
Citation: Qianqian Cui. Global stability of multi-group SIR epidemic model with group mixing and human movement[J]. Mathematical Biosciences and Engineering, 2019, 16(4): 1798-1814. doi: 10.3934/mbe.2019087
[1] | Pengyan Liu, Hong-Xu Li . Global behavior of a multi-group SEIR epidemic model with age structure and spatial diffusion. Mathematical Biosciences and Engineering, 2020, 17(6): 7248-7273. doi: 10.3934/mbe.2020372 |
[2] | Jinliang Wang, Hongying Shu . Global analysis on a class of multi-group SEIR model with latency and relapse. Mathematical Biosciences and Engineering, 2016, 13(1): 209-225. doi: 10.3934/mbe.2016.13.209 |
[3] | Zhisheng Shuai, P. van den Driessche . Impact of heterogeneity on the dynamics of an SEIR epidemic model. Mathematical Biosciences and Engineering, 2012, 9(2): 393-411. doi: 10.3934/mbe.2012.9.393 |
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[6] | Toshikazu Kuniya, Yoshiaki Muroya, Yoichi Enatsu . Threshold dynamics of an SIR epidemic model with hybrid of multigroup and patch structures. Mathematical Biosciences and Engineering, 2014, 11(6): 1375-1393. doi: 10.3934/mbe.2014.11.1375 |
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[9] | Yoichi Enatsu, Yukihiko Nakata, Yoshiaki Muroya . Global stability for a class of discrete SIR epidemic models. Mathematical Biosciences and Engineering, 2010, 7(2): 347-361. doi: 10.3934/mbe.2010.7.347 |
[10] | Shuang-Hong Ma, Hai-Feng Huo . Global dynamics for a multi-group alcoholism model with public health education and alcoholism age. Mathematical Biosciences and Engineering, 2019, 16(3): 1683-1708. doi: 10.3934/mbe.2019080 |
Since Kermack and Mckendrick [1] formulated the compartmental ODE model to study epidemiology, extensively mathematical models have been used to explore the transmission dynamics of infectious diseases. Most of these mathematical models are assumed that the host population is homogeneously mixed. In reality, the host population is often heterogenous and it can be divided into several groups with different transmission patterns [2]. For example, it seems more reasonable to make a division into two groups for measles and mumps due to the different contact patterns between children and adults. The sexually transmitted diseases (such as, HIV/AIDS and gonorrhea) can be divided into serval groups according to the number of sexual partners. Therefore, multi-group epidemic models are emerged to investigate how the population heterogeneity affect the spread of disease.
Note that the study of the mathematical properties of multi-group epidemic model can obtain suitable measures for the control of infectious diseases. Recently, numerous literatures (see for example, [3,4,5,6,7,9,8,10,11,12,13,2] and the references therein) are dedicated to study such models on the theoretical and analytical properties including the existence, uniqueness of solutions and global stability of each equilibrium of the model. Particularly, Guo et al. [3,4] proposed a graph theory to Lyapunov functional technique, which simplified the proof on the global stability for the positive equilibrium of multi-group model. Hereafter, the graph-theoretical approach was widely used in studying the global dynamics of various multi-group models (see for example, [6,10,12] and references therein).
Nowadays, with the recent development of worldwide transportation, infected individuals can easily travel from one place to another which is thought to be one of the main reasons of the global pandemic of diseases. For instance, SARS first appeared in Guangdong Province of China in November, 2002. This destructive disease soon spread to other areas of China and, in the days that followed, to other parts of the world [13]. Ebola appeared in Guinea in March, 2014. It then spread to other countries including the United States, Spain and the United Kingdom [15]. Thus, it is necessary to incorporate human movement into epidemic model to clarifying how it affects the pattern of disease prevalence.
Recently, several researchers focus on the dynamics of multi-group models that incorporate the movement of human movement. In [16], Arino et al. explored the dynamics of a multi-group epidemic model with individuals movement. Liu and Takeuchi obtained the local stability of a two-species epidemic model with transport-related infection [17]. Wang and Yang studied the global dynamics of a two-patch SIS model with infection during transport [14]. In [18], Sun and Wu gained the stability of multi-group models with cross-dispersal. However, fewer studies obtained the global dynamics of general multi-group model with human movement.
