Loading [MathJax]/jax/element/mml/optable/BasicLatin.js
Research article Special Issues

Equilibrium properties of a coupled contagion model of mosquito-borne disease and mosquito preventive behaviors

  • Received: 01 February 2025 Revised: 20 May 2025 Accepted: 27 May 2025 Published: 18 June 2025
  • Although different strategies for mosquito-borne disease prevention can vary significantly in their efficacy and scale of implementation, they all require that individuals comply with their use. Despite this, human behavior is rarely considered in mathematical models of mosquito-borne diseases. Here, we sought to address that gap by establishing general expectations for how different behavioral stimuli and forms of mosquito prevention shape the equilibrium prevalence of disease. To accomplish this, we developed a coupled contagion model tailored to the epidemiology of dengue and preventive behaviors relevant to it. Under our model's parameterization, we found that mosquito biting was the most important driver of behavior uptake. In contrast, encounters with individuals experiencing disease or engaging in preventive behaviors themselves had a smaller influence on behavior uptake. The relative influence of these three stimuli reflected the relative frequency with which individuals encountered them. We also found that two distinct forms of mosquito prevention—namely, personal protection and mosquito density reduction—mediated different influences of behavior on equilibrium disease prevalence. Our results highlight that unique features of coupled contagion models can arise in disease systems with distinct biological features.

    Citation: Marya L. Poterek, Mauricio Santos-Vega, T. Alex Perkins. Equilibrium properties of a coupled contagion model of mosquito-borne disease and mosquito preventive behaviors[J]. Mathematical Biosciences and Engineering, 2025, 22(8): 1875-1897. doi: 10.3934/mbe.2025068

    Related Papers:

    [1] Chentong Li, Jinyan Wang, Jinhu Xu, Yao Rong . The Global dynamics of a SIR model considering competitions among multiple strains in patchy environments. Mathematical Biosciences and Engineering, 2022, 19(5): 4690-4702. doi: 10.3934/mbe.2022218
    [2] Maoxing Liu, Yuhang Li . Dynamics analysis of an SVEIR epidemic model in a patchy environment. Mathematical Biosciences and Engineering, 2023, 20(9): 16962-16977. doi: 10.3934/mbe.2023756
    [3] Siyu Liu, Yong Li, Yingjie Bi, Qingdao Huang . Mixed vaccination strategy for the control of tuberculosis: A case study in China. Mathematical Biosciences and Engineering, 2017, 14(3): 695-708. doi: 10.3934/mbe.2017039
    [4] Lili Liu, Xi Wang, Yazhi Li . Mathematical analysis and optimal control of an epidemic model with vaccination and different infectivity. Mathematical Biosciences and Engineering, 2023, 20(12): 20914-20938. doi: 10.3934/mbe.2023925
    [5] Mostafa Adimy, Abdennasser Chekroun, Claudia Pio Ferreira . Global dynamics of a differential-difference system: a case of Kermack-McKendrick SIR model with age-structured protection phase. Mathematical Biosciences and Engineering, 2020, 17(2): 1329-1354. doi: 10.3934/mbe.2020067
    [6] Holly Gaff, Elsa Schaefer . Optimal control applied to vaccination and treatment strategies for various epidemiological models. Mathematical Biosciences and Engineering, 2009, 6(3): 469-492. doi: 10.3934/mbe.2009.6.469
    [7] Kento Okuwa, Hisashi Inaba, Toshikazu Kuniya . Mathematical analysis for an age-structured SIRS epidemic model. Mathematical Biosciences and Engineering, 2019, 16(5): 6071-6102. doi: 10.3934/mbe.2019304
    [8] Eunha Shim . A note on epidemic models with infective immigrants and vaccination. Mathematical Biosciences and Engineering, 2006, 3(3): 557-566. doi: 10.3934/mbe.2006.3.557
    [9] Muntaser Safan . Mathematical analysis of an SIR respiratory infection model with sex and gender disparity: special reference to influenza A. Mathematical Biosciences and Engineering, 2019, 16(4): 2613-2649. doi: 10.3934/mbe.2019131
    [10] Steady Mushayabasa, Drew Posny, Jin Wang . Modeling the intrinsic dynamics of foot-and-mouth disease. Mathematical Biosciences and Engineering, 2016, 13(2): 425-442. doi: 10.3934/mbe.2015010
  • Although different strategies for mosquito-borne disease prevention can vary significantly in their efficacy and scale of implementation, they all require that individuals comply with their use. Despite this, human behavior is rarely considered in mathematical models of mosquito-borne diseases. Here, we sought to address that gap by establishing general expectations for how different behavioral stimuli and forms of mosquito prevention shape the equilibrium prevalence of disease. To accomplish this, we developed a coupled contagion model tailored to the epidemiology of dengue and preventive behaviors relevant to it. Under our model's parameterization, we found that mosquito biting was the most important driver of behavior uptake. In contrast, encounters with individuals experiencing disease or engaging in preventive behaviors themselves had a smaller influence on behavior uptake. The relative influence of these three stimuli reflected the relative frequency with which individuals encountered them. We also found that two distinct forms of mosquito prevention—namely, personal protection and mosquito density reduction—mediated different influences of behavior on equilibrium disease prevalence. Our results highlight that unique features of coupled contagion models can arise in disease systems with distinct biological features.



    1. Introduction

    With the development of transportation and urbanisation, population migration across regions becomes more frequent, and more and more rural population crowded into cities. The increasing mobility among regions might lead to the spread of the infectious diseases regionally and globally much faster than ever before [19]. For example, SARS was first reported in Guangdong Province of China in November of 2002, and in late June of 2003, the emerging infectious disease had spread to 32 countries and regions due to the human mobility [21,25]. In February 2014 Ebola virus appeared in Guinea and then due to the human mobility the disease spread very quickly to other countries including the United States, Spain and the United Kingdom et al [12], and has caused about 6070 reported deaths and 17145 reported cases of Ebola virus disease up to December 3,2014 according to the report from the World Health Organization (WHO) [6]. All the above facts show that the population dispersal can affect transmission dynamics of the infectious diseases.

    In the recent years, the impact of population dispersal has received increasing attention, and many mathematical patch models are formulated to investigate this hot issue (see [24,3,14] and the references cited therein). Here, the patches can be cities, towns, states, countries or other appropriate community divisions. Wang and Zhao [24] proposed an epidemic model with population dispersal to describe the dynamics of disease spread between two patches and n patches. Arino and van den Driessche [3] developed a multi-city epidemic model to analyze the spatial spread of infectious diseases. In 2011, Gao and Ruan [15] formulated an SIS patch model with non-constant transmission coefficients to investigate the effect of media coverage and human movement on the spread of infectious diseases among patches, and soon after, Gao and Ruan [13] proposed a multi-patch model to study the impacts of population dispersal on the spatial spread of malaria between patches. All the above mathematical models have provided useful information about the effect of host mobility on transmission dynamics of infectious diseases, but almost these models do not include the control measures, such as vaccination in it.

    There is no doubt that the top priority of global public security is to prevent and contain the spread of infectious diseases. Thus it is important to study how to control the spread of infectious diseases in patchy environment and how the increasing mobility of hosts affects the current public health security. In this paper, we will use a mathematical model to explore this important issue. As we all know, vaccination is one of the most effective biological means of containing the outbreak of infectious diseases, which inoculates antigenic material into the individuals to stimulate immune system to develop adaptive immunity to a pathogen. Since Edward Jenner, the founder of vaccinology, inoculated a 13 year-old-boy with vaccinia virus (cowpox) and demonstrated immunity to smallpox [18] in 1796, vaccination has played an important role in controlling and preventing the outbreak of infectious diseases. The widespread immunity due to vaccination is largely responsible for the worldwide eradication of smallpox and the restriction of infectious diseases, such as polio, measles, and tetanus from much of the world [17]. Over the past two decades, many modeling studies have been conducted the effect of vaccination on transmission dynamics of infectious diseases (see [1,2] and reference therein). However, most of the epidemic models with vaccination are formulated in an isolated patch, ignoring spatial heterogeneity both for populations and disease transmissions.

    The main purpose of the paper is to formulate an SIR epidemic model to study the impact of vaccination on transmission dynamics of infectious disease in patchy environment and the impact of the increasing mobility of hosts on the current immunization strategy. The paper is organized as follows. In Section 2, based on the SIR model with birth targeted vaccination we propose an SIR epidemic model with vaccination in patchy environment. In Section 3, we mainly present some preliminary results and derive the reproduction number. A classification of the equilibria of system on two patches and its the local dynamical behavior is provided in Section 4. We conclude with some numerical simulations in Section 5 and give a brief conclusion in the final section.


    2. Model formulation

    In this section, we employ an n-patch SIR epidemic model capable of informing vaccination policy to illustrate the impact of population migration between patches on the transmission dynamics of an infectious disease.

    First, let us formulate a model for the spread of the disease in the i-th patch. Suppose there is no host migration among patches, i.e., the patches are isolated. We assume that the total host population Ni(t) in the ith patch is partitioned into three distinct epidemiological subclasses which are susceptible, infectious and removed either by recovery from infection or by vaccination, with sizes denoted by Si(t),Ii(t) and Ri(t), respectively. Our assumptions on the dynamical transfer of the host population in the ith patch are demonstrated in Figure 1.

    Figure 1. Diagram of transitions between epidemiological classes in the i-th patch.

    We assume that the hosts are recruited at a rate μiNi into the susceptible class and die of natural causes at a rate μi. All individuals are born susceptible, and a fraction pi of newborns will receive vaccination. The newborns that successfully take the vaccine will then develop immunity to infection. The force of infection for susceptible is βiSiIiNi, where βi denotes the transmission coefficient. An infected host recovers at the rate γi.

    Based on the transfer diagram 1, the spread of an infectious disease in the i-th patch can be described by the following equations:

    {dSidt=(1pi)μiNiβiIiNiSiμiSi,dIidt=βiIiNiSi(μi+γi)Ii,dRidt=piμiNi+γiIiμiRi. (1)

    When n patches are connected, we assume that only susceptible and recovered hosts can migrate among the patches and the infected hosts cannot migrate among patches due to health problems or strict border inspection. Let mij0 denotes the per capita rate that susceptible or recovered hosts of patch i leave for patch j, where ij; d represents the migration period, and lij denotes the fraction of the hosts in patch i that move to patch j and satisfies nj=1lij=1, then the migration rate mij can be calculated or estimated from available data. If we given the fraction lij of the hosts migrate from patch i to patch j within d days, the migration rate mij can be determined from using the relationship 1emijd=lij, that is

    mij=ln(1lij)1d,  i,j=1,2,,n, ij. (2)

    Then the dynamics of the hosts with migration is governed by the following model:

    {dSidt=(1pi)μiNiβiIiNiSiμiSi+nji(mjiSjmijSi),dIidt=βiIiNiSi(μi+γi)Ii,dRidt=piμiNi+γIiμiRi+nji(mjiRjmijRi),Ni=Si+Ii+Ri,i=1,2,,n. (3)

    In this paper, we will use the system (3) to investigate the effect of vaccination on transmission dynamics of infectious disease in patchy environment and the impact of the increasing mobility of hosts on the current immunization strategy.


    3. Preliminary results and the reproduction number

    We first introduce some notations which will be used throughout this paper. Let x,yRn+, where Rn+={xRn:xi0 for 1in} be the positive orthant in Rn. We write xy=(x1y1,x2y2,,xnyn), yx whenever yxRn+, y>x whenever yxRn+ and xy, and Diag(x) the n×n matrix whose diagonal is given by the components of x and the other terms are zero.

