping cough and tetanus has been reducing in numerous countries; the advent of many antibiotics has made the "plague", which once caused great calamity to human, no longer harm the world [16]. However, the World Health Report published by World Health Organization (WHO) has shown that infectious disease is still the greatest threat to mankind [39]. For example, the most widespread epidemic of Ebola virus in history began in Guinea in December 2013 and has continued for over two years. As of 17 March 2016, WHO and respective governments have reported over 28,000 suspected cases and about 11,000 deaths [17]. In 2014, dengue fever broke out in Guangdong, China and it was reported that there were more than 30,000 infected cases [18]. There are about 20,000 people died of dengue fever worldwide each year [33]. The latest threat is from Zika [13] and there is no vaccine or medicine for it. The Zika virus has now been detected in more than 50 countries and the epidemic situation it caused is declared by WHO a public health emergency of international concern.

    The earliest differential equation model, concerning malaria transmission, was probably introduced by Dr. Ross. He showed from this mathematical model that if the number of malaria-carrying mosquitoes reduced below a critical value, the prevalence of malaria would be controlled. In 1927, Kermack and Mckendrick constructed the famous SIR compartment model to study the transmission dynamics of the Black Death in London from 1665 to 1666 and those of plague in Mumbai in 1906 [20]. They also proposed the SIS compartment model [21], and presented a "threshold value" which would determine the extinction and persistence of diseases based on the analysis of the established model.

    Over the past 30 years, the research on epidemic dynamics has made much progress, and a large number of mathematical models are used to describe and analyze various infectious diseases. Most of mathematical models are governed by ordinary differential systems ([11,12,19,26,37]). Considering the spatial diffusion, the reaction-diffusion systems are used to describe spatial transmission of infectious diseases [1,5,22,23]. These models usually assume that the effective contact rate and recovery rate are constants ([1,23]). However, this assumption may hold only for a short time and for the homogeneous environment. To capture the impact of spatial heterogeneity of environment on the dynamics of disease transmission, Allen et al. proposed in [2] an epidemic model as follows,

    {StdSΔS=β(x)SIS+I+γ(x)I,xΩ,t>0,ItdIΔI=β(x)SIS+Iγ(x)I,xΩ,t>0,Sη=Iη=0,xΩ,t>0, (1)

    where S and I represent the density of susceptible and infected individuals, respectively. β(x) and γ(x) account for spatial dependent rates of disease contact transmission and disease recovery at x, respectively.

    Infectious disease often starts at a source location and gradually spreads over places where contact transmission occurs. For example, West Nile virus (WNv) is endemic in Africa, the Middle East and other regions. This virus was first detected in New York in 1999 [6], but it reached New Jersey and Connecticut in the second year and till 2002, it has spread across almost the whole America continent. This implies that the disease gradually spreads and the infected environment is changing with time t. Hence, for infectious diseases such as WNv, it is natural to understand the changing of the infected environment. Considering the moving front of the infected environment, the following epidemic model with the free boundary was recently studied in [23],

    {Std1ΔS=bβSIμ1S,r>0,t>0,Itd2ΔI=βSIμ2IαI,0<r<h(t),t>0,Rtd3ΔR=αIμ3R,0<r<h(t),t>0,Sr(0,t)=Ir(0,t)=Rr(0,t)=0,t>0,I(r,t)=R(r,t)=0,rh(t),t>0,h(t)=μIr(h(t),t),h(0)=h0>0,t>0,S(r,0)=S0(r),I(r,0)=I0(r),R(r,0)=R0(r),r0, (2)

    where r=|x| and xRn. The governed equation for the moving front r=h(t) is the well-known Stefan condition, which was established in [28] for an invasive species. Stefan condition can be found in research of many applied areas, such as ice melting in contact with water [32], image processing [3], vapor infiltration of pyrolytic carbon in chemistry [31], tumor cure [35] and wound healing [7] in medicine, and spreading of invasive species [8,9,10,15,25,36,38,40]. Recently, it has been used to describe the moving front of diseases [1,14,23,29].

    In addition, the spread of disease is different from the "random walk" of particle, which follows the Fick's law. The disease tends to move towards the feasible environment and spread along the human's movement. For instance, in the second year after WNv was detected, the wave front traveled 1100 km to the warmer South and 187 km to the colder North [30]. In 2008, according to reports from the Division of Disease Control, Public Health Department (DPH) of Indonesia, dengue cases (about 217-668 cases) were found in some more prosperous and densely-populated cities such as Makassar and Gowa, but no case was found in other sparsely-populated cities such as Jeneponto and Selayar [34]. To consider the impact of advection on transmission of disease, the authors in [14] proposed the following simplified SIS epidemic model,

    {ItdIIxx+αIx=(β(x)γ(x))Iβ(x)NI2,g(t)<x<h(t),t>0,I(g(t),t)=0,g(t)=μIx(g(t),t),t>0,I(h(t),t)=0,h(t)=μIx(h(t),t),t>0,g(0)=h0,h(0)=h0,I(x,0)=I0(x),h0xh0, (3)

    in which they presented the sufficient conditions for the disease to spread or vanish, and discussed the impacts of the advection and the expanding capability on the spreading fronts.

    Motivated by the above research, we will study the general SIR epidemic model with moving fronts and spatial advection,

    {StSxx+αSx=bβ(x)SIμ1S,<x<,t>0,ItIxx+αIx=β(x)SIγ(x)Iμ2I,g(t)<x<h(t),t>0,RtRxx+αRx=γ(x)Iμ3R,g(t)<x<h(t),t>0,I(x,t)=R(x,t)=0,xg(t)orxh(t),t>0,g(t)=μIx(g(t),t),g(0)=h0<0,t>0,h(t)=μIx(h(t),t),h(0)=h0>0,t>0,S(x,0)=S0(x),I(x,0)=I0(x),R(x,0)=R0(x),<x<, (4)

    where x=g(t) and x=h(t) are the moving left and right boundaries to be determined, the governing equations g(t)=μIx(g(t),t) and h(t)=μIx(h(t),t) are the special Stefan conditions. The death rates for the S, I and R classes are given by μ1, μ2 and μ3, respectively. The influx of the S class comes from a constant recruitment rate b, and h0, μ, α are all positive constants, where μ and α represent the expanding capability and advection rate, respectively. The functions β(x) and γ(x) are positive H¨older continuous and satisfy

    (H1) limx±β(x)=β>0 and limx±γ(x)=γ>0.

    Epidemiologically, it means that the far sites are similar.

    As in [2], if the disease transmission rate β(x) at the site x is greater than the recovery rate γ(x), we call the location x a high-risk site, we say it is low-risk if the disease transmission rate β(x) is less than the recovery rate γ(x). If the spatial average value 1|Ω|Ωβ(x)dx of transmission rate is greater than (or less than) the spatial average value 1|Ω|Ωγ(x)dx of the recovery rate, we call the habitat Ω a high-risk (or low-risk) domain.