Motivated by these facts, in this paper we aim to study the global dynamics of a general multi-group SIR model that incorporate explicit human movement between groups. The whole population is divided into n distinct groups (n≥1). The i-th (1≤i≤n) group is further partitioned into three compartments: the susceptible, infectious and removed, the number of individuals at time t are denoted by Si(t),Ii(t) and Ri(t), respectively. Like in [16], the diseases is assumed to be horizontally transmitted between humans according to standard incidence (see, for example, [19]) with βij the rate of disease transfer from infective individual in group j to susceptible individual in group i. The rate of human movement, from group i to group j, is given by mij with mij≥0 and is assumed to be the same for each type of individual. Therefore, the multi-group SIR epidemic model with human movement can be described by the following system of 3n ordinary differential equations
{S′i=(1−pi)μiNi−n∑j=1βijIjNjSi−μiSi+n∑j=1(mjiSj−mijSi),I′i=n∑j=1βijIjNjSi−μiIi−γiIi+n∑j=1(mjiIj−mijIi),R′i=piμiNi+γiIi−μiRi+n∑j=1(mjiRj−mijRi), | (1.1) |
where the prime (′) denotes the differentiation with respect to time t and the sub-population number Ni=Si+Ii+Ri. In patch i, μi is both the birth and death rate; pi is the proportion of immune at birth; γi is the recovery rate. Here, parameters μi,γi are positive constants and pi,βij,mij are non-negative constants.
In this model, we consider disease transmission can occur not only in the same groups (βij>0 for i=j) but also in different groups (βij>0 for some i≠j). This kind of system is called epidemic model with hybrid of multi-group [3] or epidemic model with group mixing [12]. To our knowledge, Kuniya and his cooperators studied several multi-group epidemic models with group mixing and population movement (see, for example [5,20,21]). In this paper, we will use the graph-theoretical approach [3,4] to present the global dynamics of multi-group SIR model (1.1) with both group mixing and human movement.
The organization of this paper is as follows. In the next section, we quote some results from graph theory which are very useful in the proof of our main results. In Section 3, we study the existence of equilibria and derive the expression of control reproduction number. We investigate the global stability of each equilibrium in Sections 4 and 5. Two numerical examples are performed to verify our theoretical results in Section 6. A brief conclusion is given in the final section.
Let A=(aij)n×n and C=(cij)n×n be nonnegative matrices, namely, all of their elements are nonnegative. We write A≥C if aij≥cij for all i and j, A>C if A≥C and A≠C, and A≫C if aij>cij for all i and j. The matrix A which satisfies A≫0 is called positive matrix.
Definition 1. ([22], p.27) An n×n matrix A is cogredient to a matrix P if for some permutation matrix Q, QAQT=P (superscript T represents transpose). A is reducible if it is cogredient to
P=(A10A2A3), |
where A1 and A3 are square matrices, or if n=1 and A=0. Otherwise, A is irreducible.
Denote G(A) as the associated directed graph of n×n matrix A, which is a set of n vertices and a set of directed arcs joining two vertices. Irreducibility of matrices can be easily tested using the associated directed graphs.
Definition 2. ([22], p.30) A directed graph G(A) is strongly connected if for any ordered pair (Qi,Qj) of vertices of G(A), there exists a sequence of edges (a path) which leads from Qi to Qj.
Theorem 1. ([22], p.30) Matrix A is irreducible if and only if G(A) is strongly connected.
The matrix A has nonpositive off-diagonal and nonnegative diagonal entries, we have the following results on A.
Definition 3. ([22], p.133) Any matrix A of the form
A=sI−B, s>0, B≥0, |
for which s≥ρ(B) (the spectral radius of B), is called an M-matrix. Here, I is identity matrix.
Lemma 1. ([22], p.134) If all off-diagonal entries of matrix A are nonpositive, then the followings are equivalent.
(ⅰ) A is a nonsingular M-matrix;
(ⅱ) A is semipositive; that is, there exists x≫0 with Ax≫0;
(ⅲ) A is inverse-positive; that is, A−1 exists and A−1≥0;
(ⅳ) A does not reverse the sign of any vector; that is, if x≠0 and y=Ax, then xiyi>0 for some subscript i.
Consider a linear system
Ax=0, | (2.1) |
where A=(aij)n×n with aii=−∑nj≠iaji and aij≤0 for all i≠j. Then the following lemma holds.
Lemma 2. ([3], Lemma 2.1) Assume that the matrix A in linear system (2.1) is irreducible and n≥2. Then the solution space of system (2.1) has dimension 1, and a basis of the solution space can be given by
(ν1,ν2,⋯,νn)=(A11,A22,⋯,Ann), |
where Aii>0 denotes the cofactor of the i-th diagonal entry of A, 1≤i≤n.
Denote contact matrix B=(βij)n×n and the movement matrix M=(mij)n×n. Unless otherwise indicated, in this paper, matrices B and M are always assumed to be irreducible. In fact, contact matrix B is irreducible which means that an infected individual in the first group can cause infection to a susceptible individual in the second group through an infection path. While, movement matrix M is irreducible which means that each patch are strongly connected with respect to human movement.
For ease of notations, let diag(ai) denote a diagonal matrix whose diagonal entries starting in the upper left corner are a1,a2,⋯,an and off-diagonal elements are all zero, and define n×n matrices
G0=diag(n∑j=1mij)−MT and Gμ=diag(μi+n∑j=1mij)−MT. |
Obviously, matrix G0 is also irreducible due to the assumption that movement matrix M is irreducible. Since all off-diagonal entries of matrix Gμ are negative and the sum of the entries in each column is positive, it follows from the equivalent conditions of Lemma 1 that matrix Gμ is a nonsingular irreducible M-matrix and is inverse-positive, i.e., G−1μ exists and G−1μ≥0.
Notice that the total population number N(t)=∑ni=1Ni(t)=∑ni=1(Si(t)+Ii(t)+Ri(t)) satisfies the equation N′(t)=∑ni=1N′i(t)=0, which implies that N(t) is always constant, denoted by Nc. Therefore, the feasible region
Γ1={(S1,I1,R1,⋯,Sn,In,Rn)∈R3n+|n∑i=1(Si+Ii+Ri)=Nc } |
is positively invariant with respect to system (1.1).
In absence of infectious disease, we have the following results on the existence and uniqueness of the disease-free equilibrium for system (1.1).
Theorem 2. (ⅰ) There exits a unique disease-free equilibrium E0=(S01,0,R01,⋯,S0n,0,R0n)∈R3n+ for system (1.1).
(ⅱ) There exists only one equilibrium whose coordinates include zero, i.e., the disease-free equilibrium E0.
Proof. First we prove (ⅰ). In absence of infectious diseases, the disease-free equilibrium of system (1.1) must satisfy the following linear system
{(1−pi)μiNi−μiSi+n∑j=1(mjiSj−mijSi)=0,piμiNi−μiRi+n∑j=1(mjiRj−mijRi)=0,n∑j=1(mjiNj−mijNi)=0,i=1,2,⋯,n. | (3.1) |
The algebraic equations (3.1) can be easily expressed by the following form of matrix system
{diag((1−pi)μi)N−GμS=0,diag(piμi)N−GμR=0,G0N=0, | (3.2) |
where # = (#1,#2,⋯,#n)T and # represents S,I,R and N. It follows from ∑ni=1Ni=Nc and Lemma 2 that linear system G0N=0 has a unique positive solution N=N0 with
N0≜(N01,N02,⋯,N0n)T=Nc∑ni=1νi(ν1,ν2,⋯,νn)T, | (3.3) |
where νi>0 is the cofactor of the i-th diagonal entry of G0. Substituting N0 into the first two equation of (3.2), it is easy to derive that the first equation of (3.2) has a unique solution S=S0 and the second equation has a unique solution R=R0, where
S0=(S01,S02,⋯,S0n)T=G−1μdiag((1−pi)μi)N0>0, |
and
R0=(R01,R02,⋯,R0n)T=G−1μdiag(piμi)N0>0. |
Next we prove (ii). Using Lemma 2 and G0 is irreducible, it follows from the third equation of (3.2) that Ni>0 at any equilibrium. Furthermore, it is impossible to have Si=0 at any equilibrium, since at Si=0 the first equation of (3.1) becomes (1−pi)μiNi+∑nj=1mjiSj>0. This is a contradiction. In the following, we only need to show that Ii=0 for some i implies that Ij=0 for all j. If Ii=0, it follows from the second equation of (1.1) that
n∑j≠iβijSiIj+n∑j=1mjiIj=0. | (3.4) |
Since Si>0,Ii≥0 for all i, then equation (3.4) implies that
n∑j=1mjiIj=0 and n∑j≠iβijSiIj=0. | (3.5) |
For the first equation of (3.5), if mji>0, then Ii=0 means Ij=0 for any 1≤i,j≤n, i.e.,
Ii=0andmji>0 implies Ij=0, ∀i,j=1,2,⋯,n. | (3.6) |
Following the Definition 2 and Theorem 1, the movement matrix M is irreducible which ensures that there exists a sequence of ordered pairs {(i,τ1),(τ1,τ2),⋯,(τq,j)} such that miτ1>0,mτ1τ2>0,⋯,mτqj>0, τk=1,2,⋯,n, k=1,2,⋯,q and q≥0. Applying (3.6) to each pair in such a sequence and using Ii=0, we derive Iτ1=0, Iτ2=0,⋯, Ij=0. Hence Ij=0 for all j provided that M is irreducible. Similarly, if B is irreducible, it follows from the second equation of (3.5) that Ij=0 for all j. Therefore, the disease-free equilibrium E0 is the only one equilibrium whose coordinates include zero.
We should remark that the system may be decoupled into several small systems and may have multiple boundary equilibria when the movement matrix M is reducible (see, for example, [26] and references therein).
Using the techniques of van den Driessche and Watmough [25], the control reproduction number can be expressed as
Rv=ρ(FV−1), | (3.7) |
where matrices F=(βijS0i/N0j)n×n and V=diag(μi+γi)+G0 respectively represent the new infection terms and the remaining transfer terms for entire population, and ρ denotes the spectral radius.
Notice that
dNidt=n∑j=1(mjiNj−mijNi),i=1,2,⋯,n. | (4.1) |
The proof of Theorem 2 implies that system (4.1) has a unique positive equilibrium N0 and one can easily testify N0 is globally asymptotically stable in Γ1 i, e., limt→∞Ni(t)=N0i. Using the results from Castillo-Chavez and Tieme [24] and Mischaikow et al. [28], we can obtain the analytical results by considering the following limit system of system (1.1) in which the sub-population is assumed to be constant N0i
{S′i=(1−pi)μiN0i−n∑j=1βijIjN0jSi−μiSi+n∑j=1(mjiSj−mijSi),I′i=n∑j=1βijIjN0jSi−μiIi−γiIi+n∑j=1(mjiIj−mijIi),R′i=piμiN0i+γiIi−μiRi+n∑j=1(mjiRj−mijRi). | (4.2) |
System (1.1) and (4.2) have the same set of equilibria and the same existence conditions as given in the previous section.
For the eventual boundedness of solutions Si,Ii,Ri, i=1,2,⋯,n of system (4.2), we have the following lemma.
Lemma 3. For any solutions in Γ1 of system (4.2), it holds that
lim supt→+∞Si(t)≤N0i,lim supt→+∞Ii(t)≤N0i,lim supt→+∞Ri(t)≤N0i,i=1,2,⋯,n, |
in particular,
lim supt→+∞Si(t)≤S0i,i=1,2,⋯,n. |
Proof. The first equation of (4.2) implies that
dSidt≤(1−pi)μiN0i−μiSi+n∑j=1(mjiSj−mijSi), i=1,2,⋯,n. | (4.3) |
Using the right hand side of (4.3), let us define an auxiliary linear system
dˉSidt=(1−pi)μiN0i−μiˉSi+n∑j=1(mjiˉSj−mijˉSi), i=1,2,⋯,n. | (4.4) |
A simple calculation shows that the positive equilibrium (ˉS01,ˉS02,⋯,ˉS0n)=(S01,S02,⋯,S0n) is the unique equilibrium of (4.4).
Let g(x)=x−1−lnx, x>0. One can easily verify that g(x)≥0 with g(x)=0 if and only if x=1 and (x−1)(1−y)=g(x)+g(y)−g(xy) for any x,y∈R+. Define
VˉSi=S0ig(¯SiS0i). |
Differentiating VˉSi along system (4.4) and using S0i is the positive equilibrium of system (4.4), simple calculation implies that
dVˉSidt|(4.4)=(1−S0iˉSi)ˉS′i=(1−S0iˉSi)[(1−pi)μiN0i−μiˉSi+n∑j=1(mjiˉSj−mijˉSi)]=(1−S0iˉSi)[−μiS0i(ˉSiS0i−1)+n∑j=1mjiS0j(ˉSjS0j−1)−n∑j=1mjiS0i(ˉSiS0i−1)]=−μiS0ig(S0iˉSi)−μiS0ig(ˉSiS0i)+n∑j=1mjiS0jg(S0jˉSj)−n∑j=1mjiS0jg(S0iˉSjˉSiS0j)+n∑j=1mjiS0jg(S0iˉSi)−n∑j=1mijS0ig(ˉSiS0i)−n∑j=1mijS0ig(S0iˉSi)=−(1−pi)μiN0ig(S0iˉSi)−n∑j=1mjiS0jg(S0iˉSjˉSiS0j)−μiS0ig(ˉSiS0i)+n∑j=1mjiS0jg(ˉSjS0j)−n∑j=1mijS0ig(ˉSiS0i). |
Let VˉS=∑ni=1VˉSi. By using ∑ni=1∑nj=1mjiS0jg(ˉSjS0j)=∑ni=1∑nj=1mijS0ig(ˉSiS0i), we have
dVˉSdt|(4.4)=−n∑i=1(1−pi)μiN0ig(S0iˉSi)−n∑i=1n∑j=1mjiS0jg(S0iˉSjˉSiS0j)−n∑i=1μiS0ig(ˉSiS0i), |
which suggests that V′ˉS|(4.4)≤0 with V′ˉS|(4.4)=0 if and only if ˉSi=S0i. Using the LaSalle's Invariance Principle [29], the unique positive equilibrium (ˉS1,ˉS2,⋯,ˉSn)=(S01,S02,⋯,S0n) is globally asymptotically stable for system (4.4), i.e., limt→∞ˉSi(t)=S0i for all i. Following the standard comparison theorem [11], we have lim supt→+∞Si(t)≤S0i, i=1,2,⋯,n.
If Si=S0i for some i and Sj≤S0j for all j≠i, it follows from Lemma 3 and the first equation of system (4.2) that
S′i≤(1−pi)μiN0i−μiS0i+n∑j=1(mjiSj−mijS0i)=n∑j=1(mjiSj−mjiS0j)≤0. |
This indicates that the subset of Γ1
Γ={(S1,I1,R1,⋯,Sn,In,Rn)∈Γ1|Si≤S0i,i=1,2,⋯,n} |
is the positively invariant with respect to system (4.2). Therefore, we can study system (4.2) in the feasible region Γ.
Theorem 3. (ⅰ) If Rv<1, then the unique disease-free equilibrium E0 of system (4.2) is globally asymptotically stable in Γ.
(ⅱ) If Rv>1, then the disease-free equilibrium E0 is unstable and system (4.2) is uniformly persistent in ˚Γ (the interior of Γ).
Proof. From Theorem 2 in van den Driessche and Watmough [25], the disease-free equilibrium E0 of system (4.2) is locally asymptotically stable if Rv<1, and unstable if Rv>1.
Let I=(I1,I2,⋯,In)T. Using the second equation of (4.2), it follows that
dIdt≤(F−V)I. |
Let u>0 be the left eigenvector of the nonnegative matrix FV−1 with respect to the eigenvalue ρ(FV−1)=Rv, that is, uTFV−1=RvuT. Construct a Lyapunov function
V=uTI. | (4.5) |
Differentiating (4.5) along the system (4.2) yields
dVdt=uTdIdt≤uT(F−V)I=(uTFV−1−uT)VI=(Rv−1)uTVI. | (4.6) |
If Rv<1, then dV/dt≤0 with dV/dt=0 if and only if Ii=0 for some i. Similar to the proof of Theorem 2, it follows that the only invariant set where V′=0 is the singleton {E0}. Therefore, by LaSalle's Invariance Principle [29], E0 is globally asymptotically stable in Γ.
If Rv>1, by continuity and (Rv−1)uTVI>0 for I>0, we have V′>0 in a neighborhood of E0 in ˚Γ. In this case, the solutions in ˚Γ sufficiently close to E0 move away from E0, that is, E0 is unstable if Rv>1. Using the uniform persistence result from [27] and the similar argument as in the proof of Proposition 3.3 of [30], we can show that the instability of E0 implies the uniform persistence of (4.2).
If Rv>1, by Theorem 2.8.6 in [23] or Theorem D.3 in [11], the uniform persistence of (4.2) and the positive invariance of the compact set Γ imply that system (4.2) admits at lest one equilibrium in ˚Γ. Let E∗=(S∗1,I∗1,R∗1,⋯,S∗n,I∗n,R∗n) be an endemic equilibrium for system (4.2), then we have
{(1−pi)μiN0i−n∑j=1βijI∗jN0jS∗i−μiS∗i+n∑j=1(mjiS∗j−mijS∗i)=0,n∑j=1βijI∗jN0jS∗i−μiI∗i−γiI∗i+n∑j=1(mjiI∗j−mijI∗i)=0,piμiN0i+γiI∗i−μiR∗i+n∑j=1(mjiR∗j−mijR∗i)=0. | (5.1) |
Define
ˉβij=βijI∗jN0jS∗i+mjiI∗j, | (5.2) |
and
ˉB=(ˉβij)n×n, B∗=diag(n∑j=1ˉβij)−ˉBT. | (5.3) |
Let
ω=(ω1,ω2,⋯,ωn)=(B∗11,B∗22,⋯,B∗nn), |
where B∗ii is the cofactor of the i-th diagonal entry of B∗ and B∗ii>0, 1≤i≤n. Then, we have the following Lemma.
Lemma 4. The positive vector ω is a basis of the solution space of linear system B∗x=0. Furthermore, positive vector ω satisfies
n∑j=1ωj(βjiS∗jN0i+mij)=ωi(μi+γi+n∑j=1mij). | (5.4) |
Proof. Matrices B and M are irreducible which imply that matrix B∗ is also irreducible. Then it follows from Lemma 2 that positive vector ω=(ω1,ω2,⋯,ωn) is a basis of the solution space of linear system B∗ω=0. This indicates that
n∑j=1ˉβijωi=n∑j=1ˉβjiωj. |
Thus, one can derive from the expressions of ˉβij given in (5.2) and the second equation of (5.1) that
n∑j=1ωjˉβji=ωin∑j=1ˉβij=ωin∑j=1(βijI∗jN0jS∗i+mjiI∗j)=ωi(μi+γi+n∑j=1mij)I∗i. |
Therefore, we have
n∑j=1ωj(βjiS∗jN0i+mij)=ωi(μi+γi+n∑j=1mij). |
Theorem 4. If Rv>1, then the endemic equilibrium E∗ of system (4.2) is unique and it is globally asymptotically stable in ˚Γ under the condition ∑nj=1ωjβjiS∗jN0i>ωiγi.
Proof. We prove that E∗ is globally asymptotically stable in ˚Γ, which implies that the endemic equilibrium is unique. Since Si+Ii+Ri=N0i and the variable Ri does not appear in the first two equations in (4.2), then we can work on the following equivalent system
{S′i=(1−pi)μiN0i−n∑j=1βijIjN0jSi−μiSi+n∑j=1(mjiSj−mijSi),I′i=n∑j=1βijIjN0jSi−μiIi−γiIi+n∑j=1(mjiIj−mijIi). | (5.5) |
Let g(x)=x−1−lnx and
VSi=S∗ig(SiS∗i), VIi=I∗ig(IiI∗i). |
Note that (x−1)(1−y)=g(x)+g(y)−g(xy) for any x,y∈R+, then using the equilibrium equations (5.1) and differentiating VSi and VIi along system (5.5), we have
dVSidt=(1−S∗iSi)S′i=(1−S∗iSi)((1−pi)μiN0i−n∑j=1βijIjN0jSi−μiSi+n∑j=1mjiSj−n∑j=1mijSi)=−n∑j=1βijS∗iI∗jN0j(SiIjS∗iI∗j−1)(1−S∗iSi)−μiS∗i(SiS∗i−1)(1−S∗iSi)+n∑j=1mjiS∗j(SjS∗j−1)(1−S∗iSi)−n∑j=1mijS∗i(SiS∗i−1)(1−S∗iSi)=−(1−pi)μiN0ig(S∗iSi)−n∑j=1βijS∗iI∗jN0jg(SiIjS∗iI∗j)+n∑j=1βijS∗iI∗jN0jg(IjI∗j)+n∑j=1mjiS∗jg(SjS∗j)−n∑j=1mjiS∗jg(S∗iSjSiS∗j)−(μi+n∑j=1mij)S∗ig(SiS∗i), | (5.6) |
and
dVIidt=(1−I∗iIi)I′i=(1−I∗iIi)(n∑j=1βijIjN0jSi−μiIi−γiIi+n∑j=1mjiIj−n∑j=1mijIi)=n∑j=1βijS∗iI∗jN0j(SiIjS∗iI∗j−1)(1−I∗iIi)−(μi+γi)I∗i(IiI∗i−1)(1−I∗iIi)+n∑j=1mjiI∗j(IjI∗j−1)(1−I∗iIi)−n∑j=1mijI∗i(IiI∗i−1)(1−I∗iIi)=n∑j=1βijS∗iI∗jN0jg(SiIjS∗iI∗j)−n∑j=1βijS∗iI∗jN0jg(SiI∗iIjS∗iIiI∗j)+n∑j=1mjiI∗jg(IjI∗j)−n∑j=1mjiI∗jg(I∗iIjIiI∗j)−(μi+γi+n∑j=1mij)I∗ig(IiI∗i). | (5.7) |
Define a Lyapunov function as follows
V=n∑i=1ωi(VSi+VIi). | (5.8) |
Then combining equations (5.6) and (5.7) together, we have
dVdt=−n∑i=1ωi(1−pi)μiN0ig(S∗iSi)−n∑i=1n∑j=1ωimjiS∗jg(S∗iSjSiS∗j)−n∑i=1n∑j=1ωiβijS∗iI∗jN0jg(SiI∗iIjS∗iIiI∗j)−n∑i=1n∑j=1ωimjiI∗jg(I∗iIjIiI∗j)+n∑i=1n∑j=1ωimjiS∗jg(SjS∗j)−n∑i=1ωi(μi+n∑j=1mij)S∗ig(SiS∗i)+n∑i=1n∑j=1ωi(βijS∗iN0j+mji)I∗jg(IjI∗j)−n∑i=1ωi(μi+γi+n∑j=1mij)I∗ig(IiI∗i) |
In fact
n∑i=1n∑j=1ωimjiS∗jg(SjS∗j)=ω(MTc1)=(ωMT)c1=n∑i=1n∑j=1ωjmijS∗ig(SiS∗i), |
n∑i=1n∑j=1ωi(βijS∗iN0j+mji)I∗jg(IjI∗j)=ω(Qc2)=(ωQ)c2=n∑i=1n∑j=1ωj(βjiS∗jN0i+mij)I∗ig(IiI∗i), |
where ω=(ω1.⋯,ωn), c1=(S∗1g(S1S∗1),⋯,S∗ng(SnS∗n))T, c2=(I∗1g(I1I∗1),⋯,I∗ng(InI∗n))T, M=(mij)n×n and Q=(βijS∗iN0j+mji)n×n. Therefore, from ∑nj=1ωj(βjiS∗jN0i+mij)=ωi(μi+γi+∑nj=1mij) and the condition ∑nj=1ωjβjiS∗jN0i>ωiγi, we have
dVdt=−n∑i=1ωi(1−pi)μiN0ig(S∗iSi)−n∑i=1n∑j=1ωimjiS∗jg(S∗iSjSiS∗j)−n∑i=1n∑j=1ωimjiI∗jg(I∗iIjIiI∗j)−n∑i=1n∑j=1ωiβijS∗iI∗jN0jg(SiI∗iIjS∗iIiI∗j)−n∑i=1n∑j=1ωjβjiS∗jN0iS∗ig(SiS∗i)+n∑i=1ωiγiS∗ig(SiS∗i)≤0. |
It is easily to verify that V′=0 if and only if Si=S∗i and
I∗iIjIiI∗j=1, that is,IiI∗i=IjI∗j, for all i,j=1,2,⋯,n. | (5.9) |
This equation is equivalent to Ii=αI∗i, where α is an arbitrary constant. Substituting Si=S∗i,Ii=αI∗i into the first equation of (5.5), we have
(1−pi)μiN0i−S∗in∑j=1βijαI∗jN0j−μiS∗i+n∑j=1(mjiS∗j−mijS∗i)=0. | (5.10) |
Since the left-hand side of (5.10) is monotonically decreasing with respect to α, it follows from the equation (5.1) that (5.10) holds if and only if α=1. That is, the only compact invariant subset of V′=0 is the only singleton point {˜E∗}, here ˜E∗=(S∗1,I∗1,S∗2,I∗2,⋯,S∗n,I∗n). Using the LaSalle's Invariance Principle [29] and the similar argument to the proof of Theorem 3, we can show that ˜E∗ is unique and globally asymptotically stable for system (5.5). That is, the endemic equilibrium E∗ is unique and globally asymptotically stable for system (4.2) in ˚Γ if Rv>1 and ∑nj=1ωjβjiS∗jN0i>ωiγi.
In this section, we mainly perform some numerical simulations to verify the validity of the theoretical results carried out in the previous sections. In this paper, the simulations are performed by using Mathematica 10 software.
We first consider the two-group case (n=2), which is thought to be suitable for infectious diseases transmitted between two cities or communities. In this paper, we consider the unit of time as a year to model the long-term spread of disease. For the two-group system, we fix
μ1=180, μ2=170, γ1=0.03, γ2=0.03, p1=0.8, p2=0.6. |
If we denote lij as the annual migration proportion from group i to j, then migration rate mij determined by mij=−ln(1−lij). Here we take migration proportion l12=0.1 and l21=0.11, which means that 10% population migrate from group 1 to group 2 during one year and 11% population migrate from group 2 to group 1 during one year. We do not give the value of lii (which determined the values of mii) due to the fact that the theoretical results are independent of migration rate mii for all i. Under these settings, we only need to change the transmission rate βij to explore the global stability of each equilibrium.
If β=(0.11440.02860.04290.1001), we have Rv=0.9938<1. Following Theorem 3, we know that the disease-free equilibrium E0=(0.2108,0,0.7396,0.2918,0,0.6578) is the unique equilibrium of the system (1.1) and it is globally asymptotically stable in Γ. In fact, Figure 1(a) provides the simulations of this case and it reveals that each infected population converges to zero.
If β=(0.120.030.0450.105), we have Rv=1.0425>1. For this case, we have min{βiiS∗i/N∗i−γi}=0.0009>0. Then, it follows from Theorem 4 that the positive equilibrium E∗=(0.2978,0.0039,0.7485,0.2801,0.0036,0.6659) is the unique endemic equilibrium and it is globally asymptotically stable in ˚Γ. In fact, Figure 1(b) gives the simulation results for this case and it shows that each infected population converges to some positive steady states.
We next consider the 50-group case (n=50), which can be considered as the system of geographical spread of disease. Referring to the pervious example, we fix
μi=180, γi=12, pi=0.2, i=1,2,⋯,50. |
We employ the following form of the movement matrix M=(mij)50×50
M=(mij)50×50=(0ˉm1ˉm200⋯0ˉm10ˉm1ˉm20⋯0ˉm2ˉm10ˉm1ˉm2⋯00⋱⋱⋱⋱⋱⋮⋮0ˉm2ˉm10ˉm10000ˉm2ˉm10), | (6.1) |
where ˉmi=−ln(1−li), i=1,2 with l1=0.15, l2=0.1. It is easy to see that the movement matrix M is irreducible. Using the diffusive-like form of contact matrix B=(βij)50×50 considered in [6], the contact matrix B in this paper can be expressed as:
B=(βij)50×50=(βxα0⋯0αβxα⋯0⋮⋱⋱⋱⋮0αβxα0⋯0αβx), | (6.2) |
where α,βx are positive constants. Obviously, contact matrix B is irreducible. For simplicity, we fix α=0.01 and only change βx to observe the dynamical behavior of each equilibrium.
The simulations of system (1.1) with n=50 can be seen in Figure 2 and Figure 3. In both figures, the discrete groups are connected smoothly by the Mathematica commands "Plot3D" and "DensityPlot".
If βx=0.62, in this case, we have Rv=0.9985<1. Figure 2 gives the simulations of this case. It shows that each infected population converges to zero, i.e., the disease-free equilibrium is globally asymptotically stable if Rv<1. This verifies the conclusion of Theorem 3.
If βx=0.66, in this case, we have Rv=1.0609>1. Simulation results for this case are presented in Figure 3. It suggests that each infected population trends to some positive steady states, i.e., the endemic equilibrium is globally asymptotically stable when Rv>1. This simulation confirms the theoretical results of Theorem 4.
In particular, by virtue of the form of contact matrix B and movement matrix M, we can observe that two infection groups can cause infection to all groups. Meanwhile, the wave-like spreading pattern which connect the disease-free equilibrium E0 and the endemic equilibrium E∗.
In this paper, we investigate the complete global dynamics of a multi-group SIR model that incorporate group mixing and human movement. The results shows that model (1.1) exists a unique disease-free equilibrium, which is the only one equilibrium whose coordinates include zero. Meanwhile, model (1.1) has a unique endemic equilibrium if the control reproduction number Rv>1. Due to the complexity of model (1.1), we simplify this model to the equivalent system (4.2). By using the graph-theoretical approach [3], we obtain that the disease-free equilibrium is global asymptotically stable if Rv<1, and the endemic equilibrium is global asymptotically stable if Rv>1 and ∑nj=1ωjβjiS∗jN0i>ωiγi.
This work was supported in part by the Natural Science Foundation of Ningxia University (No. ZR18011), the National Natural Science Foundation of China (Nos. 11671206 and 61662060). The author would like to thank Prof. Zhipeng Qiu at Nanjing University of Science and Technology for his valuable suggestions.
The author declare there is no conflict of interest in this paper.
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