    Let Ni(t)=Si(t)+Ii(t)+Ri(t) be the total population in patch i at time t and let the new infection term in patch i equal zero if Ni=0, see Adding all equations in (3) together leads to (N1(t)+N2(t)++Nn(t))=0, giving that the total population N(t)=ni=1Ni(t) is always a constant. If the total initial population given by N(0), then the fesible region

    Γ={(S1,I1,R1,,Sn,In,Rn)R3n+:ni=1(Si+Ii+Ri)N(0),i=1,2,,n},

    is positively invariant with respect to system (3).

    Define movement matrix

    M=(nj1m1jm21mn1m12nj2m2jmn2m1nm2nnjnmnj). (4)

    In this paper, we always assume that the movement matrix is irreducible, that is, the graph of the patches are strongly connected through the movement of hosts with respect to disease. If the movement matrix is reducible, the system may be decoupled into several samll systems (see [11] and reference therein).

    To find the disease-free equilibrium with all Ii=0 of system (3), consider the following linear systems

    {(1pi)μiNiμiSi+nji(mjiSjmijSi)=0,piμiNiμiRi+nji(mjiRjmijRi)=0,Ni=Si+Ri,i=1,2,,n, (5)

    or in the form of matrix systems

    {Diag((1p)μ)N(M+Diag(μ))S=0,Diag(pμ)N(M+Diag(μ))R=0,MN=0, (6)

    where μ=(μ1,μ2,,μn), 1=(1,1,,1) and X=(X1,X2,,Xn)T (subscript T denotes transpose), X represents S,I,R,N and p.

    We first solve the third equation of (5) or (6) which independent of the first two equations. Applying the results presented in Lemma 2.1 [16], the general solution to the third equation of (6) can be given as N=k(c11,c22,,cnn)T, where ckk>0, (k=1,2,,n) is the co-factor of the k-th diagonal entry of M and k is a constant to be specified later. It follows from ni=1Ni=N(0) that k=N(0)ni=1cii>0, then the third equation of (6) has a unique positive solution

    N0(N01,N02,,N0n)T=N(0)ni=1cii(c11,c22,,cnn)T.

    Substituting N0 back into the first two equations of (6) yields that

    S0(S01,S02,,S0n)=(M+Diag(μ))1Diag((1p)μ)N0,R0(R01,R02,,R0n)=(M+Diag(μ))1Diag(pμ)N0. (7)

    Since all off-diagonal entries of matrix M+Diag(μ) are negative (i.e., the Z-sign pattern) and the sum of the entries in each column is positive, it follows from Chapter 6 in [5] that M+Diag(μ) is a nonsingular irreducible M-matrix and (M+Diag(μ))1>0. Therefore, the linear system (6) has a unique positive solution S0,R0,N0, that is, system (3) always has unique disease-free equilibrium E0=(S0,0,R0).

    In absence of infectious disease, adding the three equations of system (3) together leads to

    dNidt=nji(mjiNjmijNi),  i=1,2,,n, (8)

    or in the form of matrix system

    dN(t)dt=MN(t). (9)

    It follows from Theorem 2.1 in [4] that the positive equilibrium N0=N(0)ni=1cii(c11,c22, ,cnn)T of system (8) is globally asymptotically stable on the affine hyperplane ni=1N0i=N(0). Using the expressions of S0,I0,N0 and the condition Ii=0 for all i, we can transfer the stability of system (3) into the following limit system

    {(SS0)=(M+Diag(μ))(SS0),(RR0)=(M+Diag(μ))(RR0). (10)

    Since the Gerschgorin circular disc theorem implies that matrix M+Diag(μ) is stable, i.e., all the eigenvalues of M+Diag(μ) have negative real parts, then equilibrium S=S0,R=R0 is global stability of system (10). Following the Theorem 2.1 in [8], we can directly obtain that the unique positive equilibrium E0 of linear system (3) is globally asymptotically stable on the affine hyperplane ni=1N0i=N(0). Summarizing the above discussions, we can obtain the following result.

    Theorem 3.1. System (3) always has a disease-free equilibrium E0(S0,0,R0), where

    S0=(M+Diag(μ))1Diag((1p)μ)N0,R0=(M+Diag(μ))1Diag(pμ)N0,N0=N(0)ni=1cii(c11,c22,,cnn)T,

    and N(0) is the initial total population and ckk>0, (k=1,2,,n) is the co-factor of the k-th diagonal entry of the movement matrix M. Moreover, the disease-free equilibrium E0(S0,0,R0) is globally asymptotically stable in

    Γ0={(S1,,Sn,I1,,In,R1,,Rn):ni=1(Si+Ri)=N(0),Ii=0,i=1,2,,n}.

    Note that the system (3) has n infected variables, namely, I1,I2,,In, it then follows that, using the notation of Driessche and Watmough [10], the matrices F and V (corresponding to the new infection terms and the remaining transfer terms, respectively) for entire population are given by

    F=Diag(β1S01N01,β2S02N02,,βnS0nN0n) and V=Diag(μ+γ).

    From literature [10], the reproduction number Rv is defined as the spectral radius of the next generation matrix FV1, that is,

    Rv=ρ(FV1)=max (11)

    where \rho(M) represents the spectral radius of the nonnegative matrix M and

    \mathfrak{R}_{vi}=\frac{\beta_i}{\mu_i+\gamma_i}\frac{S_i^0}{N_i^0}, (12)

    which represents the reproduction number in the i-th patch. It is clearly that the domain \mathfrak{R}_v implicitly depend on the movement of susceptible individuals and vaccination coverage through S_i^0. For disease-free equilibrium, we then have the following result based on the Theorem 2 in [10].

    Theorem 3.2. The disease-free equilibrium E^0 of system (3) is locally asymptotically stable if \mathfrak{R}_v<1, whereas it is unstable if \mathfrak{R}_v>1.

    In the special case n=1, the control reproduction number has the explicit expression

    \mathfrak{R}_v=(1-p_1)\frac{\beta_1}{\mu_1+\gamma_1}. (13)

    which represents the numbers of secondary cases directly produced by infectious diease during the period of infection in a susceptible population.

    In the special case of no movement between patches (i.e., M=0), the control reproduction number \mathfrak{R}_v defined in (11) is given by the maximum value of control reproduction numbers \mathfrak{R}_{vi} in all patches. Namely,

    \mathfrak{R}_v= \max\{\mathfrak{R}_{v1},\mathfrak{R}_{v2},\cdots,\mathfrak{R}_{vn}\}, (14)

    with \mathfrak{R}_{vi}=(1-p_i)\frac{\beta_i}{\mu_i+\gamma_i}.

    Theorem 3.3. If \mathfrak{R}_{v}<1, then system (3) exists only one equilibrium whose coordinates includes zero, that is, the disease-free equilibrium E^0.

    Proof. For any equilibrium E({\bf{S}},{\bf{I}},{\bf{R}}) of system (3), it must satisfy the matrix system:

    \left\{ \begin{array}{ll} \displaystyle {\rm Diag}((1-p)*\mu) {\bf{N}}-{\rm Diag}(\mu+\gamma) {\bf{I}}-(M+{\rm Diag}(\mu)){\bf{S}}=0,\\[2ex] \displaystyle\displaystyle {\rm Diag}({\bf{I}})({\bf{S}}-B{\bf{N}})=0,\\[2ex] \displaystyle {\rm Diag}(p*\mu) {\bf{N}}+{\rm Diag}(\gamma) {\bf{I}}-(M+{\rm Diag}(\mu) {\bf{R}}=0,\\[2ex] \displaystyle {\bf{N}} = {\bf{S}}+{\bf{I}}+{\bf{R}}. \end{array}\right. (15)

    where B={\rm Diag}(\frac{\mu_1+\gamma_1}{\beta_1},\frac{\mu_2+\gamma_2}{\beta_2},\cdots, \frac{\mu_n+\gamma_n}{\beta_n}).

    Adding the first three equations of (15) together yields M({\bf{N}}-{\bf{I}})=0, whose general solution can be given as (see Lemma 2.1 [16])

    {\bf{N}}-{\bf{I}}=k(c_{11},c_{22},\cdots,c_{nn})^T,

    where c_{kk}>0,\ (k=1,2,\cdots,n) is the co-factor of the k-th diagonal entry of M and k is constant to be specified later. Since N(0)=\sum_{i=1}^nN_i, then direct calculation implies that k=\frac{1}{\sum_{i=1}^nc_{ii}}N(0)-\frac{1}{\sum_{i=1}^nc_{ii}}{\bf{1}} \cdot {\bf{I}}. Therefore, we can rewrite {\bf{N}} as

    \begin{array}{rl} {\bf{N}}={\bf{N}}^0+(\mathbb{E}-C){\bf{I}}, \end{array} (16)

    where {\bf{N}}^0= \frac{N(0)}{\sum_{i=1}^nc_{ii}}(c_{11},c_{22},\cdots,c_{nn})^T, C=\big(\frac{c_{11}}{\sum_{i=1}^nc_{ii}},\frac{c_{22}}{\sum_{i=1}^nc_{ii}}, \cdots,\frac{c_{nn}}{\sum_{i=1}^nc_{ii}}\big)^T\cdot {\bf{1}} and \mathbb{E} is the identity matrix. Substituting (16) into the first equation of (15) leads to

    \begin{array}{rl} {\bf{S}}=&{\bf{S}}^0+(M+{\rm Diag}(\mu))^{-1}\Big({\rm Diag}(({\bf{1}}-{\bf{p}})*\mu)(\mathbb{E}-C)-{\rm Diag}(\mu+\gamma)\Big){\bf{I}}, \end{array} (17)

    where {\bf{S}}^0=(M+{\rm Diag}(\mu))^{-1}{\rm Diag}(({\bf{1}}-{\bf{p}})\mu) {\bf{N}}^0.

    Substituting (16), (17) into the second equation of (15), the system of equation (15) can be reduced to the following equation with one single equation of {\bf{I}}

    \begin{array}{l} \displaystyle {\rm Diag}({\bf{I}})\Big({\bf{S}}^0-B{\bf{N}}^0-((M+{\rm Diag}(\mu))^{-1}{\rm Diag}(({\bf{1}}-{\bf{p}})\mu)C-B C){\bf{I}}\\ -(B+(M+{\rm Diag}(\mu))^{-1}({\rm Diag}(\mu+\gamma)-{\rm Diag}(({\bf{1}}-{\bf{p}})\mu)){\bf{I}}\Big)=0. \end{array} (18)

    In the following, we only need to solve (18) for {\bf{I}} and then back-substitute into (15), the solutions for other variables will be found.