    Furthermore, we only consider the case of the small advection in a habitat with high-risk far sites for problem (4) and assume that

    (H2) bμ1βγμ2>0 and α<2bμ1βγμ2.

    It is well-known that the basic reproduction number for the system

    {˙S(t)=bβSIμ1S,˙I(t)=βSIγIμ2I,˙R(t)=γIμ3R.

    is R0=bβμ1(r+μ2), R0 is the number of secondary cases which one case would produce on average over the course of its infectious period, in a completely susceptible population. The first inequality in (H2) means that R0>1 and the far sites are high-risk. The constant 2bμ1βγμ2 in (H2) is the minimal speed of the traveling waves to the Cauchy problem

    ItIxx=I(bμ1βγμ2dI)

    with any d>0.

    The initial functions S0, I0 and R0 are nonnegative and satisfy

    {S0C2(,)L(,+), I0,R0C2([h0,h0]);I0(x)=R0(x)=0,  x(,h0][h0,),I0(x)>0,R0(x)>0,  x(h0,h0), (5)

    here (5) indicates that the infected individuals exist in the area x(h0,h0) at the beginning, and no infection happens in the area |x|h0. For model (4), one can see that there are no infected or recovered individuals beyond the left boundary x=g(t) and the right x=h(t).

    We are interested in the impacts of environmental heterogeneity and small advection on the persistence of the disease, and the paper is organized as follows. Firstly, we present the global existence and uniqueness of the solution to problem (4) by the contraction mapping theorem in section 2. In section 3, we first present the definition and exhibit properties of the basic reproduction number for the corresponding model with Dirichlet boundary conditions, and then give the definition and properties of the spatio-temporal risk index RF0(t) for problem (4). Section 4 deals with the sufficient conditions for the disease to vanish and Section 5 is devoted to the sufficient conditions for the disease to spread. The paper closes with some numerical simulations and a brief discussion.


    2. Preliminaries

    The contraction mapping theorem will be first used to prove the local existence and uniqueness of the solution to (4). Then suitable estimates will be exhibited to show that the solution is defined for all t>0, and the comparison principle will also be presented.

    Theorem 2.1. Given any ν(0,1) and (S0,I0,R0) satisfying (5), there is a T>0 such that problem (4) admits a unique bounded solution

    (S,I,R;g,h)C1+ν,1+ν2(DT)×[C1+ν,1+ν2(¯D(g,h)T)]2×[C1+ν2([0,T])]2,

    and

    SC1+ν,1+ν2(DT)+IC1+ν,1+ν2(¯D(g,h)T)+RC1+ν,1+ν2(¯D(g,h)T)C,
    gC1+ν2([0,T])+hC1+ν2([0,T])C,

    where

    DT  ={(x,t)R2:x(,),t[0,T]},D(g,h)T={(x,t)R2:x(g(t),h(t)),t(0,T]}. (6)

    Here C and T only depend on h0,ν,S0C2((,)),S0L((,)),I0C2([h0,h0]) and R0C2([h0,h0]).

    Proof. The idea of this proof is to straighten the free boundaries to circumvent the difficulty caused by the unknown boundaries, and then to construct a mapping. The conclusions of this theorem follow from the contraction mapping theorem together with Lp theory and Sobolev's imbedding theorem [24], we omit it here since it is similar to that of Theorem 2.1 in [23] with obvious modifications, see also [7,8] and references therein.

    We derive the following estimates, which will be used to show that the local solution obtained in Theorem 2.1 can be extended to all t>0.

    Lemma 2.2. Let T0(0,+) and (S,I,R;g,h) be a solution to problem (4) defined for t[0,T0]. Then there exist the constants C1 and C2, independent of T0, such that

    0<S(x,t)C1,<x<+,0<tT0,0<I(x,t), R(x,t)C2,g(t)<x<h(t),0<tT0.

    Proof. It is easy to see that S0,I0 and R0 in (,+)×[0,T0] as long as the solution exists. Moreover, using the strong maximum principle to the first equation of (4) in [g(t),h(t)]×[0,T0] gives that

    S(x,t)>0,<x<,0<tT0,
    I(x,t), R(x,t)>0,g(t)<x<h(t),0<tT0.

    It is easily verified that any constant C is an upper solution of S in (,+)×[0,T0) if C>bμ1 and CS0(x). Hence,

    0<S(x,t)max{bμ1,S0L}:=C1,  <x<,0<t<T0.

    Furthermore, adding the first three equations of (4) leads to

    (S+I+R)t(S+I+R)xx+α(S+I+R)x=bμ1Sμ2Iμ3Rbμ0(S+I+R)

    for g(t)<x<h(t) and 0<tT0, where μ0=min{μ1,μ2,μ3}. Therefore, we have

    S+I+Rmax{bμ0,S0+I0+R0L}:=C2.

    The next lemma displays the monotonicity of free boundaries for problem (4). The proof is similar as that of Lemma 2.3 in [23] for an SIR epidemic model without advection, or that of Lemma 2.3 in [27] for a mutualistic model with advection, we omit it here.

    Lemma 2.3. Let T0(0,+) and (S,I,R;g,h) be a solution to problem (4) defined for t(0,T0]. Thenthere exists a constant C3 independent of T0 such that

    C3g(t)<0and0<h(t)C3fort(0,T0].

    With the above bounds independent of T0, we can extend the solution. The following theorem guarantees the global existence of the solution to problem (4), and the reader can refer to [23] for a similar standard proof.

    Theorem 2.4. Problem (4) admits a unique solution (S,I,R;g,h), which exists globally in [0,) with respect to t.

    In what follows, we exhibit the comparison principle for convenience of later analysis, which are similar to Lemma 3.5 in [9].

    Lemma 2.5. (Comparison principle) Assume that T(0,), ¯g,g_, ¯h,h_C1([0,T]), ¯S(x,t),S_(x,t)C(DT)C2,1(DT), ¯I(x,t)C(D(¯g,¯h)T)C2,1(D(¯g,¯h)T), I_(x,t)C(D(g_,h_)T)C2,1(D(g_,h_)T), here the definitions of DT,D(¯g,¯h)T and D(g_,h_)T are the same as those in (6). Moreover, assume

    {¯St¯Sxx+α¯Sxbμ1¯SI_μ1¯S,<x<,0<tT,S_tS_xx+αS_xbμ1S_¯Iμ1S_,<x<,0<tT,¯It¯Ixx+α¯Ix(β(x)¯Sγ(x)μ2)¯I,¯g(t)<x<¯h(t),0<tT,I_tI_xx+αI_x(β(x)S_γ(x)μ2)I_,g_(t)<x<h_(t),0<tT,¯I(x,t)=0, ¯g(t)μ¯Ix(¯g(t),t),x¯g(t),0<tT,I_(x,t)=0, g_(t)μI_x(g_(t),t),xg_(t),0<tT,¯I(x,t)=0, ¯h(t)μ¯Ix(¯h(t),t),x¯h(t),0<tT,I_(x,t)=0, h_(t)μI_x(h_(t),t),xh_(t),0<tT,¯g(0)h0g_(0)<h_(0)h0¯h(0),I_(x,0)I0(x)¯I(x,0),h0xh0,S_(x,0)S0(x)¯S(x,0),<x<.

    Then the solution (S,I,R;g,h) of problem (4) satisfies

    ¯g(t)g(t)g_(t), h_(t)h(t)¯h(t),0<tT,S_(x,t)S(x,t)¯S(x,t),<x<,0<tT,I_(x,t)I(x,t)¯I(x,t),g(t)xh(t),0<tT.

    3. The risk index

    The objective of this section is to discuss the risk index for the free boundary problem (4), we first present the basic reproduction number of the following reaction-diffusion-advection problem with Dirichlet boundary condition,

    {ItIxx+αIx=bμ1β(x)Iγ(x)Iμ2I,x(p,q),t>0,I(x,t)=0,x=p or q,t>0, (7)

    where p<q. Now the basic reproduction number of (7) is defined by

    RDA0=RDA0((p,q),β(x),γ(x))=supϕH10((p,q))ϕ0qpbμ1β(x)ϕ2dxqp(ϕ2x+(α24+γ(x)+μ2)ϕ2)dx (8)

    and the following lemma was given in [14].

    Lemma 3.1. sign(1RDA0)=sign(λ0), where λ0 is the principal eigenvalue for the reaction-diffusion-advection problem

    {ψxx+αψx=bμ1β(x)ψγ(x)ψμ2ψ+λ0ψ,x(p,q),ψ(x)=0,x=p or q,

    here ψ(x) is the corresponding eigenfunction and ψ(x)>0 in (p,q).

    With the above definition of RDA0, we have some properties for it.

    Theorem 3.2. The following assertions hold.

    (i) If Ω1Ω2R1, then RDA0(Ω1)RDA0(Ω2), and the strict inequality holds if Ω2Ω1 is a nonempty open set. Moreover, lim(qp)+RDA0((p,q))βα24+γ+μ2 provided by (H1) holds;

    (ii) If β(x)β and γ(x)γ, then

    RDA0=bμ1β(πqp)2+α24+γ+μ2.

    Proof. The proof of the monotonicity in assertion (ⅰ) is similar as that of Corollary 2.3 in [5], and the limit in assertion (ⅱ) can be calculated directly.

    We now turn to the limit in (ⅰ). Since limxβ(x)=β,limxγ(x)=γ, we deduce that for any ε>0, there exists L>0 such that for |x|L,

    βεβ(x)β+ε,γεγ(x)γ+ε.

    If q2L, according to (8) and the monotonicity in assertion (ⅰ), we can get

    RDA0((p,q),β(x),γ(x))RDA0((L,2L),β(x),γ(x))RDA0((L,2L),βε,γ+ε)=supϕH10(L,2L)ϕ02LLbμ1(βε)ϕ2dx2LL(ϕ2x+(α24+γ+ε+μ2)ϕ2)dx. (9)

    At the same time, λ=(πL)2 is the principal eigenvalue for the following problem

    {ϕxx=λϕ,x(L,2L),ϕ(L)=ϕ(2L)=0

    with the corresponding eigenfunction ϕ=sin(π(xL)L). Plugging such ϕ into (9), one easily obtains

    RDA0((p,q),β(x),γ(x))bμ1(βε)(πL)2+(α24+γ+ε+μ2). (10)

    Similarly, if p2L, we can also obtain (10) by replacing (L,2L) by (2L,L). Hence, if (qp)4L, the inequality (10) holds. Letting L gives

    lim(qp)+RDA0bμ1(βε)α24+γ+ε+μ2.

    Because of the arbitrariness of ε, it follows that

    lim(qp)+RDA0bμ1βα24+γ+μ2.

    For the free boundary problem (4), the infected interval (g(t),h(t)) is changing with t, so the basic reproduction number is not a constant and should be a function of t. Now we define it as the risk index RF0(t), whose expression is given by

    RF0(t):=RDA0((g(t),h(t)),β(x),γ(x))=supϕH10((g(t),h(t)))ϕ0h(t)g(t)bμ1β(x)ϕ2dxh(t)g(t)(ϕ2x+(α24+γ(x)+μ2)ϕ2)dx. (11)

    Owing to the monotonicity of g(t) and h(t) in Lemma 2.3, we have the limits g[,h0] and h[h0,+] such that limtg(t)=g and limth(t)=h. Moreover, (g(t),h(t)) is expanding and then RF0(t) is increasing, we then denote

    RF0():=limtRF0(t)=RDA0((g,h),β(x),γ(x)). (12)

    Using the above notations, Lemma 2.3 and Theorem 3.2 lead to the following result.

    Theorem 3.3. RF0(t) is a strictly monotone increasing function of t, that is RF0(t1)<RF0(t2) if t1<t2. Additionally, under the assumption of (H1), if hg=, then RF0()bμ1βα24+γ+μ2.

    Remark 1. Epidemiologically, the monotonicity in Theorem 3.3 implies that the risk of the disease increases with time. By Theorem 3.3, we further obtain that RF0()>1 if (H2) holds and hg=.


    4. The vanishing of disease

    Usually, if the infected domain no longer expands and the infected individuals eventually disappear, we say the epidemic has been controlled. Mathematically, we say the disease vanishes and have the following definition.

    Definition 4.1. The disease is vanishing if hg< and limtI(,t)C([g(t),h(t)]) =0, while the disease is spreading if hg= and lim suptI(,t)C([g(t),h(t)]) >0.

    Thus, our natural question is: What conditions can make the disease vanish?

    Theorem 4.2. Assume that (H2) holds. If RF0()<1, then hg< and

    limtI(,t)C([g(t),h(t)])=0.

    Moreover, we have limtR(,t)C([g(t),h(t)])=0 and limtS(x,t)=bμ1 uniformly for x(,).

    Proof. On the contrary we assume that hg+ as t. Together with assumption (H2) and Remark 1, we can get RF0()bμ1βα24+γ+μ2>1. This contradicts to RF0()<1.

    Now it follows from Lemma 2.5 that S(x,t)¯S(t) for (x,t)(,)×[0,), where

    ¯S(t)=bμ1+(S0Lbμ1)eμ1t,

    which satisfies

    {d¯Sdt=bμ1¯S,   t[0,),¯S(0)=S0L.

    Since limt¯S(t)=bμ1, we deduce that

    lim suptS(x,t)limt¯S(t)=bμ1uniformly for x(,). (13)

    Next we claim that limtI(,t)C([g(t),h(t)])=0. Noting

    RF0()=RDA0((g,h),β(x),γ(x))<1

    and hg<+, it follows from the continuity that RDA0((g,h),β(x)(bμ1+δ),γ(x))<1 for some small δ>0. Then, due to Lemma 3.1, there are λδ0>0 and ψ(x)>0 in (g,h) such that

    {ψxx+αψx=(β(x)(bμ1+δ)γ(x)μ2)ψ+λδ0ψ,x(g,h),ψ(x)=0,x=g or h.

    For δ given above, there exists Tδ>0 such that S(x,t)bμ1+δ for tTδ and x(,). Let ¯I(x,t) be the unique solution of the problem

    {¯It¯Ixx+α¯Ix=(β(x)(bμ1+δ)γ(x)μ2)¯I,g<x<h,t>Tδ,¯I(g,t)=0,¯I(h,t)=0,t>Tδ,¯I(x,Tδ)=I0(x,Tδ),g<x<h.

    Using the comparison principle (Lemma 2.5) with ¯S=bμ1+δ yields

    0I(x,t)¯I(x,t)Meλδ02(tTδ)ψ(x), g(t)xh(t),tTδ,

    for some large M>0. Therefore,

    limtI(,t)C([g(t),h(t)])=0 (14)

    due to Meλδ02(tTδ)ψ(x)0 as t. It then follows from the third equations of (4) that

    limtR(,t)C([g(t),h(t)])=0.

    It remains to show the limit of S. Owing to (14), for any ε>0, there exists Tε>0 such that

    0β(x)SIβLC1I(x,t)ε,     (x,t)(,+)×[Tε,),

    here C1 is the upper bound of S defined in Lemma 2.2. Thus, we have S(x,t)S_(t) in (,+)×[Tε,), where S_(t) satisfies

    {dS_dt=bεμ1S_,t>Tε,S_(T)=inf(,+)S(x,Tε)0.

    It is easy to see that S_(t)bεμ1 as t. Therefore,

    lim inft+S(x,t)bεμ1,    x(,+).

    Since ε is arbitrary, we get

    lim inft+S(x,t)bμ1uniformly for  x(,+),

    which together with (13) gives

    limtS(x,t)=bμ1uniformly for x(,+).

    This completes the proof.

    Theorem 4.3. Suppose RF0(0)<1. Then hg< and

    limtI(,t)C([g(t),h(t)])=0

    provided that S0bμ1 in (,+) and I0C([h0,h0]) is sufficiently small.

    Proof. Since RF0(0)=RDA0((h0,h0))<1, it follows from Lemma 3.1 that there exist λ00>0 and ψ(x)>0 in (h0,h0) such that

    {ψxx+αψx=(β(x)bμ1γ(x)μ2)ψ+λ00ψ,h0<x<h0,ψ(x)=0,x=±h0. (15)

    We first assert that there exists some constant M0>0 such that

    xψ(x)M0ψ(x),h0xh0. (16)

    In fact, let x1 be the first stationary point of ψ(x) (i. e. ψ(x1)=0) when x moves to the right from h0 to h0, and oppositely x2 the first one from h0 to h0. It is easy to see that h0<x1x2<h0. Denoting y1=min{x1,0} and y2=max{x2,0}, we have h0<y10y2<h0, which divides the interval [h0,h0] into three subintervals [h0,y1),[y1,y2] and (y2,h0].

    Noting that for x[h0,y1), x<0 and ψ(x)>0, we have xψ(x)<0. Similarly, for x(y2,h0], ψ(x)>0 and xψ(x)<0.

    Since that ψ(x)>0 for x[y1,y2], we can choose some large M0>0 such that

    xψ(x)h0ψLM0min[y1,y2]ψ(x)M0ψ(x), x[y1,y2],

    therefore (16) holds for M0(h0ψL)/min[y1,y2]ψ(x).

    Now we prove that the vanishing happens. Owing to λ00>0, we can choose some small δ>0 such that

    δ(1+δ)2+αh04δ2+M02(1+δ)δ2+βLbμ1((1+δ)21)λ00. (17)

    Next we define

    σ(t)=h0(1+δδ2eδt), t>0, (18)

    and

    U(x,t)=εeαx2α2xh0σ(t)eδtψ(xh0σ(t)),σ(t)xσ(t), t>0.

    Direct calculations show that

    σ(t)+μUx(σ(t),t)=h02δ2eδt+μεeδteα2(σ(t)h0)ψ(h0)h0σ(t)h0eδt(δ22+μεh0eα2h0δψ(h0)).

    Similarly,

    σ(t)+μUx(σ(t),t)h0eδt(δ22+μεh0eα2h0δψ(h0)).

    Selecting ε=δ2h02μeα2h0δmin{1ψ(h0),1ψ(h0)} leads to

    σ(t)μUx(σ(t),t)andσ(t)μUx(σ(t),t).

    By (16), (17) and (18), a routine computation gives rise to the inequality as follows

    UtUxx+αUx(β(x)bμ1γ(x)μ2)U=U[δ+α2xh0σ2(t)σ(t)σ(t)σ(t)xh0σ(t)ψψ1+α24(1h20σ2(t))   +h20σ2(t)(ψ"+αψ)ψ1(β(x)bμ1γ(x)μ2)]=U[δ+α2xh0σ2(t)σ(t)σ(t)σ(t)xh0σ(t)ψψ1(1h20σ2(t))(β(x)bμ1γ(x)μ2α24)   +h20σ2(t)λ00]U[δα2h20σ2(t)σ(t)σ(t)σ(t)M0(1h20σ2(t))βLbμ1+h20σ2(t)λ00]Uh20σ2(t)[δ(1+δ)2αh04δ2M02(1+δ)δ2βLbμ1((1+δ)21)+λ00]0. (19)

    Because of the assumption that S0bμ1 for x(,+), we derive S(x,t)bμ1 for <x<+,t0. Therefore, if I0LU(x,0)=εeαx2αx2h0σ(0)ψ(xh0σ(0)) for x[h0,h0], we can apply the comparison principle (Lemma 2.5) with ¯S=bμ1 to conclude that g(t)σ(t),h(t)σ(t) and I(x,t)U(x,t) for g(t)xh(t),t>0. It follows that hlimtσ(t)=h0(1+δ)<, gσ(t)> and then limtI(,t)C([g(t),h(t)])=0.

    Theorem 4.4. Suppose RF0(0)<1. Then hg< and

    limtI(,t)C([g(t),h(t)])=0

    provided that S0bμ1 in (,+) and μ is sufficiently small.

    Proof. Similar to Theorem 4.3, we define

    W(x,t)=Meαx2α2xh0σ(t)eδtψ(xh0σ(t)),σ(t)xσ(t), t>0,

    where M>0 is large enough such that I0LW(x,0)=Meαx2αx2h0σ(0)ψ(xh0σ(0)) for x[h0,h0]. Using the same calculation as (19) yields

    WtWxx+αWx(β(x)bμ1γ(x)μ2)W0.

    Additionally, straightforward calculations tell us that

    σ(t)μWx(σ(t),t)andσ(t)μWx(σ(t),t)

    if μ is sufficiently small. The result for vanishing is a direct application of Lemma 2.5.


    5. The spreading of disease

    In this section, our aim is to present the sufficient conditions for the spreading. First of all, we give a lemma for the following initial-boundary value problem

    {utuxx+αux=f(x,t)u,g(t)<x<h(t),t>0,u(x,t)=0,xg(t) or xh(t),t>0,g(t)=μux(g(t),t),g(0)=h0<0,t>0,h(t)=μux(h(t),t),h(0)=h0>0,t>0,u(x,0)=u0(x),h0<x<h0, (20)

    where α>0 is a constant, f(x,t) is a continuous function, u0(x)C2[h0,h0], u0(±h0)=0 and u0(x)>0,x(h0,h0).

    Lemma 5.1. Suppose the following conditions hold.

    (i) There exists a constant M1>0 such that |f(x,t)|M1 for <x<, t>0;

    (ii) u(x,t), g(t) and h(t) are bounded.

    Then the unique solution (u;g(t),h(t)) of problem (20) satisfies

    limtu(,t)C([g(t),h(t)])=0. (21)

    Proof. Since f(x,t) is bounded, it is well-known that problem (20) admits a unique global solution (u(x,t);g(t),h(t)) and g(t) is decreasing, h(t) is increasing. Furthermore, straightening the free boundaries as follows

    y=2h0xh(t)g(t)h0(h(t)+g(t))h(t)g(t),   w(y,t)=u(x,t)

    leads to a related problem with the fixed boundaries. Similarly as Lemma 3.2 in [1], it follows that for 0<ν<1, there exists a constant ˆC that depends on ν,h0,g0,u0C2[h0,h0] and g,h such that

    wC1+ν,1+ν2([h0,h0]×[τ,τ+1])ˆC,

    for any τ1. Noting that τ is arbitrary and ˆC is independent of τ, we can obtain

    u(,t)C1([g(t),h(t)])˜C,   t1, (22)

    which together with the free boundary conditions in (20) yields

    hCν2([1,)),  gCν2([1,))˜C,   t1, (23)

    for some positive constant ˜C.

    Next, we prove (21). Arguing by contradiction, we assume that

    lim suptu(,t)C([g(t),h(t)])=δ>0. (24)

    Thus, there exists a sequence {(xk,tk):g(tk)<xk<h(tk),tk>0} with tk as k such that u(xk,tk)δ2 for all kN. Owing to <g<g(tk)<xk<h(tk)<h<, we can extract a subsequence of {xk}, still denoted by it, converges to x0[g,h]. Moreover, it follows from (22) that x0(g,h). Define

    uk(x,t)=u(x,t+tk),   x(g(t+tk),h(t+tk)),t(tk,).

    From condition (i), (22) and the standard parabolic regularity, it follows that {uk} has a subsequence {uki} such that uki˜u(i) and ˜u satisfies

    ˜ut˜uxx+α˜ux=f(x,t)˜uM1˜u,   (x,t)(g,h)×(,),

    which together with

    ˜u(x0,0)=limkiuki(xki,0)=limkiu(xki,tki)δ2,  ˜u(h,0)=0

    gives that ˜u>0 in (g,h)×(,) via the maximum principle. Hence, applying the Hopf boundary lemma at the point (h,0) leads to

    ˜ux(h,0)σ<0

    for some σ>0. From (22) and the above fact, we conclude

    ux(h(tki),tki)=xuki(h(tki),0)σ2<0

    for all large ki, which together with the Stefan condition implies that

    h(tki)μσ2>0. (25)

    On the other hand, (23) and the assumption that hg<0 give rise to

    h(t)0andg(t)0. (26)

    Comparing (25) and (26), it yields a contradiction so that (24) doesn't hold, that is, we arrive at (21).

    Theorem 5.2. If there exists t00 such that RF0(t0)1, then hg= and

    lim suptI(,t)C([g(t),h(t)])>0, (27)

    namely, spreading happens.

    Proof. Since S is bounded, from the second equation in (4), we conclude

    ItIxx+αIxM1I

    by M1:=βLmax{bμ1,S0L}+γL+μ2. Assuming that hg< by contradiction, it follows from Lemma 5.1 that

    limtI(,t)C([g(t),h(t)])=0, (28)

    which together with the first equation in (4) gives

    limtS(x,t)=bμ1uniformly for x(,). (29)

    Additionally, we know that there exists T0>t0 such that

    RF0(T0)=RDA0((g(T0),h(T0)),bμ1β(x),γ(x))>1 (30)

    based on the hypothesis RF0(t0)1 and the monotonicity of RF0(t) with respect to t. By continuity, there exists ε0>0 sufficiently small (ε0<bμ1) such that

    RF0(T0,ε0):=RDA0((g(T0),h(T0)),β(x)(bμ1ε0),γ(x))>1. (31)

    For ε0 given above, it follows from (29) that there is T>T0 such that

    S(x,t)bμ1ε0,x(g,h), tT,

    and the monotonicity of RF0(t) implies that

    RF0(T,ε0)=RDA0((g(T),h(T)),β(x)(bμ1ε0),γ(x))>1, (32)

    which together with Lemma 3.1 shows that the principal eigenvalue λ0<0 for the following problem

    {ψxx+αψx=(β(x)(bμ1ε0)γ(x)μ2)ψ+λ0ψ,x(g(T),h(T)),ψ(x)=0,x=g(T) or h(T), (33)

    and ψ(x)>0 in (g(T),h(T)). Now we set

    u_(x,t)=δeλ0(tT)ψ(x),     x(g(T),h(T)),tT,

    where δ is sufficiently small such that u_(x,T)=δψ(x)I(x,T), and in light of (33), we get

    u_tu_xx+αu_x=(β(x)(bμ1ε0)γ(x)μ2)u_. (34)

    Employing the comparison principle with S_=bμ1ε0 in [g(T),h(T)]×[T,) deduces that

    I(,t)C([g(t),h(t)])δeλ0(tT)ψ(0)+ast.

    This is a contradiction to (28), which concludes that hg=.

    Now, we turn to prove (27). If not, then

    lim suptI(,t)C([g(t),h(t)])=0, (35)

    thus, we can obtain (29) again. Following the same procedure, we can prove that (31) and (32) hold for given ε0,T0,T. Therefore I admits a lower solution u, which is unbounded. This leads to a contradiction to (35), which completes the proof.

    Recalling Theorem 4.4, we know that if the expanding capability μ is sufficiently small, accompanied with other conditions, the disease will vanish. However, another question arises: if μ is large, what will happen? To answer this question, we need the following lemma. Meanwhile, in order to stress the dependence of the solutions on μ for problem (4) and (20), we substitute (Iμ;gμ,hμ) and (uμ;gμ,hμ) for (I;g,h) and (u;g,h) respectively in the following lemma and theorem.

    Lemma 5.3. Assume that in problem (20), there exists a constant M2>0 such that f(x,t)M2. Then for any given constant H>0, there exists μH>0 such that when μ>μH, the unique solution (uμ;gμ(t),hμ(t)) satisfies

    lim suptgμ(t)<H,  and  lim infthμ(t)>H. (36)

    Proof. This can be proved in a similar way as shown in [38,Lemma 3.2]. It is clear that

    uμ(x,t)vμ(x,t),pμ(t)xqμ(t), t>0.gμ(t)pμ(t), hμ(t)qμ(t),t>0. (37)

    where (vμ;pμ(t),qμ(t)) satisfies

    {vtvxx+αvx=M2v,p(t)<x<q(t),t>0,v(x,t)=0,xp(t) or xq(t),t>0,p(t)=μvx(p(t),t),p(0)=h0<0,t>0,q(t)=μvx(q(t),t),q(0)=h0>0,t>0,v(x,0)=u0(x),h0<x<h0, (38)

    and (pμ)(t)<0,(qμ)(t)>0 for t>0.

    We are in a position to prove that for all large μ,

    pμ(2)H   and   qμ(2)H. (39)

    To this end, we first choose smooth functions p_(t) and q_(t) with

    p_(0)=h02,p_(t)<0,p_(2)=H, and  q_(0)=h02,q_(t)>0,q_(2)=H.

    We then invoke the following initial-boundary value problem

    {v_tv_xx+αv_x=M2v_,p_(t)<x<q_(t),t>0,v_(x,t)=0,xp_(t) or xq_(t),t>0,v_(x,0)=v_0(x),h02xh02, (40)

    where the smooth initial value v_0(x) satisfies

    {0<v_0(x)<u0(x),   h02xh02,v_0(h02)=v_0(h02)=0, v_0(h02)>0, v_0(h02)<0. (41)

    Thus, the standard theory for parabolic equations ensures that (40) admits a unique solution v_, and the Hopf boundary lemma shows that v_x(p_(t),t)>0 and v_x(q_(t),t)<0 for t[0,2].

    According to our choice of v_0(x), p_(t) and q_(t), there exists a constant μH such that for all μ>μH,

    p_(t)μv_x(p_(t),t)  and  q_(t)μv_x(q_(t),t),  0t2. (42)

    Obviously,

    p_(0)=h02>h0=pμ(0),    q_(0)=h02<h0=qμ(0).

    The comparison principle together with (38), (40), (41) and (42) gives rise to

    vμ(x,t)v_(x,t), pμ(t)p_(t), qμ(t)q_(t),  for  p_(t)xq_(t),0t2,

    which implies (39) hold. Hence, owing to (37) and (39), we obtain

    lim suptg(t)limtpμ(t)<pμ(2)H,lim infth(t)limtqμ(t)>qμ(2)H.

    Theorem 5.4. Suppose RF0(0)<1. Then hg= and

    lim suptI(,t)C([g(t),h(t)])>0 (43)

    if μ is sufficiently large, that is, spreading happens.

    Proof. It has been proven successfully for the similar result, which adopts the method of constructing a lower solution and can be found in [36,Lemma 3.13]. To more simple, we will apply Lemma 5.3 to prove here. Clearly,

    ItIxx+αIxM2I, (44)

    where M2 is the same as M1 defined in Theorem 5.2 and independent of μ.

    Recalling assertion (i) of Theorem 3.2, we can select some H>0 such that RDA0((H,H))>1. For H chosen above, it follows from (44) and Lemma 5.3 that there exists a μH such that when μ>μH,

    lim suptgμ(t)<H  and  lim infthμ(t)>H.

    Combining with the monotonicity of gμ(t) and hμ(t) gives that there is T0>0 such that gμ(T0)<H, hμ(T0)>H, thus,

    RF0(T0)=RDA0((gμ(T0),hμ(T0)))>RDA0((H,H))>1.

    Therefore, for μ>μH, we can use Theorem 5.2 to conclude that hg= and lim suptI(,t)C([g(t),h(t)])>0.

    The following result follows directly from the comparison principle (Lemma 2.5), Theorems 4.4 and 5.4, see also the similar proof of Theorem 5.5 in [14].

    Theorem 5.5. (Sharp threshold) For fixed h0, I0 and S0 (S0bμ1), there exists μ[0,) such that vanishing occurs when 0<μμ, and spreading occurs when μ>μ .


    6. Numerical simulation and discussion

    In this section, we first carry out numerical simulations to illustrate the impact of expanding capability μ. Fixing some coefficients and functions as follows:

    α=1.5, b=1, μ1=0.5, μ2=0.6, h0=1,S0(x)=1+12sinx,   I0(x)=cos(π2x),β(x)=1+21+x2(sinπ2x+1), γ(x)=0.5+201+x2(cosπ2x+1),

    we can see that β=1, γ=0.5, S0(x)bμ1 and (H2) holds. Further, we have by (11) that

    RF0(0)11bμ1β(x)ϕ2dx11(α24+γ(x)+μ2)ϕ2dxbμ1maxx[1,1]β(x)11ϕ2dx(α24+minx[1,1]γ(x)+μ2)11ϕ2dx811<1.

    Thus, the asymptotic behaviors of the solution to problem (4) and the changing of free boundaries are illustrated by choosing different expanding capabilities.

    Example 6.1. Fix small μ=20. Theorem 4.4 gives that the solution is vanishing for small μ. We can see from Figure 1 that the disease I tends to extinction quickly, and the free boundaries don't expand.

    Figure 1. μ=20. The left graph shows that the solution I decays to zero quickly. The right graph is the corresponding contour graph, which shows the free boundaries expand slowly and will be limited in a long run.

    Example 6.2. Fix big μ=40. Theorem 5.4 tells us that the spreading of solution happens if μ is sufficiently large. Comparing with Figure 1, it is easy to see from Figure 2 that a spatially inhomogeneous stationary endemic state appears and is globally asymptotically stable for bigger μ. The two fronts expand quickly.

    Figure 2. μ=40. The solution I in the left graph keeps positive and stabilizes to an equilibrium. The right contour graph shows that the free boundaries expand fast.

    In this paper, we consider a reaction-diffusion-advection SIR model (4) with double free boundaries, which describes the left and right fronts of the infected habitat. The model extends the existing models such as (2) for a model without advection and (3) for a simplified SIS model.

    We introduce the basic reproduction number RDA0 for system (7) with Dirichlet boundary and the risk index RF0(t) for model (4), respectively. Based on the risk index RF0(t), we exhibit some sufficient conditions to ensure spreading or vanishing of the disease. Specifically, our results reveal that if RF0(t0)1 for some t0, spreading always happens, namely, the disease will become endemic (Theorem 5.2), and if RF0()<1, vanishing always happens, namely, the disease will be controlled (Theorem 4.2). But if RF0(0)<1, vanishing will happen for the small initial value I0 of infected individuals (Theorem 4.3) or the small expanding capability μ (Theorem 4.4), however, spreading can also happen for the large μ (Theorem 5.4).

    In our work, three basic reproduction numbers are introduced, one is R0 (:=bβμ1(μ2+α)) for SIR model (2) without advection, one is RDA0 defined by (8) for SIR model with fixed boundaries, another one is RF0(t) defined by (11) for SIR model (4) with free boundaries. Their differences and correlations have been discussed in [14,Section 7].

    It is worthwhile to point out that our risk index RF0(t) is related not only with the advection α, but also with the contact transmission rate β(x) and recovery rate γ(x). In detail, RF0(t) increases with β(x), and decreases with γ(x). These facts suggest that all epidemiological parameters affect the transmission dynamics of disease. Specially, decreasing of β(x) or increasing of γ(x) can lower the risk index and prevent the further spreading of the disease. For instance, in the control of infectious diseases such as the Ebola epidemics in West Africa ([17]), applying some proper isolation facilities, which can reduce the contact rate, was shown to be a crucial factor in preventing the spread to neighboring countries. Another alternative way is improving medical technical level, which can increase the recovery rate and thus become a vital factor in controlling the spread.

    We close this paper by recalling the advection coefficient α. To avoid complexity, we begin with a small advection. But big advection, we believe, will cause more complex dynamical behaviors, and interested readers can refer to [4]. We will continue to focus on the dynamics induced by big advection.


    [1] [ I. Ahn,S. Baek,Z. G. Lin, The spreading fronts of an infective environment in a man-environment-man epidemic model, Appl. Math. Modelling, 40 (2016): 7082-7101.
    [2] [ L. J. S. Allen,B. M. Bolker,Y. Lou,A. L. Nevai, Asymptotic profiles of the steady states for an SIS epidemic reaction-diffusion model, Discrete Contin. Dyn. Syst. Ser. A, 21 (2008): 1-20.
    [3] [ A. L. Amadori,J. L. Vázquez, Singular free boundary problem from image processing, Math. Model. Methods. Appl. Sci., 15 (2005): 689-715.
    [4] [ A. Bezuglyy,Y. Lou, Reaction-diffusion models with large advection coefficients, Appl. Anal., 89 (2010): 983-1004.
    [5] [ R. S. Cantrell and C. Cosner, Spatial Ecology via Reaction-Diffusion Equations, John Wiley & Sons, Ltd, 2003.
    [6] [ Center for Disease Control and Prevention (CDC), Update: West Nile-like viral encephalitis-New York, 1999, Morb. Mortal Wkly. Rep., 48 (1999): 890-892.
    [7] [ X. F. Chen,A. Friedman, A free boundary problem arising in a model of wound healing, SIAM J. Math. Anal., 32 (2000): 778-800.
    [8] [ Y. H. Du,Z. G. Lin, Spreading-vanishing dichotomy in the diffusive logistic model with a free boundary, SIAM J. Math. Anal., 42 (2010): 377-405.
    [9] [ Y. H. Du,Z. G. Lin, The diffusive competition model with a free boundary: Invasion of a superior or inferior competitor, Discrete Contin. Dyn. Syst. Ser. B, 19 (2014): 3105-3132.
    [10] [ Y. H. Du,B. D. Lou, Spreading and vanishing in nonlinear diffusion problems with free boundaries, J. Eur. Math. Soc., 17 (2015): 2673-2724.
    [11] [ A. M. Elaiw,N. H. AlShamrani, Global stability of humoral immunity virus dynamics models with nonlinear infection rate and removal, Nonlinear Anal. Real World Appl., 26 (2015): 161-190.
    [12] [ X. M. Feng,S. G. Ruan,Z. D. Teng,K. Wang, Stability and backward bifurcation in a malaria transmission model with applications to the control of malaria in China, Math. Biosci., 266 (2015): 52-64.
    [13] [ D. Z. Gao, Y. J. Lou and D. H. He, et al., Prevention and control of Zika as a mosquito-borne and sexually transmitted disease: A mathematical modeling analysis, Scientific Reports 6, Article number: 6 (2016), 28070.
    [14] [ J. Ge,K. I. Kim,Z. G. Lin,H. P. Zhu, A SIS reaction-diffusion model in a low-risk and high-risk domain, J. Differential Equation, 259 (2015): 5486-5509.
    [15] [ H. Gu,B. D. Lou,M. L. Zhou, Long time behavior of solutions of Fisher-KPP equation with advection and free boundaries, J. Funct. Anal., 269 (2015): 1714-1768.
    [16] [ Globalization and disease Available from: https://en.wikipedia.org/wiki/Globalization_and_disease.
    [17] [ West African Ebola virus epidemic Available from: https://en.wikipedia.org/wiki/West_African_Ebola_virus_epidemic.
    [18] [ Epidemic situation of dengue fever in Guangdong, 2014 (Chinese) Available from: http://www.rdsj5.com/guonei/1369.html.
    [19] [ S. Iwami,Y. Takeuchi,X. N. Liu, Avian-human influenza epidemic model, Math. Biosci., 207 (2007): 1-25.
    [20] [ W. O. Kermack,A. G. Mckendrick, Contributions to the mathematical theory of epidemics, Proc. Roy. Soc., A115 (1927): 700-721.
    [21] [ W. O. Kermack,A. G. Mckendrick, Contributions to the mathematical theory of epidemics, Proc. Roy. Soc., A138 (1932): 55-83.
    [22] [ K. I. Kim,Z. G. Lin,L. Zhang, Avian-human influenza epidemic model with diffusion, Nonlinear Anal. Real World Appl., 11 (2010): 313-322.
    [23] [ K. I. Kim,Z. G. Lin,Q. Y. Zhang, An SIR epidemic model with free boundary, Nonlinear Anal. Real World Appl., 14 (2013): 1992-2001.
    [24] [ O. A. Ladyzenskaja, V. A. Solonnikov and N. N. Ural'ceva, Linear and Quasilinear Equations of Parabolic Type, Amer. Math. Soc, Providence, RI, 1968.
    [25] [ C. X. Lei,Z. G. Lin,Q. Y. Zhang, The spreading front of invasive species in favorable habitat or unfavorable habitat, J. Differential Equations, 257 (2014): 145-166.
    [26] [ C. Z. Li,J. Q. Li,Z. E. Ma,H. P. Zhu, Canard phenomenon for an SIS epidemic model with nonlinear incidence, J. Math. Anal. Appl., 420 (2014): 987-1004.
    [27] [ M. Li,Z. G. Lin, The spreading fronts in a mutualistic model with advection, Discrete Contin. Dyn. Syst. Ser. B, 20 (2015): 2089-2105.
    [28] [ Z. G. Lin, A free boundary problem for a predator-prey model, Nonlinearity, 20 (2007): 1883-1892.
    [29] [ Z. G. Lin and H. P. Zhu, Spatial spreading model and dynamics of West Nile virus in birds and mosquitoes with free boundary, J. Math. Biol., (2017), 1–29, http://link.springer.com/article/10.1007/s00285-017-1124-7?wt_mc=Internal.Event.1.SEM.ArticleAuthorOnlineFirst.
    [30] [ N. A. Maidana,H. Yang, Spatial spreading of West Nile Virus described by traveling waves, J. Theoret. Biol., 258 (2009): 403-417.
    [31] [ W. Merz,P. Rybka, A free boundary problem describing reaction-diffusion problems in chemical vapor infiltration of pyrolytic carbon, J. Math. Anal. Appl., 292 (2004): 571-588.
    [32] [ L. I. Rubinstein, The Stefan Problem, Amer. Math. Soc, Providence, RI, 1971.
    [33] [ C. Shekhar, Deadly dengue: New vaccines promise to tackle this escalating global menace, Chem. Biol., 14 (2007): 871-872.
    [34] [ S. Side,S. M. Noorani, A SIR model for spread of Dengue fever disease (simulation for South Sulawesi, Indonesia and Selangor, Malaysia), World Journal of Modelling and Simulation, 9 (2013): 96-105.
    [35] [ Y. S. Tao,M. J. Chen, An elliptic-hyperbolic free boundary problem modelling cancer therapy, Nonlinearity, 19 (2006): 419-440.
    [36] [ J. Wang,J. F. Cao, The spreading frontiers in partially degenerate reaction-diffusion systems, Nonlinear Anal., 122 (2015): 215-238.
    [37] [ J. Y. Wang,Y. N. Xiao,Z. H. Peng, Modelling seasonal HFMD infections with the effects of contaminated environments in mainland China, Appl. Math. Comput., 274 (2016): 615-627.
    [38] [ M. X. Wang,J. F. Zhao, Free boundary problems for a Lotka-Volterra competition system, J. Dynam. Differential Equations, 26 (2014): 655-672.
    [39] [ World Health Organization, World Health Statistics 2006-2012.
    [40] [ P. Zhou,D. M. Xiao, The diffusive logistic model with a free boundary in heterogeneous environment, J. Differential Equations, 256 (2014): 1927-1954.
  • This article has been cited by:

    1. Min Zhu, Zhigui Lin, Lai Zhang, Spatial-temporal risk index and transmission of a nonlocal dengue model, 2020, 53, 14681218, 103076, 10.1016/j.nonrwa.2019.103076
    2. Shaon Bhatta Shuvo, Bonaventure C. Molokwu, Ziad Kobti, 2020, Simulating the Impact of Hospital Capacity and Social Isolation to Minimize the Propagation of Infectious Diseases, 9781450379984, 3451, 10.1145/3394486.3412859
    3. Min Zhu, Yong Xu, A time-periodic dengue fever model in a heterogeneous environment, 2019, 155, 03784754, 115, 10.1016/j.matcom.2017.12.008
    4. Zhengdi Zhang, Abdelrazig K. Tarboush, The diffusive model for West Nile virus with advection and expanding fronts in a heterogeneous environment, 2020, 13, 1793-5245, 2050057, 10.1142/S1793524520500576
    5. Malú Grave, Alvaro L. G. A. Coutinho, Adaptive mesh refinement and coarsening for diffusion–reaction epidemiological models, 2021, 67, 0178-7675, 1177, 10.1007/s00466-021-01986-7
    6. Nao Yamamoto, Bohan Jiang, Haiyan Wang, Quantifying compliance with COVID-19 mitigation policies in the US: A mathematical modeling study, 2021, 6, 24680427, 503, 10.1016/j.idm.2021.02.004
    7. Ru-Qi Li, Yu-Rong Song, Guo-Ping Jiang, Prediction of epidemics dynamics on networks with partial differential equations: A case study for COVID-19 in China* , 2021, 30, 1674-1056, 120202, 10.1088/1674-1056/ac2b16
    8. Vanshika Aggarwal, Geeta Arora, Homan Emadifar, Faraidun K. Hamasalh, Masoumeh Khademi, Sania Qureshi, Numerical Simulation to Predict COVID-19 Cases in Punjab, 2022, 2022, 1748-6718, 1, 10.1155/2022/7546393
    9. Yachun Tong, Inkyung Ahn, Zhigui Lin, The impact factors of the risk index and diffusive dynamics of a SIS free boundary model, 2022, 7, 24680427, 605, 10.1016/j.idm.2022.09.003
    10. 2023, 9780443186790, 229, 10.1016/B978-0-44-318679-0.00013-2
    11. Min Zhu, Yong Xu, Lai Zhang, Jinde Cao, A dengue fever model with free boundary incorporating the time‐periodicity and spatial‐heterogeneity, 2022, 45, 0170-4214, 301, 10.1002/mma.7776
    12. Jingli Ren, Haiyan Wang, 2023, 9780443186790, 173, 10.1016/B978-0-44-318679-0.00012-0
    13. Shaon Bhatta Shuvo, Bonaventure Chidube Molokwu, Samaneh Miri Rostami, Ziad Kobti, Anne W Snowdon, 2021, Simulating and Predicting the Active Cases and Hospitalization Considering the Second Wave of COVID-19, 978-1-6654-2744-9, 1, 10.1109/ISCC53001.2021.9631420
    14. Xieer Dai, Michael Beenstock, Daniel Felsenstein, David Genesove, Nikita Kotsenko, 'Traffic light' theory for Covid-19 spatial mitigation policy design, 2023, 4, 2662-2998, 10.1007/s43071-022-00033-8
    15. Yachun Tong, Inkyung Ahn, Zhigui Lin, Threshold dynamics of a nonlocal dispersal SIS epidemic model with free boundaries, 2025, 18, 1793-5245, 10.1142/S179352452350095X
    16. Zhiguo Wang, Hua Nie, Sanyi Tang, Dynamics of an epidemic model arising in a spatial segregation control strategy, 2025, 90, 0303-6812, 10.1007/s00285-025-02195-z
  • Reader Comments
  • © 2017 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(3756) PDF downloads(710) Cited by(16)

Article outline

Figures and Tables

Figures(2)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog