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Threshold dynamics of a time-periodic two-strain SIRS epidemic model with distributed delay

  • In this paper, a two-strain SIRS epidemic model with distributed delay and spatiotemporal heterogeneity is proposed and investigated. We first introduce the basic reproduction number Ri0 and the invasion number ˆRi0(i=1,2) for each strain i. Then the threshold dynamics of the model is established in terms of Ri0 and ˆRi0 by using the theory of chain transitive sets and persistence. It is shown that if ˆRi0>1(i=1,2), then the disease in two strains is persist uniformly; if Ri0>1Rj0(ij,i,j=1,2), then the disease in i-th strain is uniformly persist, but the disease in j-th strain will disappear; if Ri0<1 or Ri0=1(i=1,2) and βi(x,t)>0, then the disease in two strains will disappear.

    Citation: Jinsheng Guo, Shuang-Ming Wang. Threshold dynamics of a time-periodic two-strain SIRS epidemic model with distributed delay[J]. AIMS Mathematics, 2022, 7(4): 6331-6355. doi: 10.3934/math.2022352

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  • In this paper, a two-strain SIRS epidemic model with distributed delay and spatiotemporal heterogeneity is proposed and investigated. We first introduce the basic reproduction number Ri0 and the invasion number ˆRi0(i=1,2) for each strain i. Then the threshold dynamics of the model is established in terms of Ri0 and ˆRi0 by using the theory of chain transitive sets and persistence. It is shown that if ˆRi0>1(i=1,2), then the disease in two strains is persist uniformly; if Ri0>1Rj0(ij,i,j=1,2), then the disease in i-th strain is uniformly persist, but the disease in j-th strain will disappear; if Ri0<1 or Ri0=1(i=1,2) and βi(x,t)>0, then the disease in two strains will disappear.



    Nowadays there are always various communicable diseases, such as malaria, dengue fever, HIV/AIDS, Zika virus, and COVID-19, which impair the health of people around the globe [2]. Especially, as of now, COVID-19 has killed more than 4 million people and is still prevailing in many countries over the world. Since Covid-19 was first identified in January 2020, thousands of mutations have been detected [34]. Moreover, it has been reported that various new strains of COVID-19 are considered as more dangerous than the original virus. In fact, the variation of pathogens is very common in epidemiology, we can refer to [4] for the instance of the mutation of influenza virus. Besides, Dengue fever is one of the most typical vector-borne infectious disease prevailing in the tropical and subtropical areas. Usually, the fever is caused by five different serotypes (DEN I-IV) and the corresponding fatality rates of these serotypes are dramatically different. This means that a person living in an endemic area might be facing the risk of infection from five distinct serotypes, and a individual who recovered form one of the serotypes could get permanent immunity to itself and only temporary cross-immune against the others. In recent years, mathematical model increasingly become a effective tool in the investigation of the spread of epidemics. With the aid of proper analysis for the mathematical models, we can better understand the transmission mechanism of infectious diseases and then take appropriate prevention and control measures to combat the diseases. In fact, the researches of epidemic dynamics models involving multi-strain interactions have attracted considerable attention of many scholars. Baba et al. [4] studied a two-strain model containing vaccination for both strains. Cai et al. [6] studied a two-strain model including vaccination, and analyzed the interaction between the strains under the vaccination theme. A class of multi-chain models with discrete time delays, moreover, is considered in the case of temporary immunity and multiple cross immunity by Bauer et al. [5]. For more literatures corresponding to pathogens with multiple strains, we can refer to [1,8,24,30,33,39] and the references.

    In reality, accumulating empirical evidence shows that seasonal factors can affect the host-pathogen interactions [3], and the incidence of many infectious diseases fluctuates over time, often with a cyclical pattern(see, e.g., [16,31,37]). In addition, Yang, et al [35] found that temperature and relative humidity were mainly the driving factors on COVID-19 transmission. It is therefore necessary to consider infectious disease models with time-dependent parameters. Martcheva et al. [24] considered a class of multi-chain models with time-periodic coefficients. Precisely speaking, they presented sufficient conditions to guarantee the coexistence of the two-strain, and further proved that competitive exclusion would occur only when the transmission rates on each chain are linearly correlated.

    At the same time, it is noticed that the resources, humidity and temperature are not uniformly distributed in space, then spatial heterogeneity should not be ignored a practical epidemiological model. From the point of view of model's rationalization, the main parameters, such as infection rate and recovery rate, should be intrinsically spatially dependent. Taking into consideration both the spatial heterogeneity of the environment and the impact of individual movement on disease transmission, Tuncer et al. [33] proposed the following two-strain model:

    {S(x,t)t=dSΔS(x,t)(β1(x)I1(x,t)+β2(x)I2(x,t))S(x,t)S(x,t)+I1(x,t)+I2(x,t)   +r1(x,t)I1(x,t)+r2(x,t)I2(x,t),I1(x,t)t=d1ΔI1(x,t)+β1(x)S(x,t)I1(x,t)S(x,t)+I1(x,t)+I2(x,t)r1(x,t)I1(x,t),I2(x,t)t=d2ΔI2(x,t)+β2(x)S(x,t)I2(x,t)S(x,t)+I1(x,t)+I2(x,t)r2(x,t)I2(x,t). (1.1)

    Furthermore, Acklehd et al. [1] studied a model with bilinear incidence, the results showed that the spatial heterogeneity facilitated the coexistence of strains. Taking into account alternation of seasons, Peng et al. [29] studied a reaction-diffusion SIS model, in which the disease transmission rate and recovery rate are all spatial-dependent and temporally periodic. The results show that temporal heterogeneity have little effect on the extinction and persistence of the diseases, nevertheless, the combination of temporal and spatial heterogeneity would increase the duration of the disease.

    It is well known that the incubation period exist commonly in most infectious diseases, and the length of the incubation periods corresponding to different diseases are often different. We can refer Leung [19] for more information about the difference of the incubation period of COVID-19 between various different variants. During the incubation period, random movements of individuals can give rise to nonlocal effects, precisely speaking, the rate of gaining infectious individuals at current position at the present time actually depends on the infections at all possible locations and all possible previous times. This nonlocal interaction will affect the global dynamic behavior of the solutions [7,13], traveling wave phenomena [14], etc. Guo et al. [12] studied the threshold dynamics of a reaction-diffusion model with nonlocal effects. In particular, Zhao et al. [38] considered the threshold dynamics of a model with fixed latent period on the basis of model (1.1). In particular, when Ri0=1 and the infection rate is assumed to be strictly positive, they studied the threshold dynamics of the model by constructing the upper control system.

    Due to the individual difference in age, nutrition, lifestyle and health status, there are significant difference in the immunity among different individuals [27]. This further lead to the difference of incubation periods in different individuals. As McAloon, et al. [27] points out, it is critically important to understand the variation in the distribution within the population. Thus, the fixed incubation period is not always an ideal description for most diseases. Takeuchi et al. [32] considered a vector-borne SIR infectious disease model with distributed time delay. Zhao et al. [39] studied a two-group reaction-diffusion model with distributed delay. In [39], the recovered individuals are assumed to be lifelong immune to the disease. However, this assumption is not suitable for all epidemics. Then it is very necessary to establish and analysis a SIRS model involving aforementioned various factors, and thus to further improve the existing relevant research. The purpose of this paper is to investigate the threshold dynamics of a two-strain SIRS epidemic model with distributed delay and spatiotemporal heterogeneity.

    The remainder of this paper is organized as follows. In the next section, we derive the model and show its well-posedness. In section 3, we established the threshold dynamics for the system in term of the basic reproduction number Ri0 and the invasion number ˆRi0(i=1,2) for each strain i. At the end of the current paper, a brief but necessary discussion is presented to show some epidemiological implications of this study.

    In this section, we propose a time-periodic two-strain SIRS model with distributed delay and spatiotemporal heterogeneity, and further analyze some useful properties of the solutions of the model.

    Let ΩRn denote the spatial habitat with smooth boundary Ω. We suppose that only one mutant can appear in a pathogen, and a susceptible individual can only be infected by one virus strain. Denote the densities of the two different infectious classes with infection age a0 and at position x, and time t by E1(x,a,t) and E2(x,a,t), respectively. By a standard argument on structured population and spatial diffusion (see e.g., [28]), we obtain

    {(t+a)Ei(x,a,t)=DiΔEi(δi(x,a,t)+ri(x,a,t)+d(x,t))Ei(x,a,t), xΩ, a>0, t>0Ei(x,a,t)n=0, xΩ, a>0, t>0,i=1,2, (2.1)

    where d(x,t) is the natural death rate at location x and time t; ri(x,a,t) and δi(x,a,t) represent the recovery rates and mortality rates induced by the disease of the i-th infectious classes with infection age a0 at position x and time t; the constants Di denote the diffusion rates of the i-th infectious class for i=1,2. We divide the population into six compartments: the susceptible group S(x,t), two latent groups Li(x,t), two infective groups Ii(x,t), and the recovered group R(x,t), i=1,2. Let N(x,t)=S(x,t)+i=1,2(Li(x,t)+Ii(x,t))+R(x,t). We assume that only a portion of recovered individuals would be permanently immune to the virus. Let α(x,a,t) be the loss of immunity rate with infection age a0 at position x and time t. In order to simplify the model reasonably, we further suppose that

    δi(x,a,t)=δi(x,t), ri(x,a,t)=ri(x,t), α(x,a,t)=α(x,t), xΩ, a,t0, i=1,2.

    On account of the individual differences of the incubation period among the different individuals, infections individuals of the i-th population be capable of infecting others until after a possible infection age a(0,τi], where the positive constant τi is the maximum incubation period of i-th strain, i=1,2. Let fi(r)dr denote the probability of becoming into the individuals who are capable of infecting others between the infection age r and r+dr, then Fi(a)=a0fi(r)dr represents the probability of turning into the individuals with infecting others before the infection age a for i=1,2. It is clear that Fi(a)0 for a(0,τi), Fi(a)1 for a[τi,+), i=1,2, and

    Li(x,t)=τi0(1Fi(a))Ei(x,a,t)da,Ii(x,t)=τi0Fi(a)Ei(x,a,t)da++τiEi(x,a,t)da, i=1,2. (2.2)

    Let

    Ii,1(x,t)=τi0Fi(a)Ei(x,a,t)da, Ii,2(x,t)=+τiEi(x,a,t)da.

    It then follows that

    Li(x,t)t=DiΔLi(x,t)(δi(x,t)+ri(x,t)+d(x,t))Li(x,t)τi0fi(a)Ei(x,a,t)da+Ei(x,0,t),

    and

    Ii,1(x,t)t=DiΔIi,1(x,t)(δi(x,t)+ri(x,t)+d(x,t))Ii,1(x,t)+τi0fi(a)Ei(x,a,t)daEi(x,τi,t),
    Ii,2(x,t)t=DiΔIi,2(x,t)(δi(x,t)+ri(x,t)+d(x,t))Ii,2(x,t)+Ei(x,τi,t)Ei(x,,t),

    where i=1,2. Biologically, we assume Ei(x,,t)=0(i=1,2). Then we have

    Ii(x,t)t=DiΔIi(x,t)(δi(x,t)+ri(x,t)+d(x,t))Ii(x,t)+τi0fi(a)Ei(x,a,t)da.

    Denote the infection rate by βi(x,t)0. Due to the fact that the contact of susceptible and infectious individuals yields the new infected individuals, we take Ei(x,0,t) as follows:

    Ei(x,0,t)=βi(x,t)S(x,t)Ii(x,t)S(x,t)+I1(x,t)+I2(x,t)+R(x,t), i=1,2.

    In the absence of disease, moreover, we suppose that the evolution of the population density follows the following equation:

    N(x,t)t=DNΔN(x,t)+μ(x,t)d(x,t)N(x,t),

    where d(x,t) is the natural death rate, μ(x,t) is the recruiting rate, and DN denotes the diffusion rate. In conclusion, the disease dynamics is expressed by the following system:

    {S(x,t)t=DSΔS(x,t)+μ(x,t)d(x,t)S(x,t)+α(x,t)R(x,t)β1(x,t)S(x,t)I1(x,t)S(x,t)+I1(x,t)+I2(x,t)+R(x,t)β2(x,t)S(x,t)I2(x,t)S(x,t)+I1(x,t)+I2(x,t)+R(x,t),Li(x,t)t=DiΔLi(x,t)(δi(x,t)+ri(x,t)+d(x,t))Li(x,t)+βi(x,t)S(x,t)Ii(x,t)S(x,t)+I1(x,t)+I2(x,t)+R(x,t)τi0fi(a)Ei(x,a,t)da,Ii(x,t)t=DiΔIi(x,t)(δi(x,t)+ri(x,t)+d(x,t))Ii(x,t)+τi0fi(a)Ei(x,a,t)da,R(x,t)t=DRΔR(x,t)+r1(x,t)(L1(x,t)+I1(x,t))+r2(x,t)(L2(x,t)+I2(x,t))d(x,t)R(x,t)α(x,t)R(x,t), i=1,2. (2.3)

    We make the following basic assumption:

    (H) DS,Di,DR>0, i=1,2, the functions d(x,t),μ(x,t),α(x,t),βi(x,t),δi(x,t),ri(x,t) are Hölder continuous and nonnegative nontrivial on ˉΩ×R, and periodic in time t with the same period T>0. Moreover, d(x,t)>0, xΩ, t>0.

    For the sake of simplicity, we let hi(x,t)=δi(x,t)+ri(x,t)+d(x,t), i=1,2. In order to determine Ei(x,a,t), let Vi(x,a,ξ)=Ei(x,a,a+ξ), ξ0, i=1,2. By a similar idea as that in [36], we have

    {Vi(x,a,ξ)a=DiΔVi(x,a,ξ)hi(x,t)Vi(x,a,ξ),Vi(x,0,ξ)=Ei(x,0,ξ)=βi(x,ξ)S(x,ξ)Ii(x,ξ)S(x,ξ)+I1(x,ξ)+I2(x,ξ)+R(x,ξ), i=1,2.

    Let Γi(x,y,t,s) with x,yΩ and t>s0 be the fundamental solution associated with the partial differential operator tDiΔhi(x,t)(i=1,2). Then we have

    Vi(x,a,ξ)=ΩΓi(x,y,ξ+a,ξ)βi(y,ξ)S(y,ξ)Ii(y,ξ)S(y,ξ)+I1(y,ξ)+I2(y,ξ)+R(y,ξ)dy. (2.4)

    According to the periodicity of hi and βi, Γi(x,y,t,s) is periodic, that is, Γi(x,y,t+T,s+T)=Γi(x,y,t,s), x,yΩ, t>s0, i=1,2. It follows from Ei(x,a,t)=Vi(x,a,ta) that

    Ei(x,a,t)=ΩΓi(x,y,t,ta)βi(y,ta)S(y,ta)Ii(y,ta)S(y,ta)+I1(y,ta)+I2(y,ta)+R(y,ta)dy. (2.5)

    Substituting (2.5) into (2.3), and dropping the Li equations from (2.3) (since they are decoupled from the other equations), we obtain the following system:

    {S(x,t)t=DSΔS(x,t)+μ(x,t)d(x,t)S(x,t)+α(x,t)R(x,t)β1(x,t)S(x,t)I1(x,t)S(x,t)+I1(x,t)+I2(x,t)+R(x,t)β2(x,t)S(x,t)I2(x,t)S(x,t)+I1(x,t)+I2(x,t)+R(x,t),Ii(x,t)t=DiΔIi(x,t)(δi(x,t)+ri(x,t)+d(x,t))Ii(x,t)+τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)S(y,ta)Ii(y,ta)S(y,ta)+I1(y,ta)+I2(y,ta)+R(y,ta)dyda,R(x,t)t=DRΔR(x,t)+r1(x,t)I1(x,t)+r2(x,t)I2(x,t)d(x,t)R(x,t)α(x,t)R(x,t), i=1,2. (2.6)

    Set τ=max{τ1,τ2}>0. Let X:=C(ˉΩ,R4) be the Banach space with a supremum norm X. Let Cτ:=C([τ,0],X) be a Banach space with the norm ϕ=maxθ[τ,0]ϕ(θ)X, ϕCτ. Define X+:=C(ˉΩ,R4+), C+τ:=C([τ,0],X+), the (X,X+) and (Cτ,C+τ) are strongly ordered spaces. For σ>0 and a given function u(t):[τ,σ]X, we denote utCτ by

    ut(θ)=u(t+θ), θ[τ,0].

    Similarly, define Y=C(ˉΩ,R) and Y+=C(ˉΩ,R+). Furthermore, we consider the following system:

    {ω(x,t)t=DSΔω(x,t)d(x,t)ω(x,t), xΩ, t>0,ω(x,t)t=0,  xΩ, t>0,ω(x,0)=ϕS(x), xΩ, ϕSY+. (2.7)

    By the arguments in [15], Eq (2.7) exists an evolution operator VS(t,s):Y+Y+ for 0st, which satisfies VS(t,t)=I, VS(t,s)VS(s,ρ)=VS(t,ρ), 0ρst, VS(t,0)ϕS=ω(x,t;ϕS), xΩ, t0, ϕSY+, where ω(x,t;ϕS) is the solution of (2.7).

    Consider the following periodic system:

    {ˉωi(x,t)t=DiΔˉωi(x,t)hi(x,t)ˉωi(x,t)),xΩ, t>0,ˉωi(x,t)n=0,xΩ, t>0,ˉωi(x,0)=ϕi(x),xΩ, ϕiY+. (2.8)

    and

    {˜ωR(x,t)t=DRΔ˜ωR(x,t)k(x,t)˜ωR(x,t)),xΩ, t>0,˜ωR(x,t)t=0,xΩ, t>0,˜ωR(x,0)=ϕR(x),xΩ, ϕRY+, (2.9)

    where k(x,t)=α(x,t)+d(x,t). Let Vi(t,s), i=1,2, and VR(t,s) be the evolution operators determined by (2.8) and (2.9), respectively. The periodicity hypothesis (H) combining with [9,Lemma 6.1] yield that VS(t+T,s+T)=VS(t,s), Vi(t+T,s+T)=Vi(t,s) and VR(t+T,s+T)=VR(t,s), ts0. In addition, for any t,sR and s<t. VS(t,s), Vi(t,s) and VR(t,s) are compact, analytic and strongly positive operators on Y+. It then follows from [9,Theorem 6.6] that there exist constants Q1, Qi1 and c0,ciR(i=1,2) such that

    VS(t,s),VR(t,s)Qec0(ts), Vi(t,s)Qieci(ts), ts, i=1,2.

    Let ci:=ˉω(Vi), where

    ˉω(Vi)=inf{ω|M1: sR, t0,||Vi(t+s,s)||Meωt}

    is the exponent growth bound of the evolution operator Vi(t,s). It is clear that ci<0.

    Define functions FS,Fi,FR:[0,)Y respectively by

    FS(t,ϕ)=μ(,t)+α(,t)ϕS(,0)2i=1βi(,0)ϕS(,0)ϕi(,0)ϕS(,0)+ϕ1(,0)+ϕ2(,0)+ϕR(,0),Fi(t,ϕ)=τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)ϕS(y,a)ϕi(y,a)ϕS(y,a)+ϕ1(y,a)+ϕ2(y,a)+ϕR(y,a)dyda,FR(t,ϕ)=r1(,0)ϕ1(,0)+r2(,0)ϕ2(,0).

    Let F=(FS,F1,F2,FR), it is clear that F is a function from [0,) to X. Define

    U(t,s):=(VS(t,s)0000V1(t,s)0000V2(t,s)0000VR(t,s)).

    Then U(t,s) is an evolution operator from X to X. Note that VS, Vi(i=1,2) and VR are analytic operators, it follows that U(t,s) is an analytic operator for (t,s)R2 with ts0. Let

    D(AS(t))={ψC2(ˉΩ)nψ=0 on Ω};[AS(t)ψ](x)=DSΔψ(x)d(x,t)ψ(x), ψD(AS(t));D(Ai(t))={ψC2(ˉΩ)nψ=0 on Ω};[Ai(t)ψ](x)=DiΔψ(x)hi(x,t)ψ(x), ψD(Ai(t)),

    and

    D(AR(t))={ψC2(ˉΩ)nψ=0 on Ω};[AR(t)ψ](x)=DRΔψ(x)k(x,t)ψ(x), ψD(AR(t)).

    Moreover, we let

    A(t):=(AS(t)0000A1(t)0000A2(t)0000AR(t)).

    Then (2.3) can be rewritten as the following Cauchy problem:

    {u(x,t)t=A(t)u(x,t)+F(t,ut), xΩ, t>0,u(x,ζ)=ϕ(x,ζ), xΩ, ζ[τ,0], (2.10)

    where u(x,t)=(S(x,t),I1(x,t),I2(x,t),R(x,t))T. Furthermore, it can be rewritten as the following integral equation

    u(t,ϕ)=U(t,0)ϕ(0)+t0U(t,s)F(t,us)ds, t0, ϕC+τ.

    Then the solution of above integral equation is called a mild solution of (2.10).

    Theorem 2.1. For each ϕC+τ, system (2.6) admits a unique solution u(t,ϕ) on [0,+) with u0=ϕ, and u(t,ϕ) is globally bounded.

    Proof. By the definition of F(t,ϕ) and the assumption (H), F(t,ϕ) is locally Lipschitz continuous on R+×C+τ. We first show

    limθ0+dist(ϕ(0)+θF(t,ϕ),X+)=0, (t,ϕ)R+×C+τ. (2.11)

    Set

    ˉβ=max{maxxˉΩ,t[0,τ]β1(x,t),maxxˉΩ,t[0,τ]β2(x,t)};mi(x,t)=βi(x,t)ϕS(x,0)ϕi(x,0)ϕS(x,0)+ϕ1(x,0)+ϕ2(x,0)+ϕR(x,0);ni(x,t)=βi(x,t)ϕS(x,t)ϕi(x,t)ϕS(x,t)+ϕ1(x,t)+ϕ2(x,t)+ϕR(x,t).

    For any t0, θ0 and xˉΩ, ϕC+τ, we have

    ϕ(x,0)+θF(t,ϕ)(x)=(ϕS(x,0)+θ[μ(x,t)+α(x,t)ϕR(x,0)2i=1mi(x,t)]ϕ1(x,0)+θτ10f1(a)ΩΓ1(x,y,t,ta)ϕ1(y,ta)dydaϕ2(x,0)+θτ20f1(a)ΩΓ2(x,y,t,ta)ϕ2(y,ta)dydaϕR(x,0)+r1(x,t)ϕ1(x,0)+r2(x,t)ϕ2(x,0))(ϕS(x,0)(1θ2i=1βi(x,t)ϕi(x,0)ϕS(x,0)+ϕ1(x,0)+ϕ2(x,0)+ϕR(x,0))ϕ1(x,0)ϕ2(x,0)ϕR(x,0))(ϕS(x,0)(1θˉβ2i=1ϕi(x,0)ϕS(x,0)+ϕ1(x,0)+ϕ2(x,0)+ϕR(x,0))ϕ1(x,0)ϕ2(x,0)ϕR(x,0)).

    The above inequality implies that (2.11) holds when θ is small enough. Consequently, by [25,Corollary 4] with K=X+ and S(t,s)=U(t,s), system (2.6) admits a unique mild solution u(x,t;ϕ) with u0(,;ϕ)=ϕ, t[0,tϕ]. Since U(t,s) is an analytic operator on X for any t,sR, s<t, it follows that u(x,t;ϕ) is a classical solution for t>τ. Set

    P(t)=Ω(S(x,t)+2i=1(Li(x,t)+Ii(x,t))+R(x,t))dx,
    μmax=sup(x,t)ˉΩ×[0,T]μ(x,t), ˉμmax=μmax|Ω|, dmin=inf(x,t)ˉΩ×[0,T]d(x,t).

    Then

    dP(t)dt=Ωμ(x,t)d(x,t)(S(x,t)+2i=1(Li(x,t)+Ii(x,t))+R(x,t))   2i=1δi(x,t)(Li(x,t)+Ii(x,t))2i=1ri(x,t)Li(x,t)dxΩμ(x,t)dxΩd(x,t)(S(x,t)+2i=1(Li(x,t)+Ii(x,t))+R(x,t))dxˉμmaxdminP(t), t>0.

    We obtain that there are l:=lϕ large enough and M=ˉμmaxdmin+1>0, so that for each ϕC+τ, one has

    P(t)M, tlT+τ.

    Then ΩIi(x,t)dxM, tlT+τ. According to [11] and assumption (H), we obtain that Γi(x,y,t,ta) and βi(x,t) are uniformly bounded functions for any x,yΩ, t[a,a+T]. Set Bi=supx,yΩ,t[a,a+T]Γi(x,y,t,ta)βi(y,ta), then we obtain

    IitDiΔIihi(x,t)Ii(x,t)+τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)Ii(y,ta)dydaDiΔIihi(x,t)Ii(x,t)+Biτi0fi(a)ΩIi(y,ta)dydaDiΔIihi(x,t)Ii(x,t)+BiMFi(τi)=DiΔIihi(x,t)Ii(x,t)+BiM, xΩ, tlT+τ. (2.12)

    Consider the following equation:

    {ωi(x,t)t=DiΔωi(x,t)hi(x,t)ωi(x,t)+BiM,xΩ, t>lT+τ,ωi(x,t)n=0,xΩ, t>lT+τ. (2.13)

    It is evident that system (2.13) admits a strictly positive periodic solution with the period T>0, which is globally attractive. According to (2.12), the first equation of system (2.6) can be dominated by (2.13) for any t>lT+τ. So there exists B1>0 such that for each ϕC+τ, we can find a li=li(ϕ)l(ϕ) satisfying Ii(x,t;ϕ)B1(i=1,2) for xˉΩ and tliT+τ. Thus

    {R(x,t)tDRΔR(x,t)k(x,t)R(x,t)+B1(r1(x,t)+r2(x,t)),xΩ, t>liT+τ,R(x,t)n=0,xΩ, t>liT+τ. (2.14)

    Similarly, there exists B2>0 such that for each ϕC+τ, there exists lR=lR(ϕ)li satisfying R(x,t;ϕ)B2 for xˉΩ and tlRT+τ. Then we have

    {S(x,t)tDSΔS(x,t)+μ(x,t)d(x,t)S(x,t)+B2α(x,t),xΩ, t>lRT+τ,S(x,t)n=0,xΩ, t>lRT+τ. (2.15)

    Hence, there are B3>0 and lS=lS(ϕ)lR such that for each ϕC+τ, S(x,t;ϕ)B3(i=1,2) for xˉΩ and tlST+τ, and hence, tϕ=+.

    Theorem 2.2. System (2.6) generates a T-periodic semi-flow Φt:=ut():C+τC+τ, namely Φt(ϕ)(x,s)=ut(ϕ)(x,s)=u(x,t+s;ϕ) for any ϕC+τ, t0 and s[τ,0]. In addition, ΦT admits a global compact attractor on C+τ, where u(x,t;ϕ) is a solution of system (2.6).

    Proof. By a similar argument as the proof of [26,Theorem 8.5.2], one can show that Φt(ϕ) is continuous for any ϕC+τ and t0. In addition, similarly as the proof of [36,Lemma 2.1], we can further verify that Φt is a T-periodic semi-flow on C+τ. According to Theorem 2.1, we obtain that Φt is dissipative. Moreover, by the arguments similar to those in the proof of [15,Proposition 21.2], we get that there exists n01 such that Φn0T=un0T is compact on C+τ for n0Tτ. Following from [23,Theorem 2.9], we have that ΦT:C+τC+τ admits a global compact attractor.

    In this section, we first analyze the threshold dynamics of a single-strain model with the help of the basic reproduction number, and then study the threshold dynamics of model (2.6).

    Let Ij(x,t)0,xΩ, t>0, j=1,2, and ij. Then system (2.6) reduces to the following single-strain model:

    {St=DSΔS+μ(x,t)d(x,t)S+α(x,t)R(x,t)βi(x,t)S(x,t)Ii(x,t)S(x,t)+Ii(x,t)+R(x,t),Iit=DiΔIi(x,t)hi(x,t)Ii(x,t)+τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)S(y,ta)Ii(y,ta)S(y,ta)+Ii(y,ta)+R(y,ta)dyda,Rt=DRΔR(x,t)+ri(x,t)Ii(x,t)d(x,t)R(x,t)α(x,t)R(x,t). (3.1)

    Consider the following linear equation:

    {S(x,t)t=DSΔS(x,t)+μ(x,t)d(x,t)S(x,t),xΩ, t>0,S(x,t)n=0,xΩ, t>0. (3.2)

    According to [36,Lemma 2.1], there is an unique T-periodic solution S(x,t) of (3.2). Linearizing the Ii-equation of system (3.1) at the disease-free periodic solution (S,0,0), we have

    {ωi(x,t)t=DiΔωi(x,t)hi(x,t)ωi(x,t)   +τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)ωi(y,ta)dyda, xΩ, t>0,ωi(x,t)n=0, xΩ, t>0. (3.3)

    Let

    CT(ˉΩ×R,R):={u|uC(ˉΩ×R,R),u(x,t+T)=u(x,t),(x,t)Ω×R,T>0},

    with the supremum norm, and define C+T as the positive cone of CT(ˉΩ×R,R), namely,

    C+T:={uCT: u(t)(x)0, tR, xˉΩ}.

    Let ψi(x,t)CT(ˉΩ×R,R) be the initial distribution of infected individuals of the i-strain at the spatial position xˉΩ and time tR, then Vi(ta,s)ψi(s)(s<ta) is the density of those infective individuals at location x who were infective at time s and retain infective at time ta when time evolved from s to ta. Furthermore, taVi(ta,s)ψi(s)ds is the density distribution of the accumulative infective individuals at positive x and time ta for all previous time s<ta. Hence the density of new infected individuals at time t and location x can be written as

    τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)ta(Vi(ta,s)ψi(s))(x)dsdyda=τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)+a(Vi(ta,ts)ψi(ts))(x)dsdyda.

    Defining operator Ci:CT(ˉΩ×R,R)CT(ˉΩ×R,R) by

    (Ciψi)(x,t)=τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)ψi(y,ta)dyda.

    Set

    Ai(ψi)(x,t)=(Ciψi)(x,t), Bi(ψi)(x,t)=+a(Vi(t,ts+a)ψi(ts+a))(x)ds.

    Defining other operators Li,ˆLi:CTCT by

    (Liψi):=τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)+aVi(ta,ts)ψi(ts)(x)dsdyda,(ˆLiψi)(x,t):=+0Vi(t,ts)(Ciψi)(ts)(x)ds, tR, s0.

    Clearly, Li=AiBi, ˆLi=BiAi, Li and ˆLi are compact, bounded and positive operators. Let r(Li) and r(ˆLi) are the spectral radius of Li and ˆLi respectively, then r(Li)=r(ˆLi). Similar to [18,20], we define the basic reproduction number for system (3.1), that is, Ri0=r(Li)=r(ˆLi).

    Define Q:=C([τ,0],Y), and let ||ϕ||Q:=maxθ[τ,0]||ϕ(θ)||Y for any ϕQ. Denote Q+:=C([τ,0],Y+) as the positive cone of Q. Then (Q,Q+) is strongly ordered Banach space. Let P:=C(ˉΩ,R3) be the Banach space with supremum norm P. For τ>0, let Dτ:=C([τ,0],P) be the Banach space with ϕ=maxθ[τ,0]ϕ(θ)P for all ϕDτ. Define P+:=C(ˉΩ,R3+) and D+τ:=C([τ,0],P+), then both (P,P+) and (Dτ,D+τ) are strongly ordered space. By the arguments in [21,39], we have the following observation:

    Theorem 3.1. The signs of Ri01 and ri1 are same.

    Consider the following equation

    {ωi(x,t)t=DiΔωi(x,t)hi(x,t)ωi(x,t)   +τi0fi(a)ΩΓi(x,y,t,ta)B3βi(y,ta)B3+ωi(y,ta)ωi(y,ta)dyda,    xΩ, t>0,ωi(x,s)=ψi(x,s), ψiQ+, xΩ, s[τi,0],ωi(x,t)n=0, xΩ, t>0, (3.4)

    where B3 is the constant in the proof of Theorem 2.1.

    Theorem 3.2. Assume that ωi(x,t;ψi) is the solution of (3.4) with an initial value of ψiQ. If Ri0=1 and βi(x,t)>0 for all xˉΩ, t>0, then ωi(x,t)0 is globally attractive.

    Proof. By a straightforward computation, one has that (3.4) is dominated by (3.3). Define the map Pnoi:QQ by Pnoi(ψi)=ωn0i,T with ωn0i,T=ωi(x,n0T+s;ψi), where ωi(x,t;ψi) is the solution of (3.3). Similar to the argument in [18], Pnoi is strongly positive on Q+ when βi(x,t)>0,xˉΩ, t>0. It follows from [20,Lemma 3.1] that Pnoi admits a positive and simple eigenvalue ri, and a strongly positive eigenfunction defined by ψi, that is Pi(ψi)=riψi. It follows from the strong positivity of ψi that ωi(x,t;ψi)0. According to Theorem 3.2, we have ri=1, and hence, μi=0. By similar arguments as the proof of [18,Lemma 3.2], we can show that there is a positive T-periodic function νi(x,t)=eμi0ωi(x,t;ψi)=ωi(x,t;ψi) such that νi(x,t) is a solution of (3.3). Then for each initial value ψi(x,s)Q, there exists a constant k>0 such that ψi(x,s)kνi(x,s) for all xΩ, t>0. Moreover, by the comparison principle, one has ωi(x,t;ψi)kνi(x,t) for all xΩ, t>0. Let

    [0,kνi]Q={uQ:0u(x,s)kνi(x,s), xˉΩ, s[τi,0]},

    then

    Sn0i(ψi):=ωi(x,noTω+S;ψI)[0,kνi]Q,  xˉΩ, s[τi,0].

    Hence the positive orbit γ+(ψi):={Skn0i(ψi):kN} of Sn0i() is precompact, and Sn0i maps [0,kνi]Q into [0,kνi]Q, Due to comparison principle, we get Sn0i() is monotone. According to [40,Theorem 2.2.2], we obtain that ωi(x,t)0 is globally attractive.

    Theorem 3.3. Suppose that ˉS(x,t;ψ)=(S(x,t;ψ),Ii(x,t;ψ),R(x,t;ψ)) is the solution of (3.1) with the initial data ψ. If Ii(x,t0;ψ)0 for some t00, then Ii(x,t;ψ)>0, xˉΩ, t>t0.

    Proof. Obviously, for the secondly equation of (3.1), we get

    {Ii(x,t)tDiΔIi(x,t)hi(x,t)Ii(x,t), xΩ, t>0,Ii(x,t)n=0, xΩ, t>0, i=1,2,

    and Ii(x,t0;ψ)0, t00, i=1,2. It follows from [15,Proposition 13.1] that Ii(x,t;ψ)>0 for all xˉΩ and t>t0.

    Theorem 3.4. Suppose that ˉS(x,t;ψ)=(S(x,t;ψ),Ii(x,t;ψ),R(x,t;ψ)) be the solution of (3.1) with the initial data ψ=(ψS,ψi,ψR)Dτ, i=1,2. Thenone has

    (1) If Ri0=1 and βi(x,t)>0 for all xΩ and t>0, then (S,0,0) is globally attractive;

    (2) If Ri0<1, then (S,0,0) is globally attractive;

    (3) If Ri0>1, then there is a M>0 such that for any ψD+τ, one has

    lim inftS(x,t;ψ)>M, lim inftIi(x,t;ψ)>M, lim inftR(x,t;ψ)>M

    uniformly for xˉΩ.

    Proof. (1) According to the proof of Theorem 2.1, for t>lsT+τ, we have S(x,t;ϕ)B3, xˉΩ, ϕC+τ. Thus, when t>lsT+τ, the second equation of (3.1) is dominated by (3.4) for xˉΩ. In addition, one has Ii(x,t;ψ)ωi(x,t) for xˉΩ and t>lsT+τ. Since Ri0=1 and βi(x,t)>0 for xˉΩ, t>0. It follows from Theorem 3.5 that limtωi(x,t)=0 for all xˉΩ. In addition, one has limtIi(x,t;ψ)=0 for all xˉΩ, and limtR(x,t;ψ)=0 for all xˉΩ. Hence the first equation of (3.1) is asymptotic to (3.2). It follows from [36,Lemma 2.1] that system (3.2) admits an unique positive T-periodic solution S(x,t), which is globally attractive.

    Let P=ΦT, J=ˉω(ψ) denotes the omega limit set for P. That is

    J={(ϕS,ϕi,ϕR)C+τ:{ki} s.t. limiPki(ϕS,ϕi,ϕR)=(ϕS,ϕi,ϕR)}.

    It follows fron [17,Lemma 2.1] that J is an internally chain transitive sets for P. Since limtIi(x,t;ψ)=0 and limtR(x,t;ψ)=0 for all xˉΩ, then J=J1×{ˆ0}×{ˆ0}. According to Theorem 3.5, one has ˆ0J1. Let ω(x,t;ψS(,0)) be the solution of (3.2) with the initial value ω(x,0)=ψS(x,0), where ψSQ+. Define

    ωt(x,θ;ψS)={ω(x,θ+t;ψS(0))  t+θ>0, t>0, θ[τ,0],ψ(x,θ+t)  t+θ0, t>0, θ[τ,0].

    Then we define the solution semiflow ωt for (3.2).

    Let ˉP=ωT(ψS), ˉω(ψS) denotes the omega limit set of ˉP. According to [36,Lemma 2.1], one has ˉω(ψS)={S}. Since P(J)=J and Ii(x,t;(ψS,ˆ0,ˆ0))0, R(x,t;(ψS,ˆ0,ˆ0))0, P(J)=ˉP(J1)×{ˆ0}×{ˆ0}, then ˉP(J1)=J1. Therefore, J1 is an internally chain transitive sets for ˉP. It follows from [36,Lemma 2.1] that {S} is globally attractive on Q+. In addition, J1WS{S}=J1 Q+=, where WS{S} is the stable set of S. According to [40,Theorem 1.2.1], one has J1{S}, then J1={S}. Consequently, J={(S,0,0)}. By the definition of J, we have

    limt(S(,t;ψ),Ii(,t;ψ),R(,t;ψ))(S(,t),0,0)∥=0.

    (2) Consider equation

    {ωi(x,t)t=DiΔωi(x,t)hi(x,t)ωi(x,t)   +τi0fi(a)ΩΓi(x,y,t,ta)(βi(y,ta)+ε)ωi(y,ta)dyda,    xΩ, t>0,ωi(x,t)n=0, xΩ, t>0. (3.5)

    Since Ri0<1, it follows from Theorem 2.1 that ri<1. Thus there exists a constant ε0>0 such that ri,ε<1 for ε[0,ε0). Then μi,ε:=lnri,εT<0 for ε[0,ε0). Similar to the proof of [18,Lemma 3.2], there is positive T-periodic function νεi(x,t) such that ωεi(x,t)=eμi,ενεi(x,t) satisfies (3.5). Since μi,ε<0, limtωεi(x,t)=0 uniformly for xΩ.

    For xΩ, t>0, one has

    {Ii(x,t)tDiΔIi(x,t)hi(x,t)Ii(x,t)   +τi0fi(a)ΩΓi(x,y,t,ta)(βi(y,ta)+ε)Ii(y,ta)dyda,    xΩ, t>0,Ii(x,t)n=0, xΩ, t>0. (3.6)

    For any given initial distribution ψD+τ, due to the boundedness of Ii(x,t;ψ), there exists α>0 such that Ii(x,t;ψ)αωεi(x,t), t[kT,kT+τ], xˉΩ, and hence, Ii(x,t;ψ)αωεi(x,t) for tkT+τ. Then limtIi(x,t;ψ)=0 and limtR(x,t;ψ)=0 for all xˉΩ. Furthermore, similar to the proof of (1), we have

    limt(S(,t;ψ),Ii(,t;ψ),R(,t;ψ))(S(,t),0,0)∥=0.

    (3) Let

    Wi0={ψ=(ψS,ψi,ψR)D+τ:ψi(,0)0},
    Wi0:=D+τWi0={ψ=(ψS,ψi,ψR)D+τ:ψi(,0)0}.

    Define Φt:D+τD+τ by Φt(ψ)(x,s)=(S(x,t+s;ψ),Ii(x,t+s;ψ),R(x,t+s;ψ)). By Theorem 3.6, we know that Ii(x,t+s;ψ)>0 for any ψW0i, xˉΩ and t>0. Thus there exists kN such that Φkn0T(Wi0)Wi0. Define

    Mi:={ψWi0:Φkn0T(ψ)Wi0, kN}.

    Let M:=(S,0,0) and ω(ψ) be the omega limit set of the orbit γ+:={Φkn0T(ψ):kN}. For any given ψMi, we have Φkn0T(ψ)Wi0. Thus Ii(x,t;ψ)0, xˉΩ, t0. Therefore R(x,t;ψ)0 for any xˉΩ and t0. By similar arguments as the proof of (1), we have

    limt(S(,t;ψ),Ii(,t;ψ),R(,t;ψ))(S(,t),0,0)∥=0.

    That is ω(ψ)=M for any ψMi.

    For sufficient small ˉθ>0, consider the following system:

    {vθi(x,t)t=DiΔvθi(x,t)hi(x,t)vθi(x,t)   +τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)(S(y,ta)ˉθ)S(y,ta)+ˉθvθi(y,ta)dyda,    xΩ, t>0,vθi(x,s)=ψi(x,s), ψiQ+, xΩ, s[τi,0],vθi(x,t)n=0, xΩ, t>0. (3.7)

    Let vθi(x,t;ψi) be the solution of (3.7). Note vθi,n0T(ψi)(x,s)=vθi(x,s+n0T;ψi) for all xΩ and s[τi,0]. Define the poincarˊe map (χiθ)n0:Q+Q+ by (χiθ)n0(ψi)=vθi,n0T(ψi). It is easy to prove that (χiθ)n0 is a compact, strongly positive operator. Let (riθ)n0 be the spectral radius of (χiθ)n0. According to [15,Theorem 7.1], there is a positive eigenvalue (riθ)n0 and a positive eigenfunction ˜φi such that (χiθ)n0=(riθ)n0˜φi. Since Ri0>1, it follows from Theorem 2.1 that ri>1. Then there exists a sufficient small number θ1>0 such that riθ>1 for θ(0,θ1).

    By the continuous dependence of solutions on initial value, there exists θ0(0,θ1) such that

    S(x,t;ϕ),Ii(x,t;ϕ),R(x,t;ϕ)(S(x,t),0,0)<ˉθ, xˉΩ, t[0,T],

    if

    (ϕS(x,s),ϕi(x,s),ϕR(x,s))(S(x,s),0,0)<θ0, xˉΩ, s[τi,0].

    Claim. M is a uniformly weak repeller for Wi0, that is,

    lim supkΦkn0T(ψ)Mθ0, ψWi0.

    Suppose, by contradiction, there exists ψ0Wi0 such that

    lim supkΦkn0T(ψ)M<θ0.

    Then there exist a k0N such that

    |S(x,kn0T+s;ψ0)S|<θ0, |Ii(x,kn0T+s;ψ0|<θ0,|R(x,kn0T+s;ψ0|<θ0, xˉΩ, s[τi,0], kk0.

    According to (3.11), for any t>kn0T and xˉΩ,

    Sˉθ<S(x,t;ψ0)<S+ˉθ, 0<Ii(x,t;ψ0)<ˉθ, 0<R(x,t;ψ0)<ˉθ.

    Therefore, for Ii-equation of (3.1), we have

    Ii(x,t)tDiΔIi(x,t)hi(x,t)Ii(x,t)   +τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)(S(y,ta)ˉθ)S(y,ta)+ˉθIi(y,ta)dyda,    xΩ,t>(k0+1)n0T. (3.8)

    Since

    Ii(x,t;ψ0)>0, xˉΩ, t>(k0+1)n0T,

    there exist some κ>0, such that

    Ii(x,(k0+1)n0T+s;ψ0)κ˜φi(x,s), xˉΩ, s[τi,0].

    By (3.12) and the comparison principle, we have

    Ii(x,t+s;ψ0)κνθi(x,t(k0+1)n0T+s;˜φi), xˉΩ, t>(k0+1)n0T.

    Therefore, we have

    Ii(x,kn0T+s;ψ0)κνθi(x,k(k0+1)n0T+s;˜φi)=κ(riθ)(kk01)n0˜φi(x,s), (3.9)

    where kk0+1, s[τi,0]. Since ˜φi(x,s)>0 for (x,s)ˉΩ×[τi,0], there is (xi,si)ˉΩ×[τi,0] such that ˆφi(xi,si)>0. It follows from (riθ)n0>1 that Ii(xi,kn0T+si;ψ0)+ as k, which contradicts to Ii(x,t;ψ0)(0,ˉθ).

    Let WS(M) be the stable set of M. In conclusion, WS(M)=Mi; M is an isolated invariant set for Φn0T in Wi0; WS(M)Wi0=MiWi0=. According to [40,Theorem 1.3.1] and [40,Remark 1.3.1], one has there is ˉσ>o such that infd(ω(ψ),Wi0)ˉσ for any ψWi0. That is lim inftd(Φkn0T,Wi0)ˉσ for any ψWi0. Therefore, Φn0T:D+τD+τ is uniformly persistent with respect to (Wi0,Wi0). Similar to Theorem 2.1, it can be proved that the solution ˉS(x,t;ψ) of 3.1 is globally bounded for any ψD+τ. Therefore, Φn0T:D+τD+τ is point dissipative. It is easy to prove that Φn0T is compact on Wi0 for n0T>τi. It follows from [40,Section 1.1] that the compact map Φn0T is an αcontraction of order 0, and an αcontraction of order 0 is αcondensing. Then according to [23,Theorem 4.5], Φn0T:Wi0Wi0 admits a compact global attractor Zi0.

    Similar to the proof of [22,Theroem 4.1], let P:D+τ[0,+) by

    P(ψ)=minxˉΩψi(x,0), ψD+τ.

    Since Φn0T(Zi0)=Zi0, we have that ψi(,0)>0 for any ψZi0. Let Bi:=t[0,n0T]Φt(Zi0), then BiWi0. In addition, we get limtd(Φt(ψ),Bi)=0 for all ψWi0. Since Bi is a compact subset of Wi0, we have minψBiP(ψ)>0. Thus, there exists a σ>0 such that lim inftIi(,t;ψ)σ. Furthermore, according to Theorem 3.6, there exists M>0 such that lim inftIi(,t;ψ)M.

    Consider the following equation:

    {ˉS(x,t)t=DˉSΔˉS(x,t)+μ(x,t)d(x,t)ˉS(x,t)β1(x,t)ˉS(x,t)β2(x,t)ˉS(x,t), xΩ, t>0,ˉS(x,t)n=0, xΩ, t>0, i=1,2. (3.10)

    According to [36,Lemma 2.1], equation (3.10) admits a unique positive solution ˉS, which is T-periodic with respect to tR. Obviously, for the S-equation of (2.6), we have

    {S(x,t)tDSΔS(x,t)+μ(x,t)d(x,t)S(x,t)β1(x,t)S(x,t),β2(x,t)S(x,t), xΩ, t>0,S(x,t)n=0, xΩ, t>0, i=1,2. (3.11)

    It follows from the comparison principle, one has

    lim inftS(x,t)ˉS(x,t), xˉΩ.

    According to Theorem 2.1, there exist constants B1,B2 and lR, such that

    Ii(x,t;ϕ)B1(i=1,2), R(x,t;ϕ)B2

    for tlRT+τ. Consider the following equation:

    {ui(x,t)t=DiΔui(x,t)hi(x,t)ui(x,t)+τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)ˉS(x,t)ˉS(x,t)+B1+B2ui(y,ta)dyda, xΩ, t>0,ui(x,t)n=0, xΩ, t>0, i=1,2. (3.12)

    Let ui(x,t;ϕi) be the solution of (3.12) for ϕiQ,(x,s)ˉΩ×[τ,0]. Define ˉPi:QQ by ˉPi(ϕi)=ui,T(ϕi) for any ϕiQ, where ui,T(ϕi)(x,t)=ui(x,s+T;ϕi), (x,s)ˉΩ×[τ,0]. Let ρ0i be the spectral of ˉPi. We define the linear operator ˉLi:CTCT by:

    ˉLi(ψi)(x,t)=τi0fi(a)ΩΓi(x,y,t,ta)βi(y,ta)S(x,t)S(x,t)+B1+B2a(Vi(ta,ts)ψi(ts))(y)dsdyda.

    Then the operator ˉLi is positive and bounded on CT(ˉΩ×R,R). Let r(ˉLi) denote the spectral radius of ˉLi. Similar to [18,20], define the invasion number ˆRi0 for strain i by ˆRi0:=r(ˉLi), and we have the following result.

    Theorem 3.5. The signs of ˆRi01 and ρ0i1 are same.

    By the arguments similar to those in the proof of [38,Proposition 5.10], we further have the following observation.

    Theorem 3.6. If ˆRi0>1, then Ri0>1, i=1,2.

    Theorem 3.7. Suppose that ˆRi0>1(i=1,2). Then for any ψ=(ψS,ψ1,ψ2,ψR)C+τ, ψi0(i=1,2), there is an η>0 such that

    lim inftS(x,t;ψ)η, lim inftIi(x,t;ψ)η, i=1,2.

    Proof. According to Theorem 3.6 and ˆRi0>1(i=1,2), one has Ri0>1(i=1,2). Let

    Z0={ψ=(ψS,ψ1,ψ2,ψR)C+τ:ψ1(,0)0  ψ2(,0)0},
    Z0:=C+τW0={ψ=(ψS,ψ1,ψ2,ψR)C+τ:ψ1(,0)0  ψ2(,0)0},

    and

    Z:={ψZ0:Φkn0T(ψ)Z0, kN}.

    Define Φt:C+τC+τ by Φt(ψ)(x,s)=˜S(x,t+s;ψ), ψC+τ and Φkn0T(ψ):=˜S(x,n0T+s;ψ) for kN and (x,s)ˉΩ×[τ,0]. It is easy to obtain that Φt(Z0)Z0 for t>0. Let

    E0:=(ˉS,0,0,0), E1:={(ψS,ψ1,0,ψR)}, E2:={(ψS,0,ψ2,ψR)},

    and ˉω(ψ) denotes the omega limit set of the orbit γ+:={Φkn0T(ψ):kN} for ψZ, we then have the following claims.

    Claim 1. ψZˉω(ψ)=E0E2E2.

    For any Φkn0T(ψ)Z, it can be see that Φkn0T(ψ)Z, kN. Then I1(x,t;ψ)0 or I2(x,t;ψ)0 for xˉΩ and t>0. Suppose, by contradiction, if there exists ti>0 such that Ii(x,t;ψ)0 on xˉΩ, i=1,2. Then the strong positivity of Vi(t,s)(t>s) implies that Ii(x,t;ψ)>0 for all t>ti and xˉΩ, i=1,2, which contradicts with the fact Φkn0T(ψ)Z. If I1(x,t;ψ)0 on (x,t)ˉΩ×R+, it follows from Theorem 3.7 that ˉω(ψ)=E0E2. If I2(x,t;ψ)0 on (x,t)ˉΩ×R+. Similarly, one has ˉω(ψ)=E0E1. Therefore, Claim 1 holds.

    Claim 2. E0 is a uniformly weak repeller for Z0, in the sense that,

    lim supkΦkn0T(ψ)E0|ε0, ψZ0

    for ε0>0. The proof of Claim 2 is similar to those in Theorem 3.4(3), so we omit it.

    Claim 3. E1 and E2 is a uniformly weak repeller for Z0, in the sense that,

    lim supkΦkn0T(ψ)Ei|ε0, ψZ0, i=1,2

    for some ε0>0 small enough. We only give the proof for E1, the proof of E2 is similar. Due to Theorem 2.1, there are B1,B2 and lR0, such that

    Ii(x,t;ϕ)B1(i=1,2), R(x,t;ϕ)B2

    for tlRT+τ. For sufficient small ε>0, we consider the following system:

    {ωε2t=D2Δωε2(x,t)h2(x,t)ωε2(x,t)+τ20f2(a)ΩΓ2(x,y,t,ta)β2(y,ta)ˉS(x,t)εˉS(x,t)+B1+B2ωε2(y,ta)dyda, xΩ, t>0,ωε2n=0, xΩ, t>0, i=1,2, (3.13)

    where ˉS is the positive periodic solution of (3.11). Let ωε2(x,t;ψ2) be the solution of (3.13) with initial data ωε2(x,s)=ψ2(x,s), ψ2Q+, xΩ, s[τ,0]. Note ωε2,n0T(ψ2)(x,s)=ωε2(x,s+n0T;ψ2) for all xΩ and s[τ1,0]. Define (Ψε2)n0:Q+Q+ by (Ψε2)n0(ψ2)=ωε2,n0T(ψ2). Let ˆr2ε and (ˆr2ε)n0 be the spectral radius of Ψε2 and (Ψε2)n0, respectively. It is easy to prove that (Ψε2)n0 is compact, strongly positive operator. According to [15,Theorem 7.1], we get that (Ψε2)n0 admits a positive and simple eigenvalue (ˆr2ε)n0 and a positive eigenfunction φ2 satisfying (Ψε2)n0=(ˆr2ε)n0φ2. Since R20>1, it follows from Theorem 3.5 that ρ02>1, then there exists a sufficient small number ε1>0 such that r2ε>1 for any ε(0,ε1).

    By the continuous dependence of solution on initial value, there exists ε0(0,ε1) such that

    ΦkT(ψ)E1<ˉε, xˉΩ, t[0,T], (3.14)

    if

    ϕ(x,s)E1<ε0, xˉΩ, s[τ,0].

    Suppose, by contradiction, there exists ψ0W0 such that

    lim supkΦkn0T(ψ)E1<ε0.

    That is, there is k0N such that

    ˉSˉε<S(x,t;ψ0)<ˉS+ˉε; 0<I1(x,t;ψ0)<B1;

    and

    0<I2(x,t;ψ0)<ˉε; 0<R(x,t;ψ0)<B2

    for all kk0. Therefore, for I2-equation of (2.6), we have

    I2(x,t)tD2ΔI2(x,t)h2(x,t)I2(x,t)+τ20f1(a)ΩΓ2(x,y,t,ta)β2(y,ta)ˉS(y,ta)ˉεˉS+B1+B2I2(y,ta)dyda (3.15)

    for xΩ and t>(k0+1)n0T. Since

    I2(x,t;ψ0)>0, xˉΩ, t>(k0+1)n0T,

    there is some κ>0, such that

    I2(x,(k0+1)n0T+s;ψ0)κφ2(x,s), xˉΩ, s[τ2,0].

    By (3.15) and the comparison principle, we have

    I2(x,t+s;ψ0)ωε2(x,t(k0+1)n0T+s;φ2), xˉΩ, t>(k0+1)n0T.

    Therefore, we have

    I2(x,kn0T+s;ψ0)κωε2(x,k(k0+1)n0T+s;φ2)=κ(ˆr2ε)(kk01)n0φ2(x,s), (3.16)

    where kk0+1, s[τ2,0]. Since φ2(x,s)>0 for (x,s)ˉΩ×[τ2,0], there is (x2,s2)ˉΩ×[τ2,0] such that φ2(x2,s2)>0. It follows from (r2ε)n0>1 that I2(x2,kn0T+s2;ψ0)+ as k, which contradicts to I2(x,t;ψ0)(0,ˉε).

    Let Θ:=E0E1E2, WS(Θ) be the stable set of Θ. In conclusion, WS(Θ)=Z; Θ is an isolated invariant set for Φn0T in Z0, WS(Θ)Z0=ZZ0=. According to [10,Theorem 1.3.1] and [10,Remark 1.3.1], there exists ˉσ>0 such that infd(ω(ψ),Z0)ˉσ for all \psi\in Z_0 . That is, \underset {t\rightarrow \infty }{\liminf }d(\Phi_{n_0T}^k, \partial Z_0)\ge \bar{\sigma} for any \psi\in Z_0 . Therefore, \Phi_{n_0T}:C_{\tau } ^+\rightarrow C_{\tau}^+ is uniformly persistent with respect to (Z_0, \partial Z_0) . Similar to Theorem 2.1 , it can be proved that the solution \tilde{S}(x, t;\psi) of (2.6) is globally bounded for any \psi\in D_{\tau}^+ . Therefore, \Phi_{n_0T}:C_{\tau}^+\rightarrow C_{\tau}^+ is point dissipative. It is easy to prove that \Phi_{n_0T} is compact on Z_0 for n_0T > \tau_1 . It then follows from [40,Section 1.1] that the compact map \Phi_{n_0T} is an \alpha- contraction of order 0 , and an \alpha- contraction of order 0 is \alpha- condensing. Then according to [23,Theorem 4.5], we obtain that \Phi_{n_0T}: Z_0\rightarrow Z_0 admits a compact global attractor N_0 .

    Similar to the proof of [22,Theroem 4.1], let P:C_{\tau }^+\rightarrow [0, +\infty) by

    P(\psi) = \min \{ \mathop {\min }\limits_{x \in \bar \Omega } {\psi _1}(x,0),\mathop {\min }\limits_{x \in \bar \Omega } {\psi _2}(x,0)\} , \ \forall \psi\in C_{\tau}^+.

    Since \Phi_{n_0T}(N_0) = N_0 , we have \psi_i(\cdot, 0) > 0 for any \psi \in N_0 . Let B_0: = \underset {t\in [0, n_0T]}{\cup}\Phi_t(N_0) , then B_0\subseteq Z_0 . In addition, we get \underset {t\rightarrow \infty }{\lim}d(\Phi_t(\psi), B_0) = 0 for all \psi\in Z_0 . Since B_0 is a compact subset of Z_0 . We have \underset {\psi\in B_0}{\min}P(\psi) > 0 . Thus, there exists \eta > 0 such that \underset {t\rightarrow \infty }{\liminf}I_1(\cdot, t; \psi)\ge \eta .

    In this subsection, under the condition that the invasion numbers on two strains are greater than 1, it is proved that two strains will always persist uniformly. By the arguments similar to those in the proof of Theorems 3.7 and 3.2, we have the following observations.

    Theorem 3.8. Suppose that \tilde{S}(x, t;\psi) = (S(x, t;\psi), I_1(x, t;\psi), I_2(x, t;\psi), R(x, t;\psi)) is the solution of (2.6) with initial data \psi = (\psi_S, \psi_1, \psi_2, \psi_R)\in C_{\tau} . If R_0^1 > 1 > R_0^2 and \psi_1(\cdot, 0)\not \equiv0 , then

    \underset {t\rightarrow \infty }{\lim}I_2(x, t;\psi) = 0,

    and there is P > 0 such that

    \begin{equation} \underset {t\rightarrow \infty }{\liminf}I_1(x, t;\psi)\ge P, \end{equation} (3.17)

    uniformly for x\in \bar{\Omega} .

    Theorem 3.9. Suppose that R_0^1 > 1 = R_0^2 and \beta_2(x, t) > 0 on (x, t)\in \bar{\Omega}\times [0, \infty) . If C_{\tau}^+ satisfies \psi_1(\cdot, 0)\not \equiv0 , then we have

    \underset {t\rightarrow \infty }{\lim}I_2(x, t;\psi) = 0,

    and there is P > 0 such that

    \underset {t\rightarrow \infty }{\liminf}I_1(x, t;\psi)\ge P,

    uniformly for x\in \bar{\Omega} .

    Theorem 3.10. Suppose that R_0^2 > 1 > R_0^1 , if \psi\in C_{\tau}^+ satisfies \psi_2(\cdot, 0)\not \equiv0 , then we have

    \underset {t\rightarrow \infty }{\lim}I_1(x, t;\psi) = 0,

    and there is P > 0 such that

    \begin{equation} \underset {t\rightarrow \infty }{\liminf}I_2(x, t;\psi)\ge P, \end{equation} (3.18)

    uniformly for x\in \bar{\Omega} .

    Theorem 3.11. Suppose that R_0^2 > 1 = R_0^1 and \beta_1(x, t) > 0 on (x, t)\in \bar{\Omega}\times [0, \infty) . If \psi\in C_{\tau}^+ satisfies \psi_2(\cdot, 0)\not \equiv0 , then we have

    \underset {t\rightarrow \infty }{\lim}I_1(x, t;\psi) = 0,

    and there is P > 0 such that

    \underset {t\rightarrow \infty }{\liminf}I_2(x, t;\psi)\ge P,

    uniformly for x\in \bar{\Omega} .

    Finally, we show that the periodic solution (S^*, 0, 0, 0) of (2.6) is globally attractive under some conditions.

    Theorem 3.12. Suppose that R_0^i < 1 for i = 1, 2 . Then the periodic (S^*, 0, 0, 0) of (2.6) is globally attractive.

    Proof. Due to R_0^i < 1, \ i = 1, 2 , similar to Theorem 3.4, one has

    \underset {t\rightarrow \infty }{\lim}I_i(x, t; \psi) = 0, \ \forall x\in \bar{\Omega}, \ \psi\in C_{\tau}^+, \ i = 1, 2.

    By using the theory of chain transitive sets, we get

    \underset {t\rightarrow \infty }{\lim}S(x, t; \psi) = S^*(x, t), \forall x\in \bar{\Omega}, \ \psi\in C_{\tau}^+.

    Therefore

    \underset {t\rightarrow \infty }{\lim }\parallel( S(\cdot , t;\psi), I_1(\cdot , t;\psi) , I_2(\cdot , t;\psi), R(\cdot , t;\psi) )-\left(S^*(\cdot, t), 0, 0, 0\right)\parallel = 0.

    That is (S^*, 0, 0, 0) is globally attractive.

    Theorem 3.13. Suppose that R_0^i = 1 and \beta_i(x, t) > 0 on \bar{\Omega}\times[0, \infty) for both i = 1, 2 . Then the periodic (S^*, 0, 0, 0) of (2.6) is globally attractive.

    Proof. The proof is similar to Theorem 3.12 by using Theorem 3.2.

    Combining Theorem 3.12 with Theorem 3.13, furthermore, we have the following conclusion.

    Theorem 3.14. If R_0^i < 1, \ R_0^j = 1 and \beta_j(x, t) > 0 on (x, t)\in \bar{\Omega}\times[0, \infty), \ i, j = 1, 2, \ i\neq j , then the periodic (S^*, 0, 0, 0) of (2.6) is globally attractive.

    In this paper, we proposed and investigated a two-strain SIRS epidemic model with distributed delay and spatiotemporal heterogeneity. The model is well suitable for simulating the pathogen mutation which is widely founded in variety viral infectious diseases. We have to remark that when the spatiotemporal heterogeneity and distributed delay are incorporated simultaneously, the analysis for the model becomes more difficult. To overcome these difficulties, we used the theory of chain transitive sets and persistence. After introducing the basic reproduction number R_0^i and the invasion number \hat{R}_0^i for each strain i , i = 1, 2 , we established the threshold dynamics for single-strain model and two-strain model, respectively. For the single-strain case, the threshold dynamics results shows that the basic reproduction number R_0^i is a threshold to determine whether the strain i can be persistent. In addition, in such case, we obtained a sufficient condition for the global attraction of the disease free equilibrium when R_0^i = 1 , i = 1, 2 . Under the condition that two strains is incorporated, we showed that if both of the invasion numbers \hat{R}_0^i are all larger than unit, then the two strains will be persistent uniformly. However, if only one of the reproduction numbers is larger than unit, that is, the other is less than unit, then the strain with larger reproduction number persists, while the strain with the smaller reproduction number dies out. This phenomenon is so called "competitive exclusion"[33]. Further, if both of the two reproduction numbers R_0^i are all less than unit, then the corresponding disease free equilibrium is globally attractive.

    Apparently, the dynamical properties of the two-strain model are much more complicated than that of the single-strain case. The most fascinating phenomenon is the appearance of "competitive exclusion" in the two strain model. Generally speaking, the strain with highest basic reproduction number will eliminate the other strain. As is well known, in reality, proper vaccination is a critical for the prevention and control of the most viral infectious disease. Thereby, with the mutating of viruses, the main thing is to ensure the vaccine as safe and effective as possible. However, it is easy to make vaccine administration error. Although some improperly administered vaccines may be valid, sometimes such errors increases the possibility of vaccine recipients being unprotected against viral infection. This paper incorporated the distributed delay, seasonal factor effects and spatial heterogeneity into a two-strain SIRS simultaneously, so the model is more in line with reality. Further, based on these realistic factors, we obtained some valuable results for proper vaccination to viral infection theoretically.

    The first author was supported by the innovation fund project for colleges and universities of Gansu Province of China (2021B-254), the second author was supported by NSF of China (12071193) and Natural Science Foundation of Gansu Province of China (21JR7RA549).

    The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



    [1] A. Ackleh, K. Deng, Y. Wu, Competitive exclusion and coexistence in a two-strain pathogen model with diffusion, Math. Biosci. Eng., 13 (2016), 1–18. http://dx.doi.org/10.3934/mbe.2016.13.1 doi: 10.3934/mbe.2016.13.1
    [2] P. Agarwal, J. J. Nieto, M. Ruzhansky, D. F. Torres, Analysis of infectious disease problems (Covid-19) and their global impact, Singapore: Springer Nature Singapore Pte Ltd, 2021. http://dx.doi.org/10.1007/978-981-16-2450-6
    [3] S. Altizer, A. Dobson, P. Hosseini, P. Hudson, M. Pascua, P. Rohani, Seasonality and the dynamics of infectious disease, Ecol. Lett., 9 (2006), 467–484. http://dx.doi.org/10.1111/j.1461-0248.2005.00879.x doi: 10.1111/j.1461-0248.2005.00879.x
    [4] I. A. Baba, B. Kaymakamzade, E. Hincal, Two-strain epidemic model with two vaccinations, Chaos Soliton. Fract., 106 (2018), 342–348. http://dx.doi.org/10.1016/j.chaos.2017.11.035 doi: 10.1016/j.chaos.2017.11.035
    [5] L. Bauer, J. Bassett, P. H\ddot{o}vel, Y. N. Kyrychko, k. B. Blyuss, Chimera states in multi-strain epidemic models with temporary immunity, Chaos, 27 (2017), 114317. http://dx.doi.org/10.1063/1.5008386 doi: 10.1063/1.5008386
    [6] L. Cai, J. Xiang, X. Z. Li, A. A. Lashari, A two-strain epidemic model with mutant strain and vaccination, J. Appl. Math. Comput., 40 (2012), 125–142. http://dx.doi.org/10.1007/s12190-012-0580-x doi: 10.1007/s12190-012-0580-x
    [7] M. X. Chang, B. S. Han, X. M. Fan, Spatiotemporal dynamics for a Belousov-Zhabotinsky reaction-diffusion system with nonlocal effects, Appl. Anal., 2021. https://doi.org/10.1080/00036811.2020.1869948
    [8] Z. W. Chen, Z. T. Xu, A delayed diffusive influenza model with two-strain and two vaccinations, Appl. Math. Comput., 349 (2019), 439–453. http://dx.doi.org/10.1016/j.amc.2018.12.065 doi: 10.1016/j.amc.2018.12.065
    [9] D. Dancer, P. Koch Medina, Abstract ecolution equations, Periodic problem and applications, Essex: Longman Scientific & Technical, 1992.
    [10] P. van den Driessche, J. Watmough, Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission, Math. Biosci., 180 (2002), 29–48. http://dx.doi.org/10.1016/S0025-5564(02)00108-6 doi: 10.1016/S0025-5564(02)00108-6
    [11] A. Friedman, Partial differential equations of parabolic type, Englewood Cliffs: Prentice-Hall, 1964.
    [12] Z. Guo, F. Wang, X. Zou, Threshold dynamics of an infective disease model with a fixed latent period and non-local infections, J. Math. Biol., 65 (2012), 1387–1410. http://dx.doi.org/10.1007/s00285-011-0500-y doi: 10.1007/s00285-011-0500-y
    [13] B. S. Han, Y. Yang, W. J. Bo, H. Tang, Global dynamics of a Lotka-Volterra competition diffusion system with nonlocal effects, Int. J. Bifurcat. Chaos, 30 (2020), 2050066. http://dx.doi.org/10.1142/S0218127420500662 doi: 10.1142/S0218127420500662
    [14] B. S. Han, Z. Feng, W. J. Bo, Traveling wave phenomena of a nonlocal reaction-diffusion equation with degenerate nonlinearity, Commun. Nonlinear Sci., 103 (2021), 105990. http://dx.doi.org/10.1016/j.cnsns.2021.105990 doi: 10.1016/j.cnsns.2021.105990
    [15] P. Hess, Periodic-parabolic boundary value problems and positivity, Essex: Longman Scientific & Technical, 1991.
    [16] H. W. Hethcote, Asymptotic behavior in a deterministic epidemic model, B. Math. Biol., 36 (1973), 607–614. http://dx.doi.org/10.1007/BF02458365 doi: 10.1007/BF02458365
    [17] M. W. Hirsch, H. L. Smith, X. Q. Zhao, Chain transitivity, attractivity and strong repellors for semidynamical systems, J. Dyn. Differ. Equ., 13 (2001), 107–131. http://dx.doi.org/10.1023/A:1009044515567 doi: 10.1023/A:1009044515567
    [18] Y. Jin, X. Q. Zhao, Spatial dynamics of a nonlocal periodic reaction-diffusion model with stage structure, SIAM J. Math. Anal., 40 (2009), 2496–2516. http://dx.doi.org/10.1137/070709761 doi: 10.1137/070709761
    [19] C. Leung, The difference in the incubation period of 2019 novel coronavirus (SARS-CoV-2) infection between travelers to Hubei and nontravelers: The need for a longer quarantine period, Infect. Cont. Hosp. Ep., 41 (2020), 594–596. http://dx.doi.org/10.1017/ice.2020.81 doi: 10.1017/ice.2020.81
    [20] X. Liang, X. Q. Zhao, Asymptotic speeds of spread and traveling waves for monotone semiflows with applications, Commun. Pure Appl. Math., 60 (2007), 1–40. http://dx.doi.org/10.1002/cpa.20154 doi: 10.1002/cpa.20154
    [21] X. Liang, L. Zhang, X. Q. Zhao, Basic reproduction ratios for periodic abstract functional differential equations (with application to a spatial model for lyme disease), J. Dyn. Differ. Equ., 31 (2019), 1247–1278. http://dx.doi.org/10.1007/s10884-017-9601-7 doi: 10.1007/s10884-017-9601-7
    [22] Y. Lou, X. Q. Zhao, Threshold dynamics in a time-delayed periodic SIS epidemic model, Discrete Cont. Dyn. B, 12 (2009), 169–186. http://dx.doi.org/10.3934/dcdsb.2009.12.169 doi: 10.3934/dcdsb.2009.12.169
    [23] P. Magal, X. Q. Zhao, Global attractors and steady states for uniformly persistent dynamical systems, SIAM J. Math. Anal., 37 (2005), 251–275. http://dx.doi.org/10.1137/S0036141003439173 doi: 10.1137/S0036141003439173
    [24] M. Martcheva, A non-autonomous multi-strain SIS epidemic model, J. Biol. Dynam., 3 (2009), 235–251. http://dx.doi.org/10.1080/17513750802638712 doi: 10.1080/17513750802638712
    [25] R. Martain, H. L. Smith, Abstract functional differential equations and reaction-diffusion system, T. Am. Math. Soc., 321 (1990), 1–44. http://dx.doi.org/10.2307/2001590 doi: 10.2307/2001590
    [26] R. H. Martin, Nonlinear operators and differential equations in Banach spaces, 1986.
    [27] C. McAloon, Á. Collins, K. Hunt, A. Barber, F. Butler, M. Casey, et al., Incubation period of COVID-19: A rapid systematic review and meta-analysis of observational research, BMJ open, 10 (2020), e039652. http://dx.doi.org/10.1136/bmjopen-2020-039652 doi: 10.1136/bmjopen-2020-039652
    [28] J. A. J. Metz, O. Diekmann, The dynamics of physiologically structured populations, Springer, 1986. http://dx.doi.org/10.1007/978-3-662-13159-6
    [29] R. Peng, X. Q. Zhao, A reaction-diffusion SIS epidemic model in a time-periodic environment, Nonlinearity, 25 (2012), 1451–1471. http://dx.doi.org/10.1088/0951-7715/25/5/1451 doi: 10.1088/0951-7715/25/5/1451
    [30] P. J. Sansonetti, J. Arondel, Construction and evaluation of a double mutant of Shigella flexneri as a candidate for oral vaccination against shigellosis, Vaccine, 7 (1989), 443–450. http://dx.doi.org/10.1016/0264-410X(89)90160-6 doi: 10.1016/0264-410X(89)90160-6
    [31] H. L. Smith, Multiple stable subharmonics for a periodic epidemic model, J. Math. Biol., 17 (1983), 179–190. http://dx.doi.org/10.1007/BF00305758 doi: 10.1007/BF00305758
    [32] Y. Takeuchi, W. Ma, E. Beretta, Global asymptotic properties of delay SIR epidemic model with finite incubation times, Nonlinear Anal., 42 (2000), 931–947. http://dx.doi.org/10.1016/S0362-546X(99)00138-8 doi: 10.1016/S0362-546X(99)00138-8
    [33] N. Tuncer, M. Martcheva, Analytical and numerical approaches to coexistence of strains in a two-strain SIS model with diffusion, J. Biol. Dynam., 6 (2012), 406–439. http://dx.doi.org/10.1080/17513758.2011.614697 doi: 10.1080/17513758.2011.614697
    [34] H. Xi, H. Jiang, M. Juhas, Y. Zhang, Multiplex biosensing for simultaneous detection of mutations in SARS-CoV-2, ACS Omega, 6 (2021), 25846–25859. http://dx.doi.org/10.1021/acsomega.1c04024 doi: 10.1021/acsomega.1c04024
    [35] X. Yang, H. Li, Y. Cao, Influence of meteorological factors on the COVID-19 transmission with season and geographic location, Int. J. Environ. Res. Public. Health, 18 (2021), 484. http://dx.doi.org/10.3390/ijerph18020484 doi: 10.3390/ijerph18020484
    [36] L. Zhang, Z. C. Wang, X. Q. Zhao, Threshold dynamics of a time periodic reaction-diffusion epidemic model with latent period, J. Differ. Equ., 258 (2015), 3011–3036. http://dx.doi.org/10.1016/j.jde.2014.12.032 doi: 10.1016/j.jde.2014.12.032
    [37] T. Zhang, Z. Teng, On a nonautonomous SEIR model in epidemiology, B. Math. Biol., 69 (2007), 2537–2560. http://dx.doi.org/10.1007/s11538-007-9231-z doi: 10.1007/s11538-007-9231-z
    [38] L. Zhao, Z. C. Wang, S. Ruan, Dynamics of a time-periodic two-strain SIS epidemic model with diffusion and latent period, Nonlinear Anal. Real, 51 (2020), 102966. http://dx.doi.org/10.1016/j.nonrwa.2019.102966 doi: 10.1016/j.nonrwa.2019.102966
    [39] L. Zhao, Z. C. Wang, L. Zhang, Threshold dynamics of a time periodic and two-group epidemic model with distributed delay, Math. Biosci. Eng., 14 (2017), 1535–1563. http://dx.doi.org/10.3934/mbe.2017080 doi: 10.3934/mbe.2017080
    [40] X. Q. Zhao, Dynamical systems in population biology, New York: Springer, 2003. http://dx.doi.org/10.1007/978-0-387-21761-1
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