    Since CN(0)=N(0)C={\bf{N}}^0\cdot {\bf{1}}, it follows from the relationship between {\bf{S}}^0 and {\bf{N}}^0 that

    \begin{array}{rl} &\displaystyle(M+{\rm Diag}(\mu))^{-1}{\rm Diag}(({\bf{1}}-{\bf{p}})*\mu)C-BC \\ &=\displaystyle (M+{\rm Diag}(\mu))^{-1}\left({\rm Diag}(({\bf{1}}-{\bf{p}})*\mu){\bf{N}}^0-(M+{\rm Diag}(\mu))B{\bf{N}}^0\right)\frac{1}{N(0)}{\bf{1}} \\ &=\displaystyle \left({\bf{S}}^0-B{\bf{N}}^0\right)\frac{1}{N(0)}{\bf{1}}, \end{array} (19)

    and the expression for \mathfrak{R}_{vi} given in (12) that

    {\bf{S}}^0-B{\bf{N}}^0=\displaystyle \left( \begin{array}{c} \displaystyle\frac{\mu_1+\gamma_1}{\beta_1}N_1^0(\mathfrak{R}_{v1}-1)\\ \displaystyle\frac{\mu_2+\gamma_2}{\beta_2}N_2^0(\mathfrak{R}_{v2}-1)\\ \vdots\\ \displaystyle\frac{\mu_n+\gamma_n}{\beta_n}N_n^0(\mathfrak{R}_{vn}-1) \end{array} \right). (20)

    Therefore, the equation (18) can be expressed as

    {\rm Diag}({\bf{I}})(M+{\rm Diag}(\mu))^{-1}({\bf{b}}-A{\bf{I}})=0, (21)

    where

    \label{2} {\bf{b}}\triangleq(b_1,b_2,\cdots,b_n)^T=(M+{\rm Diag}(\mu))({\bf{S}}^0-B{\bf{N}}^0),

    and

    \label{1} \begin{array}{rl} A\triangleq (a_{ij})_{n\times n}=&{\rm Diag}(\gamma+{\bf{p}}\mu)+(M+{\rm Diag}(\mu))B\\[2ex] &\displaystyle +(M+{\rm Diag}(\mu))\left({\bf{S}}^0-B{\bf{N}}^0\right)\frac{1}{N(0)}{\bf{1}}.\\[2ex] \end{array}

    Note that M+{\rm Diag}(\mu) is a nonsingular M-matrix, it follows from Chapter 6 in [5] and equation (20) that {\bf{b}}<{\bf{0}} if \mathfrak{R}_v<1. Since all off-diagonal entries are negative and every column sum of matrix A is positive if \mathfrak{R}_v<1, then matrix A is a nonsingular M-matrix. Denote sub-matrix A(i_1,i_2,\cdots,i_k) which composed by the i_1-th, i_2-th, \cdots,i_k-th rows and columns of A, similarly, one can verify that sub-matrix A(i_1,i_2,\cdots,i_k) is also a non-singular M-matrix.

    It is easily to see that {\bf{I}}={\bf{0}} is one solution of (21). Except {\bf{I}}={\bf{0}}, the other solution of equation (21) should be {\bf{I}}\neq{\bf{0}}. For ease of presentation, we discuss the cases I_i\neq0 for all i and I_i\neq0 for some i separately. If I_i\neq 0 for all i, then the solution of {\bf{I}} must satisfy {\bf{b}}-A{\bf{I}}=0, it follows from {\bf{b}}<{\bf{0}} and A is a nonsingular M-matrix that {\bf{I}}=A^{-1}{\bf{b}}<{\bf{0}}. If I_i\neq0 for some i, without loss of generality, we assume that I_{i1}\neq0,I_{i2}\neq0,\cdots,I_{ik}\neq0 and I_{i,k+1}=I_{i,k+2}=\cdots=I_{in}=0, then solution of I_{i1},I_{i2},\cdots,I_{ik} satisfy {\bf{b}}(i_1,i_2,\cdots,i_k)-A(i_1,i_2,\cdots,i_k)(I_{i1},I_{i2},\cdots,I_{ik})^T=0, where {\bf{b}}(i_1,i_2,\cdots,i_k) composed with the i_1-th, i_2-th, \cdots,i_k-th rows of {\bf{b}}. It follows from {\bf{b}}(i_1,i_2,\cdots,i_k)<{\bf{0}} and A(i_1,i_2,\cdots,i_k) is a nonsingular M-matrix that I_{ij}<0 for j=1,2,\cdots,k. That is, the solutions of (21) when \mathfrak{R}_v<1 either equal to zero or less than zero. Considering the biological significance, we omit the solution including the element I_i<0 (i=1,2,\cdots,n). Then back-substituting {\bf{I}}=0 into (21), we obtain the expression of E({\bf{S}},{\bf{I}},{\bf{R}}) which in fact is the disease-free equilibrium E^0. Therefore, the disease-free equilibrium E^0 is the unique equilibrium under the condition \mathfrak{R}_v<1 for system (3). This completes the proof.


    4. The SIR model on two patches

    In this section, we mainly consider the dynamic behaviors for system (3) with n=2 due to it is hard to find the explicit solutions of (21) when n is very large as \mathfrak{R}_v>1. In this case, following the results presented in the previous section, we know that disease-free equilibrium E^0=(S_1^0,S_2^0,0,0,R_1^0,R_2^0) always exists and the explicit expression can be computed as

    \label{dfe2} \begin{array}{l} \displaystyle S_1^0=\frac{((1-p_1)(\mu_1\mu_2+\mu_1m_{21})+(1-p_2)\mu_2m_{12})m_{21}N(0)} {(\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12})(m_{12}+m_{21})},\\[2ex] \displaystyle S_2^0=\frac{((1-p_1)\mu_1m_{21}+(1-p_2)(\mu_1\mu_2+\mu_2m_{12})m_{12}N(0)} {(\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12})(m_{12}+m_{21})},\\[2ex] \displaystyle R_1^0=\frac{(p_1(\mu_1\mu_2+\mu_1m_{21})+p_2\mu_2m_{12})m_{21}N(0)} {(\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12})(m_{12}+m_{21})},\\[2ex] \displaystyle R_2^0=\frac{(p_1\mu_1m_{21}+p_2(\mu_1\mu_2+\mu_2m_{12})m_{12}N(0)} {(\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12})(m_{12}+m_{21})}.\\[2ex] \end{array}

    From (11) and (12), the control reproduction number for this case can be given by

    \mathfrak{R}_v=\max\{\mathfrak{R}_{v1},\mathfrak{R}_{v2}\}, (22)

    where

    \begin{array}{l} \displaystyle\mathfrak{R}_{v1}=\frac{\beta_1}{\mu_1+\gamma_1}\frac{(1-p_1)(\mu_1\mu_2+\mu_1m_{21})+(1-p_2)\mu_2m_{12}}{\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12}},\\ \displaystyle \mathfrak{R}_{v2}=\frac{\beta_2}{\mu_2+\gamma_2}\frac{(1-p_1)\mu_1m_{21}+(1-p_2)(\mu_1\mu_2+\mu_2m_{12})}{\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12}}, \end{array} (23)

    represent the control reproduction number correspond to the sub-patch 1 and 2, respectively.

    Like in the single patch model (1) or many other epidemic models, we have the global stability of the disease-free equilibrium for system (3) with n=2 as \mathfrak{R}_v<1.

    Theorem 4.1. If \mathfrak{R}_v<1, then E^0 is globally asymptotically stable for system (3) without vaccination, whereas if \mathfrak{R}_v>1, E^0 is unstable

    The proof of Theorem (4.1) is analogous to those of Theorem 2.4 in Gao and Ruan [15] and Theorem 3.2 in Sun et al. [23]. We omit the details here.

    Following Theorem 4.1 and the proof of Theorem 4.1, when \mathfrak{R}_v<1, there does not exist any endemic equilibrium. We now turn to the case where \mathfrak{R}_v>1. We first study the existence of other equilibria for system (3) with n=2 when \mathfrak{R}_v>1, and then establish its the stability.

    For convenience of presentation, set

    \begin{array}{l} \xi_1=\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12}, \ \xi_2=(\gamma_2+p_2\mu_2)\beta_2, \ \xi_3=(\gamma_1+p_1\mu_1)\beta_1, \\ \xi_4=(\mu_1+\gamma_1)(\mu_2+\gamma_2)(\mu_2+m_{21})+(\mu_1+\gamma_1)\xi_2+(\mu_2+\gamma_2)^2m_{12},\\ \xi_5=(\mu_1+\gamma_1)(\mu_2+\gamma_2)(\mu_1+m_{12})+(\mu_2+\gamma_2)\xi_3+(\mu_1+\gamma_1)^2m_{21}, \end{array}

    and define

    \begin{array}{rl} \displaystyle \mathfrak{\bar{R}}_{v1}=\frac{((\mu_2+\gamma_2)(\mu_2+m_{21})+\xi_2)(1-p_1)\mu_1\beta_1+(\mu_2+\gamma_2)^2m_{12}\beta_1} {(\mu_1+\gamma_1)((\mu_2+\gamma_2)\xi_1+(\mu_1+m_{12})\xi_2)},\\ \displaystyle \mathfrak{\bar{R}}_{v2}=\frac{((\mu_1+\gamma_1)(\mu_1+m_{12})+\xi_3)(1-p_2)\mu_2\beta_2+(\mu_1+\gamma_1)^2m_{21}\beta_2} {(\mu_2+\gamma_2)((\mu_1+\gamma_1)\xi_1+(\mu_2+m_{21})\xi_3)}, \end{array} (24)

    which can be considered as a second threshold for epidemic invasion of sub-populations 1 and 2, respectively.

    Theorem 4.2. The system (3) can have other three equilibria, and we have the following results:

    1. Boundary equilibria \hat{E}=(\hat{S}_1,\hat{S}_2,\hat{I}_1,0,\hat{R}_1,\hat{R}_2) exists if and only if \mathfrak{R}_{v1}>1, and \bar{E}=(\bar{S}_1,\bar{S}_2,0,\bar{I}_2,\bar{R}_1,\bar{R}_2) exists if and only if \mathfrak{R}_{v2}>1. Here,

    \label{en:boundaryI2}\begin{array}{l} \displaystyle \hat{S}_1\mspace{-3mu}=\mspace{-3mu}\frac{((\mu_1+\gamma_1)(\mu_2+m_{21})\mspace{-3mu}+\mspace{-3mu}m_{12}(1-p_2)\mu_2)(\mu_1+\gamma_1)m_{21}N(0)} {(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(m_{12}\xi_1\mspace{-3mu}+\mspace{-3mu} (\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})m_{21}\beta_1)\mspace{-3mu}+\mspace{-3mu}m_{12} (\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})\xi_3\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_2)\mu_2\beta_1},\\ \displaystyle\hat{S}_2\mspace{-3mu}=\mspace{-3mu}\frac{((\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)^2m_{21}\mspace{-3mu} +\mspace{-3mu}((\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(\mu_1\mspace{-3mu} +\mspace{-3mu}m_{12})\mspace{-3mu}+\mspace{-3mu}(\gamma_1\mspace{-3mu} +\mspace{-3mu}p_1\mu_1)\beta_1)(1\mspace{-3mu}-\mspace{-3mu}p_2)\mu_2)m_{12}N(0)} {(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(m_{12}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})m_{21}\beta_1)\mspace{-3mu}+\mspace{-3mu}m_{12}(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})\xi_3\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_2)\mu_2\beta_1},\\ \displaystyle\hat{I}_1\mspace{-3mu}=\mspace{-3mu}\frac{(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)\xi_1m_{21}(\mathfrak{R}_{v1}-1)N(0)} {(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(m_{12}\xi_1\mspace{-3mu}+\mspace{-3mu} (\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})m_{21}\beta_1)\mspace{-3mu}+\mspace{-3mu}m_{12} (\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})\xi_3\mspace{-3mu}+m_{12}m_{21} (1-p_2)\mu_2\beta_1},\\ \displaystyle\hat{R}_1\mspace{-3mu}=\mspace{-3mu}\frac{((\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})(\xi_3-(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)\gamma_1) \mspace{-3mu}+\mspace{-3mu}m_{12}(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)p_2\mu_2)m_{21}N(0)} {(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(m_{12}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})m_{21}\beta_1)\mspace{-3mu}+\mspace{-3mu}m_{12}(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})\xi_3\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_2)\mu_2\beta_1},\\ \displaystyle\hat{R}_2\mspace{-3mu}=\mspace{-3mu}\frac{(m_{21}(\xi_3-(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)\gamma_1)\mspace{-3mu}+\mspace{-3mu}((\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12}) \mspace{-3mu}+\mspace{-3mu}(\gamma_1\mspace{-3mu}+\mspace{-3mu}p_1\mu_1)\beta_1)p_2\mu_2)m_{12}N(0)} {(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(m_{12}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})m_{21}\beta_1)\mspace{-3mu}+\mspace{-3mu}m_{12}(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})\xi_3\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_2)\mu_2\beta_1}, \end{array}

    and

    \label{en:boundaryI1} \begin{array}{l} \displaystyle \displaystyle \bar{S}_1\mspace{-3mu}=\mspace{-3mu}\frac{((\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)^2m_{12}\mspace{-3mu}+\mspace{-3mu}((\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21})\mspace{-3mu}+\mspace{-3mu}(\gamma_2\mspace{-3mu}+\mspace{-3mu}p_2\mu_2)\beta_2)(1-p_1)\mu_1)m_{21}N(0)} {(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(m_{21}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})m_{12}\beta_2)\mspace{-3mu}+\mspace{-3mu}m_{21}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})\xi_2\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_1)\mu_1\beta_2}, \\ \displaystyle \bar{S}_2\mspace{-3mu}=\mspace{-3mu}\frac{((\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})\mspace{-3mu}+\mspace{-3mu}m_{21}(1-p_1)\mu_1)(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)m_{12}N(0)} {(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(m_{21}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})m_{12}\beta_2)\mspace{-3mu}+\mspace{-3mu}m_{21}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})\xi_2\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_1)\mu_1\beta_2},\\ \displaystyle\bar{I}_2\mspace{-3mu}=\mspace{-3mu}\frac{(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)\xi_1m_{12}(\mathfrak{R}_{v2}-1)N(0)} {(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(m_{21}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})m_{12}\beta_2)\mspace{-3mu}+\mspace{-3mu}m_{21}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})\xi_2\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_1)\mu_1\beta_2},\\%[11pt] \end{array}
    \begin{array}{l} \displaystyle \bar{R}_1\mspace{-3mu}=\mspace{-3mu}\frac{(m_{12}(\xi_2-(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)\gamma2)\mspace{-3mu}+\mspace{-3mu}((\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(\mu_2\mspace{-3mu}+\mspace{-3mu}m_{21}) \mspace{-3mu}+\mspace{-3mu}(\gamma_2\mspace{-3mu}+\mspace{-3mu}p_2\mu_2)\beta_2)p_1\mu_1)m_{21}N(0)} {(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(m_{21}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})m_{12}\beta_2)\mspace{-3mu}+\mspace{-3mu}m_{21}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})\xi_2\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_1)\mu_1\beta_2},\\ \displaystyle\bar{R}_2\mspace{-3mu}=\mspace{-3mu}\frac{((\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})(\xi_2-(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)\gamma_2) \mspace{-3mu}+\mspace{-3mu}m_{21}(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)p_1\mu_1)m_{12}N(0)} {(\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_2)(m_{21}\xi_1\mspace{-3mu}+\mspace{-3mu}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})m_{12}\beta_2)\mspace{-3mu}+\mspace{-3mu}m_{21}(\mu_1\mspace{-3mu}+\mspace{-3mu}m_{12})\xi_2\mspace{-3mu}+\mspace{-3mu}m_{12}m_{21} (1-p_1)\mu_1\beta_2}.\\%[11pt] \end{array}

    2. System (3) has a unique endemic equilibrium E^*=(S_1^*,S_2^*,I_1^*,I_2^*,R_1^*,R_2^*) if and only if \mathfrak{\bar{R}}_{v1}>1 and \mathfrak{\bar{R}}_{v2}>1. Here

    \begin{split} \displaystyle S_1^*=&\frac{((\mu_1+\gamma_1)((\mu_2+\gamma_2)(\mu_2+m_{21})+\xi_2)+(\mu_2+\gamma_2)^2m_{12})(\mu_1+\gamma_1)m_{21}N(0)} {m_{21}\beta_1\xi_4+m_{12}\beta_2\xi_5},\\ \displaystyle S_2^*=&\frac{((\mu_2+\gamma_2)((\mu_1+\gamma_1)(\mu_1+m_{12})+\xi_3)+(\mu_1+\gamma_1)^2m_{21})(\mu_2+\gamma_2)m_{12}N(0)} {m_{21}\beta_1\xi_4+m_{12}\beta_2\xi_5},\\ \displaystyle I_1^*=&\frac{(\mu_1+\gamma_1)((\mu_1+m_{12})\xi_2+(\mu_2+\gamma_2)\xi_1)(\mathfrak{\bar{R}}_{v1}-1)m_{21}N(0)} {m_{21}\beta_1\xi_4+m_{12}\beta_2\xi_5},\\ \displaystyle I_2^*=&\frac{(\mu_2+\gamma_2)((\mu_2+m_{21})\xi_3+(\mu_1+\gamma_1)\xi_1)(\mathfrak{\bar{R}}_{v2}-1)m_{12}N(0)} {m_{21}\beta_1\xi_4+m_{12}\beta_2\xi_5},\\ \displaystyle R_1^*=&\frac{(\xi_2 +(\mu_2+ \gamma_2) (\mu_2 + m_{21}) ) (\xi_3- \gamma_1(\mu_1 + \gamma_1) ) m_{21} N (0)} {m_{21}\beta_1\xi_4 + m_{12}\beta_2\xi_5}\\ &+\frac{m_{12}(\mu_1 + \gamma_1) (\xi_2 - \gamma_2(\mu_2 + \gamma_2) ) m_{21} N (0)}{m_{21}\beta_1\xi_4 + m_{12}\beta_2\xi_5},\\ \displaystyle R_2^*=&\frac{ (\xi_3 + (\mu_1 + \gamma_1) (\mu_1 + m_{12}) ) (\xi_2 - \gamma_2 (\mu_2 + \gamma_2) )m_{12} N (0)} {m_{21}\beta_1\xi_4 + m_{12}\beta_2\xi_5}\\ &+\frac{ m_{21}(\mu_2 + \gamma_2) (\xi_3 - \gamma_1(\mu_1 + \gamma_1) ) m_{12} N (0)} {m_{21}\beta_1\xi_4 + m_{12}\beta_2\xi_5}.\\%[9pt] \end{split}

    It follows from the expressions of \mathfrak{\bar{R}}_{vi} and \mathfrak{R}_{vi} (i=1,2) that

    \label{d} \begin{array}{l} \displaystyle \mathfrak{\bar{R}}_{v1}-\mathfrak{R}_{v1}=\frac{(\mu_2+\gamma_2)(\gamma_2+p_2\mu_2)m_{12}\beta_1} {(\mu_1+\gamma_1)((\mu_2+\gamma_2) \xi_1+(\mu_1+m_{12})\xi_2)}(1-\mathfrak{R}_{v2}),\\ \displaystyle \mathfrak{\bar{R}}_{v2}-\mathfrak{R}_{v2}=\frac{(\mu_1+\gamma_1)(\gamma_1+p_1\mu_1)m_{21}\beta_2} {(\mu_2+\gamma_2)((\mu_1+\gamma_1) \xi_1+(\mu_2+m_{21})\xi_3)}(1-\mathfrak{R}_{v1}). \end{array}

    Thus, if \mathfrak{R}_v>1, the inequalities \mathfrak{R}_{v1}>\mathfrak{\bar{R}}_{v1}>1 and \mathfrak{R}_{v2}>\mathfrak{\bar{R}}_{v2}>1 hold. Therefore, system (3) coexists at most four equilibriums if \mathfrak{\bar{R}}_{v1}>1 and \mathfrak{\bar{R}}_{v2}>1.

    Using N(0)=N_1+N_2, we can reduce system (3) with n=2 as follows

    \left\{ \begin{array}{ll} \displaystyle \frac{dS_1}{dt}=(1-p_1)\mu_1 N_1-\beta_1\frac{I_1}{N_1} S_1-\mu_1 S_1+m_{21}S_2-m_{12} S_1,\\ \displaystyle \frac{dS_2}{dt}=(1-p_2)\mu_2 (N(0)-N_1)-\beta_2\frac{I_2}{N(0)-N_1} S_2-\mu_2 S_1+m_{12}S_1-m_{21} S_2,\\ \displaystyle \frac{dI_1}{dt}=\beta_1\frac{I_1}{N_1} S_1-(\mu_1+\gamma_1) I_1, \displaystyle \frac{dI_2}{dt}=\beta_2\frac{I_2}{N(0)-N_1} S_2-(\mu_2+\gamma_2) I_2,\\ \displaystyle \frac{dN_1}{dt}=m_{21}(N(0)-N_1-I_2)-m_{12}(N_1-I_1), \end{array}\label{model:n2}\right. (25)

    which can be used to study the local behavior of system (3) near the boundary equilibria. By considering the linear system for (25), we have the following theorems.

    Theorem 4.3. If \mathfrak{R}_{v1}>1 and \mathfrak{\bar{R}}_{v2}<1, then \hat{E} is locally asymptotically stable, whereas if \mathfrak{\bar{R}}_{v2}>1, then \hat{E} is unstable.

    Proof. Evaluating system (25) at boundary equilibrium \hat{E}, we have the following Jacobian matrix

    \begin{split} J\mspace{-2mu}(\hat{E})\mspace{-5mu}=\mspace{-5mu}\left(\begin{array}{cccccc} -\mspace{-4mu}2\mu_1\mspace{-5mu} -\mspace{-5mu}\gamma_1\mspace{-5mu}-\mspace{-5mu}m_{12}\mspace{-3mu}&m_{21}& \mspace{-3mu}-\mspace{-3mu}\beta_1\mspace{-3mu}\frac{\hat{S}_1}{\hat{N}_1}&0& (\mspace{-3mu}1\mspace{-5mu}-\mspace{-5mu}p_1)\mu_1\mspace{-5mu}+\mspace{-5mu} (\mu_1\mspace{-5mu}+\mspace{-5mu}\gamma_1)\mspace{-3mu}\frac{\hat{I}_1}{\hat{N}_1}\\ m_{12}& \mspace{-4mu}-\mspace{-4mu}\mu_2\mspace{-5mu}-\mspace{-5mu}m_{21}&0&-\beta_2\frac{\hat{S}_2}{\hat{N}_2}&-(1-p_2)\mu_2\\ \beta_1\frac{\hat{I}_1}{\hat{N}_1}&0&0&0&-(\mu_1+\gamma_1)\frac{\hat{I}_1}{\hat{N}_1}\\ 0&0&0&\beta_2\mspace{-4mu}\frac{\hat{S}_2}{\hat{N}_2}\mspace{-5mu}-\mspace{-5mu} \mu_2\mspace{-5mu}-\mspace{-5mu}\gamma_2&0\\ 0&0&m_{12}&-m_{21}&-(m_{12}+m_{21}) \end{array}\right). \end{split}

    It is clearly that one of the eigenvalue of J(\hat{E}) is

    \lambda_1=\beta_2\frac{\hat{S}_2}{\hat{N}_2}-(\mu_2+\gamma_2)=(\mu_2+\gamma_2)(\mathfrak{\bar{R}}_{v2}-1),

    where \mathfrak{\bar{R}}_{v2} given in (24). After complexity calculation, the other eigenvalues of J(\hat{E}) are the solutions of quartic equation

    \lambda^4+\alpha_3\lambda_3+\alpha_2\lambda_2+\alpha_1\lambda_1+\alpha_0=0, (26)

    where

    \begin{array}{rl} \alpha_0=&m_{12}(\mu_1\mu_2+\mu_1m_{21}+\mu_2m_{12}(\mu_1+\gamma_1)\hat{N}_1^3\hat{I}_1+m_{12}m_{21}(1-p_2)\mu_2\hat{N}_1^4\\ &+(\mu_1\gamma_1)^2(\mu_2+m_{21})m_{21}\hat{N}_1^4+(\gamma_1+p_1\mu_1)(\mu_2+m_{21})m_{12}\hat{N}_1^4>0,\\ \alpha_1=&(\mu_1+\gamma_1)(\mu_1+\mu_2+m_{12}+m_{21})m_{12}\hat{N}_1^2\hat{I}_1+((2\mu_1+\gamma_1)m_{21}^2+\mu_2m_{12}^2)\hat{N}_1^2\\ &+(\mu_2(\mu_1+\gamma_1)^2+(m_{12}+2m_{21})\gamma_1^2+2\mu_1(\mu_1+\mu_2)+(4\mu_1+\mu_2)\gamma_1)\hat{N}_1^2\\ &+(m_{21}(2\mu_1+\mu_2+\gamma_1)+\mu_1(\gamma_1+p_1\mu_1+p_1\gamma_1)+\mu_2(\gamma_1+2\mu_1))\hat{N}_1^2>0,\\ \alpha_2=&m_{12}(\mu_1+\gamma_1)\hat{N}_1\hat{I}_1+(m_{12}^2+m_{21}^2+(\mu_1+\gamma_1)^2+\mu_2\gamma_1+2\mu_1\mu_2)\hat{N}_1^2\\ &+(m_{21}(2\gamma_1+4\mu_1+\mu_2) +m_{12}(2m_{21}+\gamma_1+2\mu_1+2\mu_2))\hat{N}_1^2>0,\\ \alpha_3=&(2\mu_1+\mu_2+\gamma_1+2m_{12}+2m_{21})\hat{N}_1>0. \end{array}

    By Routh-Hurwitz theorem, (26) has roots with negative real parts only requires that \alpha_1>0,\alpha_3>0 and \alpha_1\alpha_2-\alpha_0\alpha_3>0. Then we only need to prove the last inequality. Direct computation gives that

    \begin{split} \alpha_1\alpha_2\mspace{-4mu}-\mspace{-4mu}\alpha_0\alpha_3 &= m_{12}^2(\mu_1+\gamma_2)^2(\mu_1+\mu_2+m_{12}+m_{21})\hat{I}_1^2\hat{N}_1^3 +(\mu_1+\gamma_1)(m_{12}^3+m_{21}^3\\ &+\mu_1\gamma_1^2 +2\mu_1^2+\gamma_1+\mu_1^3+2\mu_2\gamma_1^2+4\mu_1\mu_2\gamma_1+2\mu_1^2\mu_2 +\mu_2^2\gamma_1+\mu_1\mu_2^2\\ &+\mspace{-3mu}(3\mu_1\mspace{-3mu}+\mspace{-3mu}2\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_1\mspace{-3mu}+\mspace{-3mu}2m_{21})m_{12}^2\mspace{-3mu}+\mspace{-3mu}(5\mu_1+2\mu_2+3\gamma_1)m_{21}^2 +(5\mu_1^2 \mspace{-3mu}+\mspace{-3mu}7\mu_1\gamma_1\\ &+\mspace{-3mu}2\gamma_1^2+4\mu_2\gamma_1+6\mu_1\mu_2+\mu_2^2)m_{21}^2+(3\mu_1^2+2\gamma_1^2+\mu_2^2+3m_{21}^2+p_1\mu_1^2\\ &+\mspace{-3mu}4\mu_1\mu_2 \mspace{-3mu}+\mspace{-3mu}4(2\mu_1\mspace{-3mu}+\mspace{-3mu}\mu_2\mspace{-3mu}+\mspace{-3mu}\gamma_1)m_{21}+(p_1+4)\mu_1\gamma_1+2\mu_2\gamma_1)m_{12})m_{12}\hat{N}_1^4\hat{I}_1\\ &+\mspace{-3mu}( m_{21}^4(2\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)\mspace{-3mu}+\mspace{-3mu}\mu_2m_{12}^4\mspace{-3mu} +\mspace{-3mu}2m_{21}^3(2\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)(2\mu_1\mspace{-3mu}+\mspace{-3mu} \gamma_1\mspace{-3mu}+\mspace{-3mu}\mu_2) m_{21}^2(2\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1) \end{split}
    \begin{split}&\times\mspace{-3mu}(4(\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1)^2\mspace{-3mu}+\mspace{-3mu} 3\mu_2\gamma_1\mspace{-3mu}+\mspace{-3mu}6\mu_1\mu_2\mspace{-3mu}+\mspace{-3mu}\mu_2^2) \mspace{-3mu}+\mspace{-3mu}(\mu_1+\gamma_1)^2\mu_2(\gamma_1^2+(2\mu_1+\mu_2)\gamma_1\\ &+\mspace{-3mu}(\mu_1\mspace{-3mu}+\mspace{-3mu}2\mu_2)\mu_1) \mspace{-3mu}+\mspace{-3mu}m_{12}^3(\gamma_1^2\mspace{-3mu}+\mspace{-3mu}p_1\mu_1^2 \mspace{-3mu}+\mspace{-3mu}4\mu_1\mu_2+2\mu_2^2+(\mu_1+p_1\mu_1+2\mu_2)\gamma_1\\ &+\mspace{-3mu}(2\mu_1\mspace{-3mu}+\mspace{-3mu}\gamma_1\mspace{-3mu}+\mspace{-3mu}3\mu_2)m_{21}) \mspace{-3mu}+\mspace{-3mu}m_{21}(2\gamma_1^4\mspace{-3mu}+\mspace{-3mu}4\gamma_1^3(2\mu_1 \mspace{-3mu}+\mspace{-3mu}\mu_2)\mspace{-3mu}+\mspace{-3mu}4\mu_1\gamma_1(2\mu_1^2\mspace{-3mu}+\mspace{-3mu}5\mu_1\mu_2\\ &+\mu_2^2)+\gamma_1^2 (12\mu_1+16\mu_1\mu_2+\mu_2^2)+2\mu_1^2(\mu_1^2+4\mu_1\mu_2+2\mu_2^2)) m_{12}^2(\gamma_1^3\\ &+3m_{21}^2(2\mu_1+\mu_2+\gamma_1)+\gamma_1^2(3\mu_2+(p_1+3)\mu_1)+\gamma_1(8\mu_1\mu_2+2\mu_2^2\\ &+\mspace{-4mu}(2\mspace{-4mu}+\mspace{-4mu}3p_1)\mu_1^2) \mspace{-3mu}+\mspace{-3mu}2\mu_1(p_1\mu^2\mspace{-4mu}+\mspace{-4mu} 3\mu_2(\mu_1\mspace{-4mu}+\mspace{-4mu}\mspace{-3mu}\mu_2))\mspace{-3mu}+\mspace{-3mu}m_{21}(3\gamma_1^2 \mspace{-3mu}+\mspace{-3mu}6\mu_1^2\mspace{-3mu}+\mspace{-3mu}2(p_2\mspace{-3mu}+\mspace{-3mu}7)\mu_1\mu_2\\ &+\mspace{-3mu}3\mu_2^2\mspace{-3mu}+\mspace{-3mu}2\gamma_1(4\mu_1\mspace{-3mu}+\mspace{-3mu} (p_2\mspace{-3mu}+\mspace{-3mu}3)\mu_2))) (\gamma_1^4\mspace{-3mu}+\mspace{-3mu}m_{21}(3\gamma_1\mspace{-3mu}+\mspace{-3mu}6\mu_1 \mspace{-3mu}+\mspace{-3mu}\mu_2)\mspace{-3mu}+\mspace{-3mu}\gamma_1^3((p_1\mspace{-3mu}+\mspace{-3mu}3)\mu_1\\ &+\mspace{-3mu}2\mu_2)\mspace{-3mu}+\mspace{-3mu}\gamma_1^2(3(p_1\mspace{-3mu}+\mspace{-3mu}1)\mu_1^2+8\mu_1\mu_2+2\mu_2^2) +\mu_1\gamma_1((1+3p_1)\mu_1^2+10\mu_1\mu_2\\ &+\mspace{-3mu}(7\mspace{-3mu}-\mspace{-3mu}p_1)\mu_2^2)\mspace{-3mu}+\mspace{-3mu} \mu_1^2(p_1\mu_1^2\mspace{-3mu}+\mspace{-3mu}4\mu_1\mu_2\mspace{-3mu}+\mspace{-3mu}(6-p_2)\mu_2^2) +m_{21}^2(4\gamma_1^2+(14-p_1)\mu_1^2\\ &+\mspace{-3mu}2(p_2\mspace{-3mu}+\mspace{-3mu}7)\mu_1\mu_2\mspace{-3mu}+\mspace{-3mu}\mu_2^2\mspace{-3mu}+\mspace{-3mu} \gamma_1((15\mspace{-3mu}-\mspace{-3mu}p_1)\mu_1\mspace{-3mu}+\mspace{-3mu}2(p_2\mspace{-3mu}+\mspace{-3mu}3)\mu_2)) \mspace{-3mu}+\mspace{-3mu}m_{21}(\gamma_1^2((15\mspace{-3mu}+\mspace{-3mu}p_1)\mu_1\\ &+\mspace{-3mu}4\gamma_1^3\mspace{-3mu}+\mspace{-3mu}(6\mspace{-3mu}+\mspace{-3mu}p_2)\mu_2)\mspace{-3mu}+\mspace{-3mu}\gamma_1((17\mspace{-3mu}+\mspace{-3mu}3p_1)\mu_1^2\mspace{-3mu}+\mspace{-3mu}(21-2p_1\mspace{-3mu}+\mspace{-3mu}3p_2)\mu_1\mu_2 \mspace{-3mu}+\mspace{-3mu}(p_2\mspace{-3mu}+\mspace{-3mu}2)\mu_2^2)\\ &+\mspace{-3mu}\mu_1(2(p_1+3)\mu_1^2+(19-2p_1+2p_2)\mu_1\mu_2+(p_2+7)\mu_2^2))) )\hat{N}_1^5>0. \end{split}

    Then all solution of (26) have negative real parts. Therefore, based on the above discussion, we know that if \mathfrak{R}_{v1}>1, there exists a boundary equilibrium \hat{E} and it is locally asymptotically stable if \mathfrak{\bar{R}}_{v2}<1. This completes the proof.

    Similar results hold for boundary equilibrium \bar{E} if \mathfrak{R}_{v2}>1.

    Theorem 4.4. If \mathfrak{R}_{v2}>1 and \mathfrak{\bar{R}}_{v1}<1, then \bar{E} is locally asymptotically stable, whereas if \mathfrak{\bar{R}}_{v1}>1, then \bar{E} is unstable.


    5. Numerical simulations

    To complement the mathematical analysis carried out in the previous sections, we now investigate some of the numerical properties of system (3). We take the default parameter values as: N(0)=10,000, \beta_1=0.5, \beta_2=0.3, \gamma=1/7, \mu=0.0006, d=360 and the initial condition for system (3) considered as (S_{1}(0),S_{2}(0),I_{1}(0),I_{2}(0),R_{1}(0),R_{2}(0))=(6489,3489,10,10,1,1). In this section, we mainly change migration rate and the vaccination coverage to simulate how migration and vaccination affect the outbreak of an infectious diseases. Since the annual (or quarter) floating population number for a region or a country (e.g. 2015 China Statistical Yearbook) determined the migration proportion l_{ij}, it follows from (2) that we can choose d=360 (or d=90) to calculate the migration rate m_{ij}. In this paper, we focus on the migration duration d=360, the corresponding results for other migration durations can be similarly obtained.

    Time evolution of system (3) in the special case of n=2 with multi-initial conditions are presented in Fig. 2. One can observe from the first figure that the trajectories of the two-patch system converge to the disease-free equilibrium E^0 when \mathfrak{R}_{v1}=0.792<1 and \mathfrak{R}_{v2}=0.421<1. This means that the disease disappears in the whole population as proved in Theorem 4.1. If \mathfrak{R}_{v1}=2.39>1,\ \mathfrak{R}_{v2}=0.85<1 and \bar{\mathfrak{R}}_{v1}=2.46>1,\ \bar{\mathfrak{R}}_{v2}=0.395<1, the trajectories of this two-patch system converge to the boundary equilibrium \hat{E}=(2046,542, 14, 0,7131,2869) as depicted in Fig. 2(b), while if \mathfrak{R}_{v1}=0.938<1,\ \mathfrak{R}_{v2}=1.24>1 and \bar{\mathfrak{R}}_{v1}=0.805<1,\ \bar{\mathfrak{R}}_{v2}=1.265>1, the trajectories converge to the boundary equilibrium \bar{E}=(1645,1375, 0, 3,7125,2875) as shown in Fig. 2(c). This suggests that the disease persist in one patch and disappear in another patch when just one patch control reproduction number larger than one as proved in Theorem 4.3 and 4.4. If the both the control reproduction number and the invasion threshold are all larger than one, as shown in Fig. 2(d) \mathfrak{R}_{v1}=2.99>\bar{\mathfrak{R}}_{v1}=2.54>1 and \mathfrak{R}_{v2}=1.84>\bar{\mathfrak{R}}_{v2}=1.81>1, then the trajectories converge to the endemic equilibrium E^*=(2046,1372, 20, 2,7131,2869). Similarly to the model considered in [15,23], the disease persist in both sub-populations if the control reproduction numbers in each patch are all larger than one, to which complement the mathematical analysis carried out in the previous section.

    Figure 2. Time evolution of system (3) with multi-initial conditions in the case of n=2 and the initial values of (S_1(0),S_2(0),I_1(0),I_2(0),R_1(0),R_2(0)) are chose as (6000,1000,320, 20,1980,780), (2000,3000, 10,230,1980,2780), (5000,3000, 5, 35,980,980), (3600,2400,700,300,1500,1500), (3000,4000, 32, 8,980,1980). Here l_1=0.1,\ l_2=0.23 and the rest parameters are default values.

    The theoretical and numerical results all show that \mathfrak{R}_v=1 acting as a sharp threshold between disease extinction and persist state, to study the influence of vaccination and migration, we can first study how the control reproduction number \mathfrak{R}_v depends on the vaccination rate p_1,p_2 and the migration rate m_{12},m_{21} (which determined by l_{12},l_{21}). Following Fig. 3, we can observe that if there is no migration between patches, then vaccines always helpful to control the spread of an infectious disease and the optimal vaccination strategy should be vaccine more individuals in patch 1 and relatively lower in patch 2. This is very reasonable, when more people in higher transmission patch (i.e., patch 1) get vaccinated, then the number of people to be infected is smaller, hence the threshold \mathfrak{R}_v will be reduced more. For the specific vaccination rate (p_1,p_2)=(0.8,0.6), if there is no migration between patches then \mathfrak{R}_v=0.83. If there exist migration between patches, then more people migrate from patch 2 to patch 1 could make the threshold \mathfrak{R}_v=0.83 marked in red curve in Fig. 3(b). Since migration rate m_{12} (m_{21}) is an increasing function of variable l_{12} (l_{21}), therefore, this figure also implies that the threshold \mathfrak{R}_v increases with the variable l_{12} and decreases with variable l_{21}. However, if we fix (p_1,p_2)=(0.6,0.8), it follows from Fig. 3(c) that threshold \mathfrak{R}_v decreases with the variable l_{12} and increases with variable l_{21}. This suggests that if we want to control the threshold \mathfrak{R}_v less than one, we should consider not only the effectiveness of vaccines but also the impact of migration.

    Figure 3. Contour plot of the control reproduction number \mathfrak{R}_v in the p_1-p_2 plane and in l_{12}-l_{21} plane. Here, (a) represents the relationship between vaccination rate (i.e., p_1,p_2) and \mathfrak{R}_v if there is no migration between patches, (b) and (c) depict the relationship between migration rate (i.e., l_{12},l_{21}) and \mathfrak{R}_v under the two specific vaccination rate marked in red point in figure (a). The red curves \mathfrak{R}_v=0.83 in (b) and \mathfrak{R}_v=1.39 in (c) respectively correspond to the red points p_1=0.8,p_2=0.6 and p_1=0.6,p_2=0.8 in (a). In these three figures, the blue curves represent the case of \mathfrak{R}_v=1. Other parameters are default values.

    To explore the effect of vaccination and migration, we also compare the second peak size and second peak time with various vaccination coverage and migration rate. For the case of p_1=0.2, p_2=0.1, although the endemic equilibrium E^* is stable due to \mathfrak{R}_{v1}=2.79>1 and \mathfrak{R}_{v1}=1.88>1, we can obtain that the second peak size decrease form 330 at 1112 day to 294 at 1450 day for patch 1, decrease from 119 at 1645 day decrease to 92 at 1906 day for patch 2, and decrease from 342 at 1110 day to 291 at 1490 day compared to the case of p_1=p_2=0 as shown in Fig.4. This figure also depicts that the disease will disappear at the first 2000 days if the vaccination rate add up to p_1=0.65,p_2=0.7, at this time, the threshold \mathfrak{R}_{v1}=1.22>1 and \mathfrak{R}_{v1}=0.627<1 and the boundary equilibrium is stable. This tells us that vaccine plays a critical role in reducing the second peak size and delay the second peak time, since the control reproduction number is decreasing with vaccination rate p_1,p_2. If there exist migration between patches in absence vaccination, then the control reproduction number \mathfrak{R}_{v1}=2.09>1 and \mathfrak{R}_{v2}=3.48>1, that is, the disease persist in both patches. In this case, we can observe from Fig. 5 that higher migration rate in patch 1 is beneficial to individuals in both patches and higher migration rate in patch 2 will magnify the second peak size of patch 1 and the entire population. This implies that, if we want to control the outbreak size during the first 2000 days, the scale of migration between patches should be considered. These figures all show that the second peaks happened after three or four years later, this may be because the decay of the effectiveness of the vaccination or individuals migration change the spatial structure of sub-populations.

    Figure 4. Comparison of the second peak size and second peak time when there is no migration between patches. Figures (a), (b) and (c) respectively represent the trajectory of infectious vary with time for patch 1, patch 2 and the entire population with different vaccination coverage. Direct calculation implies that \mathfrak{R}_{v1} equal to 3.48, 2.179, 1.22 and \mathfrak{R}_{v2} equal to 2.09, 1.88, 0.627 are respectively corresponding to the vaccination coverage p_1=p_2=0, p_1=0.2, p_2=0.1 and p_1=0.65, p_2=0.7. The results show that lower vaccination coverage delay the second peak time and slightly reduce the second peak size for patch 1, patch 2 even the entire population. Whereas the higher coverage will not generate a second outbreak during the first 2000 days.
    Figure 5. Comparison of the second peak size and peak time with different migration rate in absence of vaccination. The trajectory of infectious varying with time for patch 1, patch 2 and the whole population are depicted in (a), (b) and (c), respectively. Figs. (a) and (c) show that human movement advanced the second peak time and increased the second peak size for patch 1 and the whole population when more individuals move to patch 1 (higher transmission rate). Fig. (b) illustrates that individuals migration can reduce the second outbreak size even no second outbreak during the first 2000 days.

    We also compared the residual values of the first peak size to investigate the impact of vaccination and migration, which shown in the histogram 6. The results show that migration can reduce the first peak size for each patches and the entire population as long as the migration rate m_{12} is less than or equal to migration rate m_{21}. Such as, for the entire population, the residual of first peak sizes almost equal to -8 in the case of l_{12}=l_{21}=0.2 and equal to -29 in the case of l_{12}=0.3, l_{21}=0.1, while the residual of first peak sizes almost equal to 24 in the case of l_{12}=0.04,l_{21}=0.36 as shown in histogram 6(c).


    6. Conclusion

    In this paper, we proposed a multi-patch SIR model with vaccination to study the influence of vaccination coverage and human mobility on disease transmission. Our theoretical results show that the control reproduction number \mathfrak{R}_v is a threshold parameter of the disease dynamics. It founds that system only exists a disease-free equilibrium E^0 if \mathfrak{R}_v<1 and is locally asymptotically stable. Particularly, in the case of n=2, boundary equilibrium \hat{E} (\bar{E}) exists if \mathfrak{R}_{v1}>1 (\mathfrak{R}_{v2}>1) and it is globally stability if \mathfrak{\bar{R}}_{v2}<1 (\mathfrak{\bar{R}}_{v1}<1), and endemic equilibrium E^* exists only when \mathfrak{\bar{R}}_{v1}>1 and \mathfrak{\bar{R}}_{v2}>1. The simulation results show that, for parameter values considered, vaccines always can shrink the outbreak of an infectious while mobility restriction (change the migration rate) dose not necessarily always have a positive impact on the overall spread of disease. An increase of migration rate from one patch to the other sometimes may prevent the outbreak of infectious in one patch while intensify the disease spread in other patch (see Figs. 5 and 6).

    Figure 6. Comparison of the residual value of first peak size (i.e., peak size with migration minus the case without migration) under different vaccination coverage. Figure (a) is for patch 1, (b) is for patch 2 and (c) is for the entire population. Here, case 1, case 2 and case 3 respectively represent l_{12}=l_{21}=0.2, l_{12}=0.3, l_{21}=0.1 and l_{12}=0.04,l_{21}=0.36, and other parameters are default values.

    In our model, we assume that the infective do not move between patches, corresponding to either a very severe disease so that infective are not able to move or move is forbidden in order to control outbreak of disease. In the further, we can generalize the current model with infective move between patches.


    Acknowledgments

    This project has been partially supported by grants from National Natural Science Foundation of China (Nos. 11671206,11271190) and Scientific Research Innovation Project of Jiangsu Province (No. KYZZ15_0130). We also thank two anonymous referees for their helpful comments.




    [1] S. Q. Deng, X. Yang, Y. Wei, J. T. Chen, X. J. Wang, H. J. Peng, A review on dengue vaccine development, Vaccines, 8 (2020), 63. https://doi.org/10.3390/vaccines8010063 doi: 10.3390/vaccines8010063
    [2] S. Rajapakse, C. Rodrigo, A. Rajapakse, Treatment of dengue fever, Infect. Drug Resist., 5 (2012), 103–112. https://doi.org/10.2147/IDR.S22613
    [3] S. J. Thomas, D. Strickman, D. W. Vaughn, Dengue Epidemiology: Virus Epidemiology, Ecology, and Emergence, Adv. Virus Res., 61 (2003), 235–289. https://doi.org/10.1016/S0065-3527(03)61006-7
    [4] N. L. Achee, F. Gould, T. A. Perkins, R. C. Reiner Jr, A. C. Morrison, S. A. Ritchie, et al., A critical assessment of vector control for dengue prevention, PLoS Negl.Trop. Dis., 9 (2015), e0003655. https://doi.org/10.1371/journal.pntd.0003655 doi: 10.1371/journal.pntd.0003655
    [5] D. Pilger, M. De Maesschalck, O. Horstick, J. L. San Martin, Dengue outbreak response: documented effective interventions and evidence gaps, TropIKA.net, 1 (2010).
    [6] P. A. Reyes-Castro, L. Castro-Luque, R. Díaz-Caravantes, K. R. Walker, M. H. Hayden, K. C. Ernst, Outdoor spatial spraying against dengue: A false sense of security among inhabitants of Hermosillo, Mexico, PLoS Negl.Trop. Dis., 11 (2017), e0005611. https://doi.org/10.1371/journal.pntd.0005611 doi: 10.1371/journal.pntd.0005611
    [7] F. Espinoza-Gómez, C. M. Hernández-Suárez, R. Coll-Cárdenas, Educational campaign versus malathion spraying for the control of Aedes aegypti in Colima, Mexico, J. Epidemiol. Community Health, 56 (2002), 148–152. https://doi.org/10.1136/jech.56.2.148 doi: 10.1136/jech.56.2.148
    [8] N. Arunachalam, B. K. Tyagi, M. Samuel, R. Krishnamoorthi, R. Manavalan, S. C. Tewari, et al., Community-based control of Aedes aegypti by adoption of eco-health methods in Chennai City, India, Pathog. Global Health, 106 (2012), 488–496. https://doi.org/10.1179/2047773212Y.0000000056 doi: 10.1179/2047773212Y.0000000056
    [9] C. Aerts, M. Revilla, L. Duval, K. Paaijmans, J. Chandrabose, H. Cox, et al., Understanding the role of disease knowledge and risk perception in shaping preventive behavior for selected vector-borne diseases in Guyana, PLoS Negl. Trop. Dis., 14 (2020), e0008149. https://doi.org/10.1371/journal.pntd.0008149 doi: 10.1371/journal.pntd.0008149
    [10] N. Andersson, E. Nava-Aguilera, J. Arosteguí, A. Morales-Perez, H. Suazo-Laguna, J. Legorreta-Soberanis, et al., Evidence based community mobilization for dengue prevention in Nicaragua and Mexico (Camino Verde, the Green Way): cluster randomized controlled trial, BMJ, 351 (2015), h3267. https://doi.org/10.1136/bmj.h3267 doi: 10.1136/bmj.h3267
    [11] J. Arosteguí, R. J. Ledogar, J. Coloma, C. Hernández-Alvarez, H. Suazo-Laguna, A. Cárcamo, et al., The Camino Verde intervention in Nicaragua, 2004–2012, BMC Public Health, 17 (2017), 406. https://doi.org/10.1186/s12889-017-4299-3 doi: 10.1186/s12889-017-4299-3
    [12] S. Funk, M. Salathé, V. A. A. Jansen, Modelling the influence of human behaviour on the spread of infectious diseases: a review, J. R. Soc. Interface, 7 (2010), 1247–1256. https://doi.org/10.1098/rsif.2010.0142 doi: 10.1098/rsif.2010.0142
    [13] T. Berry, M. Ferrari, T. Sauer, S. J. Greybush, D. Ebeigbe, A. J. Whalen, et al., Stabilizing the return to normal behavior in an epidemic, medRxiv, 2023.03.13.23287222.
    [14] S. Del Valle, H. Hethcote, J. M. Hyman, C. Castillo-Chavez, Effects of behavioral changes in a smallpox attack model, Math. Biosci., 195 (2005), 228–251. https://doi.org/10.1016/j.mbs.2005.03.006 doi: 10.1016/j.mbs.2005.03.006
    [15] M. J. Ferrari, S. Bansal, L. A. Meyers, O. N. Bjørnstad, Network frailty and the geometry of herd immunity, Proc. R. Soc. B, 273 (2006), 2743–2748. https://doi.org/10.1098/rspb.2006.3636 doi: 10.1098/rspb.2006.3636
    [16] E. P. Fenichel, C. Castillo-Chavez, M. G. Ceddia, G. Chowell, P. A. Gonzalez Parra, G. J. Hickling, et al., Adaptive human behavior in epidemiological models, Proc. Natl. Acad. Sci. U.S.A., 108 (2011), 6306–6311. https://doi.org/10.1073/pnas.101125010 doi: 10.1073/pnas.101125010
    [17] L. LeJeune, N. Ghaffarzadegan, L. M. Childs, O. Saucedo, Mathematical analysis of simple behavioral epidemic models, Math. Biosci., 375 (2024), 109250. https://doi.org/10.1016/j.mbs.2024.109250 doi: 10.1016/j.mbs.2024.109250
    [18] C. Eksin, K. Paarporn, J. S. Weitz, Systematic biases in disease forecasting – The role of behavior change, Epidemics, 27 (2019), 96–105. https://doi.org/10.1016/j.epidem.2019.02.004 doi: 10.1016/j.epidem.2019.02.004
    [19] T. Boccia, M. N. Burattini, F. A. B. Coutinho, E. Massad, Will people change their vector-control practices in the presence of an imperfect dengue vaccine?, Epidemiol. Infect., 142 (2014), 625–633. https://doi.org/10.1017/S0950268813001350 doi: 10.1017/S0950268813001350
    [20] V. M. Alvarado-Castro, C. Vargas-De-León, S. Paredes-Solis, A. Li-Martin, E. Nava-Aguilera, A. Morales-Pérez, et al., The influence of gender and temephos exposure on community participation in dengue prevention: a compartmental mathematical model, BMC Infect. Dis., 24 (2024), 463. https://doi.org/10.1186/s12879-024-09341-w doi: 10.1186/s12879-024-09341-w
    [21] J. Jiao, G. P. Suarez, N. H. Fefferman, How public reaction to disease information across scales and the impacts of vector control methods influence disease prevalence and control efficacy, PLoS Comput. Biol., 17 (2021), e1008762. https://doi.org/10.1371/journal.pcbi.1008762 doi: 10.1371/journal.pcbi.1008762
    [22] K. Roosa, N. H. Fefferman, A general modeling framework for exploring the impact of individual concern and personal protection on vector-borne disease dynamics, Parasites Vectors, 15 (2022), 361. https://doi.org/10.1186/s13071-022-05481-7 doi: 10.1186/s13071-022-05481-7
    [23] J. M. Epstein, J. Parker, D. Cummings, R. A. Hammond, Coupled contagion dynamics of fear and disease: mathematical and computational explorations, PLoS One, 3 (2008), e3955. https://doi.org/10.1371/journal.pone.0003955 doi: 10.1371/journal.pone.0003955
    [24] K. Jain, V. Bhatnagar, S. Prasad, S. Kaur, Coupling fear and contagion for modeling epidemic dynamics, IEEE Trans. Network Sci. Eng., 10 (2023), 20–34. https://doi.org/10.1109/TNSE.2022.3187775 doi: 10.1109/TNSE.2022.3187775
    [25] J. M. Epstein, E. Hatna, J. Crodelle, Triple contagion: a two-fears epidemic model, J. R. Soc. Interface, 18 (2021), 20210186. https://doi.org/10.1098/rsif.2021.0186 doi: 10.1098/rsif.2021.0186
    [26] N. Perra, D. Balcan, B. Gonçalves, A. Vespignani, Towards a characterization of behavior-disease models, PLoS One, 6 (2011), e23084. https://doi.org/10.1371/journal.pone.0023084 doi: 10.1371/journal.pone.0023084
    [27] S. A. Pedro, F. T. Ndjomatchoua, P. Jentsch, J. M. Tchuenche, M. Anand, C. T. Bauch, Conditions for a second wave of COVID-19 due to interactions between disease dynamics and social processes, Front. Phys., 8 (2020), 574514. https://doi.org/10.3389/fphy.2020.574514 doi: 10.3389/fphy.2020.574514
    [28] A. Bernardin, A. J. Martínez, T. Perez-Acle, On the effectiveness of communication strategies as non-pharmaceutical interventions to tackle epidemics, PLoS One, 16 (2021), e0257995. https://doi.org/10.1371/journal.pone.0257995 doi: 10.1371/journal.pone.0257995
    [29] Mathematica 14.0, 2024. Available from: http://www.wolfram.com.
    [30] M. M. Andersen, S. Højsgaard, caracas: Computer Algebra, 2023. Available from: https://github.com/r-cas/caracas.
    [31] P. Driessche, J. Watmough, Further notes on the basic reproduction number, Math. Epidemiol., 2008 (2008), 159–178. https://doi.org/10.1007/978-3-540-78911-6_6 doi: 10.1007/978-3-540-78911-6_6
    [32] A. B. Sabin, Research on dengue during World War II, Am. J. Trop. Med. Hyg., 1 (1952), 30–50. https://doi.org/10.4269/ajtmh.1952.1.30 doi: 10.4269/ajtmh.1952.1.30
    [33] C. Probst, T. M. Vu, J. M. Epstein, A. E. Nielsen, C. Buckley, A. Brennan, et al., The normative underpinnings of population-level alcohol use: An individual-level simulation model, Health Educ. Behav., 47 (2020), 224–234. https://doi.org/10.1177/1090198119880545 doi: 10.1177/1090198119880545
    [34] J. M. Epstein, Agent_Zero, Princeton University Press, 2014.
    [35] T. M. Vu, C. Probst, J. M. Epstein, A. Brennan, M. Strong, R. C. Purshouse, Toward inverse generative social science using multi-objective genetic programming, in Proceedings of the Genetic and Evolutionary Computation Conference, ACM, Prague Czech Republic, (2019), 1356–1363.
    [36] L. Cattarino, I. Rodriguez-Barraquer, N. Imai, D. A. T. Cummings, N. M. Ferguson, Mapping global variation in dengue transmission intensity, Sci. Transl. Med., 12 (2020), eaax4144. https://doi.org/10.1126/scitranslmed.aax4144 doi: 10.1126/scitranslmed.aax4144
    [37] Y. Liu, K. Lillepold, J. C. Semenza, Y. Tozan, M. B. M. Quam, J. Rocklöv, Reviewing estimates of the basic reproduction number for dengue, Zika and chikungunya across global climate zones, Environ. Res., 182 (2020), 109114. https://doi.org/10.1016/j.envres.2020.109114 doi: 10.1016/j.envres.2020.109114
    [38] A. C. Morrison, R. C. Reiner, W. H. Elson, H. Astete, C. Guevara, C. del Aguila, et al., Efficacy of a spatial repellent for control of Aedes-borne virus transmission: A cluster-randomized trial in Iquitos, Peru, Proc. Natl. Acad. Sci., 119 (2022), e2118283119. https://doi.org/10.1073/pnas.2118283119 doi: 10.1073/pnas.2118283119
    [39] H. J. Wearing, P. Rohani, Ecological and immunological determinants of dengue epidemics, Proc. Natl. Acad. Sci., 103 (2006), 11802–11807. https://doi.org/10.1073/pnas.0602960103 doi: 10.1073/pnas.0602960103
    [40] N. G. Reich, S. Shrestha, A. A. King, P. Rohani, J. Lessler, S. Kalayanarooj, et al., Interactions between serotypes of dengue highlight epidemiological impact of cross-immunity, J. R. Soc. Interface, 10 (2013), 20130414. https://doi.org/10.1098/rsif.2013.0414 doi: 10.1098/rsif.2013.0414
    [41] C. B. F. Vogels, C. Rückert, S. M. Cavany, T. A. Perkins, G. D. Ebel, N. D. Grubaugh, Arbovirus coinfection and co-transmission: A neglected public health concern?, PLoS Biol., 17 (2019), e3000130. https://doi.org/10.1371/journal.pbio.3000130 doi: 10.1371/journal.pbio.3000130
    [42] M. Chan, M. A. Johansson, The incubation periods of dengue viruses, PLoS One, 7 (2012), e50972. https://doi.org/10.1371/journal.pone.0050972 doi: 10.1371/journal.pone.0050972
    [43] Q. A. Ten Bosch, J. M. Wagman, F. Castro-Llanos, N. L. Achee, J. P. Grieco, T. A. Perkins, Community-level impacts of spatial repellents for control of diseases vectored by Aedes aegypti mosquitoes, PLoS Comput. Biol., 16 (2020), e1008190. https://doi.org/10.1371/journal.pcbi.1008190 doi: 10.1371/journal.pcbi.1008190
    [44] L. C. Harrington, J. P. Buonaccorsi, J. D. Edman, A. Costero, P. Kittayapong, G. G. Clark, et al., Analysis of survival of young and old Aedes aegypti (Diptera: Culicidae) from Puerto Rico and Thailand, J. Med. Entomol., 38 (2001), 537–547. https://doi.org/10.1603/0022-2585-38.4.537 doi: 10.1603/0022-2585-38.4.537
    [45] T. W. Scott, P. H. Amerasinghe, A. C. Morrison, L. H. Lorenz, G. G. Clark, D. Strickman, et al., Longitudinal studies of Aedes aegypti (Diptera: Culicidae) in Thailand and Puerto Rico: blood feeding frequency, J. Med. Entomol., 37 (2000), 89–101. https://doi.org/10.1603/0022-2585-37.1.89 doi: 10.1603/0022-2585-37.1.89
    [46] D. L. Smith, K. E. Battle, S. I. Hay, C. M. Barker, T. W. Scott, F. E. McKenzie, Ross, Macdonald, and a theory for the dynamics and control of mosquito-transmitted pathogens, PLoS Pathogens, 8 (2012), e1002588. https://doi.org/10.1371/journal.ppat.1002588 doi: 10.1371/journal.ppat.1002588
    [47] R Core Team, R: A Language and Environment for Statistical Computing, 2021. Available from: https://www.R-project.org/.
    [48] K. Soetaert, T. Petzoldt, R. W. Setzer, Solving differential equations in R: package deSolve, J. Stat. Software, 33 (2010), 1–25. https://doi.org/10.18637/jss.v033.i09 doi: 10.18637/jss.v033.i09
    [49] A. Puy, S. Lo Piano, A. Saltelli, S. A. Levin, Sensobol: An R package to compute variance-based sensitivity indices, J. Stat. Software, 102 (2022), 1–37. https://doi.org/10.18637/jss.v102.i05 doi: 10.18637/jss.v102.i05
    [50] R. M. Anderson, R. M. May, Infectious Diseases of Humans: Dynamics and Control, Oxford University Press, Oxford, New York, 1992.
    [51] M. Martcheva, Introduction to epidemic modeling, in An Introduction to Mathematical Epidemiology (ed. M. Martcheva), Springer US, Boston, MA, (2015), 9–31. https://doi.org/10.1007/978-1-4899-7612-3_2
    [52] F. Brauer, C. Castillo-Chavez, Z. Feng, Endemic disease models, Math. Models Epidemiol., 69 (2019), 63–116. https://doi.org/10.2478/acph-2019-0006
    [53] R. C. Reiner, S. T. Stoddard, B. M. Forshey, A. A. King, A. M. Ellis, A. L. Lloyd, et al., Time-varying, serotype-specific force of infection of dengue virus, Proc. Natl. Acad. Sci., 111 (2014), E2694–E2702. https://doi.org/10.1073/pnas.13149331 doi: 10.1073/pnas.13149331
    [54] M. Ryan, E. Brindal, M. Roberts, R. I. Hickson, A behaviour and disease transmission model: incorporating the Health Belief Model for human behaviour into a simple transmission model, J. R. Soc. Interface, 21 (215), 20240038. https://doi.org/10.1098/rsif.2024.0038
    [55] J. Cascante-Vega, S. Torres-Florez, J. Cordovez, M. Santos-Vega, How disease risk awareness modulates transmission: coupling infectious disease models with behavioural dynamics, R. Soc. Open Sci., 9 (2022), 210803. https://doi.org/10.1098/rsos.210803 doi: 10.1098/rsos.210803
    [56] V. Vanlerberghe, M. E. Toledo, M. Rodriguez, D. Gomez, A. Baly, J. R. Benitez, et al., Community involvement in dengue vector control: cluster randomised trial, BMJ, 338 (2009), b1959–b1959. https://doi.org/10.1136/bmj.b1959 doi: 10.1136/bmj.b1959
    [57] J. Quintero, N. R. Pulido, J. Logan, T. Ant, J. Bruce, G. Carrasquilla, Effectiveness of an intervention for Aedes aegypti control scaled-up under an inter-sectoral approach in a Colombian city hyper-endemic for dengue virus, PLoS One, 15 (2020), e0230486. https://doi.org/10.1371/journal.pone.0230486 doi: 10.1371/journal.pone.0230486
    [58] J. Raude, K. MCColl, C. Flamand, T. Apostolidis, Understanding health behaviour changes in response to outbreaks: Findings from a longitudinal study of a large epidemic of mosquito-borne disease, Soc. Sci. Med., 230 (2019), 184–193. https://doi.org/10.1016/j.socscimed.2019.04.009 doi: 10.1016/j.socscimed.2019.04.009
    [59] L. S. Lloyd, P. Winch, J. Ortega-Canto, C. Kendall, The design of a community-based health education intervention for the control of Aedes aegypti, Am. J. Trop. Med. Hyg., 50 (1994), 401–411. https://doi.org/10.4269/ajtmh.1994.50.401 doi: 10.4269/ajtmh.1994.50.401
    [60] A. Caprara, J. W. D. O. Lima, A. C. R. Peixoto, C. M. V. Motta, J. M. S. Nobre, J. Sommerfeld, et al., Entomological impact and social participation in dengue control: a cluster randomized trial in Fortaleza, Brazil, Trans. R. Soc. Trop. Med. Hyg., 109 (2015), 99–105. https://doi.org/10.1093/trstmh/tru187 doi: 10.1093/trstmh/tru187
    [61] A. M. Buttenheim, V. Paz-Soldan, C. Barbu, C. Skovira, J. Q. Calderón, L. M. M. Riveros, et al., Is participation contagious? Evidence from a household vector control campaign in urban Peru, J Epidemiol. Community Health, 68 (2014), 103–109. https://doi.org/10.1136/jech-2013-202661 doi: 10.1136/jech-2013-202661
    [62] J. Bedson, L. A. Skrip, D. Pedi, S. Abramowitz, S. Carter, M. F. Jalloh, et al., A review and agenda for integrated disease models including social and behavioural factors, Nat. Hum. Behav., 5 (2021), 834–846. https://doi.org/10.1038/s41562-021-01136-2 doi: 10.1038/s41562-021-01136-2
    [63] K. Magori, M. Legros, M. E. Puente, D. A. Focks, T. W. Scott, A. L. Lloyd, et al., Skeeter Buster: a stochastic, spatially explicit modeling tool for studying Aedes aegypti population replacement and population suppression strategies, PLoS Negl. Trop. Dis., 3 (2009), e508. https://doi.org/10.1371/journal.pntd.0000508 doi: 10.1371/journal.pntd.0000508
    [64] E. L. Davis, T. D. Hollingsworth, M. J. Keeling, An analytically tractable, age-structured model of the impact of vector control on mosquito-transmitted infections, PLoS Comput. Biol., 20 (2024), e1011440. https://doi.org/10.1371/journal.pcbi.1011440 doi: 10.1371/journal.pcbi.1011440
    [65] M. Predescu, G. Sirbu, R. Levins, T. Awerbuch-Friedlander, On the dynamics of a deterministic and stochastic model for mosquito control, Appl. Math. Lett., 20 (2007), 919–925. https://doi.org/10.1016/j.aml.2006.12.001 doi: 10.1016/j.aml.2006.12.001
    [66] J. Elsinga, H. T. Van Der Veen, I. Gerstenbluth, J. G. M. Burgerhof, A. Dijkstra, M. P. Grobusch, et al., Community participation in mosquito breeding site control: an interdisciplinary mixed methods study in Curaçao, Parasites Vectors, 10 (2017), 434. https://doi.org/10.1186/s13071-017-2371-6 doi: 10.1186/s13071-017-2371-6
    [67] A. N. Rakhmani, Y. Limpanont, J. Kaewkungwal, K. Okanurak, Factors associated with dengue prevention behaviour in Lowokwaru, Malang, Indonesia: a cross-sectional study, BMC Public Health, 18 (2018), 619. https://doi.org/10.1186/s12889-018-5553-z doi: 10.1186/s12889-018-5553-z
    [68] A. J. Mackay, M. Amador, A. Diaz, J. Smith, R. Barrera, Dynamics of Aedes aegypti and Culex quinquefasciatus in septic tanks, J. Am. Mosq. Control Assoc., 25 (2009), 409–416. https://doi.org/10.2987/09-5888.1 doi: 10.2987/09-5888.1
  • This article has been cited by:

    1. Jiawei Xu, Yincai Tang, Bayesian Framework for Multi-Wave COVID-19 Epidemic Analysis Using Empirical Vaccination Data, 2021, 10, 2227-7390, 21, 10.3390/math10010021
    2. Ke-Lu Li, Jun-Yuan Yang, Xue-Zhi Li, Analysis of an environmental epidemic model based on voluntary vaccination policy, 2022, 1025-5842, 1, 10.1080/10255842.2022.2079080
    3. Yuan Liu, Bin Wu, Coevolution of vaccination behavior and perceived vaccination risk can lead to a stag-hunt-like game, 2022, 106, 2470-0045, 10.1103/PhysRevE.106.034308
    4. Cássio de Lima Quiroga, Pedro Henrique Triguis Schimit, A multi-city epidemiological model based on cellular automata and complex networks for the COVID-19, 2023, 42, 2238-3603, 10.1007/s40314-023-02401-y
    5. Maoxing Liu, Yuhang Li, Dynamics analysis of an SVEIR epidemic model in a patchy environment, 2023, 20, 1551-0018, 16962, 10.3934/mbe.2023756
    6. Tingting Zheng, Yantao Luo, Linfei Nie, Zhidong Teng, Analysis of transmission dynamics of dengue fever on a partially degenerated weighted network, 2025, 142, 10075704, 108495, 10.1016/j.cnsns.2024.108495
    7. Yingzi He, Linhe Zhu, Theoretical analysis and practical application of multi-patch infectious disease model, 2025, 198, 09600779, 116519, 10.1016/j.chaos.2025.116519
  • Reader Comments
  • © 2025 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(184) PDF downloads(25) Cited by(0)

Article outline

Figures and Tables

Figures(9)  /  Tables(2)

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog