The food and beverage packaging industry has experienced remarkable growth in recent years. Particularly the requirement for appropriate packaging materials used for the sale of fermented products is boosted due to the rising acceptance of economical functional foods available to consumers on the shelves of their local supermarkets. The most popular nutraceutical foods with increased sales include natural yogurts, probiotic-rich milk, kefir, and other fermented food and beverage products. These items have mainly been produced from dairy-based or non-dairy raw materials to provide several product options for most consumers, including vegan and lactose-intolerant populations. Therefore, there is a need for an evaluation of the potential developments and prospects that characterize the growth of the food packaging industry in the global market. The article is based on a review of information from published research, encompassing current trends, emerging technologies, challenges, innovations, and sustainability initiatives for food industry packaging.
Citation: Dali Vilma Francis, Divakar Dahiya, Trupti Gokhale, Poonam Singh Nigam. Sustainable packaging materials for fermented probiotic dairy or non-dairy food and beverage products: challenges and innovations[J]. AIMS Microbiology, 2024, 10(2): 320-339. doi: 10.3934/microbiol.2024017
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The food and beverage packaging industry has experienced remarkable growth in recent years. Particularly the requirement for appropriate packaging materials used for the sale of fermented products is boosted due to the rising acceptance of economical functional foods available to consumers on the shelves of their local supermarkets. The most popular nutraceutical foods with increased sales include natural yogurts, probiotic-rich milk, kefir, and other fermented food and beverage products. These items have mainly been produced from dairy-based or non-dairy raw materials to provide several product options for most consumers, including vegan and lactose-intolerant populations. Therefore, there is a need for an evaluation of the potential developments and prospects that characterize the growth of the food packaging industry in the global market. The article is based on a review of information from published research, encompassing current trends, emerging technologies, challenges, innovations, and sustainability initiatives for food industry packaging.
Vector-borne diseases are infectious diseases caused by pathogens and parasites in human populations that are transmitted to people by blood-sucking arthropods, such as mosquitoes, ticks and fleas. They include some of the world's most destructive diseases, for instance, malaria, schistosomiasis, plague, and dengue fever. According to WHO [1], vector-borne diseases account for more than 17 % of all infectious diseases, causing more than 1 million deaths annually. In the past two decades, some vector-borne diseases, such as malaria and schistosomiasis, have continued to threaten human health. Furthermore, other vector-borne diseases have reemerged and broken out in different parts of the world, such as the 2014 Guangzhou outbreak of dengue fever and the outbreak of West Nile virus in North America since 1999. Any outbreak of the vector-borne diseases causes great harm to public health. As far as the 2014 Guangzhou outbreak of dengue fever is concerned, the total number of dengue fever cases reached 36,889 as of October 21st, 2014 [2], according to the provincial health and family planning commission. Due to the great harm to the public health caused by the vector diseases, it is imperative to understand the transmission dynamics of the vector-borne diseases firstly, and then discuss strategies to prevent and contain their outbreaks.
Mathematical modeling has contributed significantly to our understanding of the epidemiology of infectious diseases [3,5]. Over the past two decades, there have been many published mathematical models focused on understanding the transmission dynamics of the vector-borne diseases ([4,12,23,26,27,30] and references therein). These models provided useful insights into the transmission dynamics of the vector-borne diseases. Almost all of the above models are described by ordinary differential equations (ODEs); therefore, some of the assumptions implicitly made in the formulation of these models [28] include: (1) infectious individuals are equally infectious during their infectious period; (2) the stage durations of the latent and infectious periods are exponentially distributed. Although in many cases these simplifying assumptions may provide a reasonable approximation to the biological process being modeled, it is important to examine how the model results may be influenced by these assumptions, which calls for an investigation of models that use more realistic assumptions [28].
In this paper, we develop an age-structured model to study how transmission dynamics of the vector-borne diseases are affected by the incubation and infectious ages. The model studied in the paper incorporates both incubation age of the exposed hosts and infection age of the infectious hosts. Incubation age of the exposed hosts describes the different removal rates in the latent period, and infection age of the infectious hosts describes the variable infectiousness in the infectious period. Several recent studies [0,16,19,20,24,25,29] on age structured models have shown that age of infection may play an important role in the transmission dynamics of infectious diseases. Thieme and Castillo-Chavez [29] studied the effect of infection-age-independent infectivity on dynamics of HIV transmission, and showed that undamped oscillations may occur in particular if the variable infectivity is highly concentrated at certain parts of the incubation period. Lloyd [19,20] studied the epidemic model with the inclusion of non-exponential distributions of infectious periods. The results indicated that the inclusion of more realistic description of the recovery process may cause a significant destabilization of the model, and less dispersed distributions are seen to have two important epidemiological consequences: (1) less stable behavior is seen within the model; (2) disease persistence is diminished.
Epidemic models with age of infection are usually described by first order partial differential equations, whose complexity makes them more difficult to theoretically analyze, particularly, their global behavior. Most existing studies on age-structured models focus only on the existence of non-trivial steady states [17,11] or give local stability results [32]. The stability analysis of nonlinear dynamical systems has always been a topic of both theoretical and practical importance since global stability is one of the most important issues related to their dynamic behaviors. However, proving the global stability is a very challenging task, especially for nonlinear systems described by PDEs due to the lack of generically applicable tools. The global stability results for the age-structured epidemic models were first obtained in [7,8,9]. The method of Lyapunov functions is the most common tool used to prove the global stability, especially for ODE models [14,15,18]. In recent years, Lyapunov function has been also used to study the global stability of epidemic models with age of infection [21,22,31].
In this paper, we also use Lyapunov functions to study the global dynamics of a vector-borne disease model with incubation age of the exposed hosts and infection age of the infectious hosts. By using a class of Lyapunov functions we show that the global dynamics of the system is completely determined by the basic reproduction number
This paper is organized as follows. In the next section we formulate a vector-borne epidemic model with incubation age of exposed hosts and infection age of infectious hosts. The two infection ages describe the different removal rates in the latent stage and the variable infectiousness in the infectious stage, respectively. We obtain an explicit formula for the basic reproduction number of system. Then we discuss the trivial and non-trivial equilibria and their stabilities. In Section 3, the global stability of the infection-free equilibrium of the system is analyzed by constructing a Lyapunov function. In Section 4, we show uniform strong persistence of the vector-borne disease if
To introduce the model, we divide the host population under consideration into four groups: susceptible hosts at time
With the above notation, we study the following infection-age-structured vector-borne epidemic model:
{S′v(t)=Λv−Sv(t)∫∞0βv(a)Ih(a,t)da−μvSv(t),I′v(t)=Sv(t)∫∞0βv(a)Ih(a,t)da−(μv+αv)Iv(t),R′v(t)=αvIv(t)−μvRv(t),S′h(t)=Λh−βhSh(t)Iv(t)−μhSh(t),∂Eh(τ,t)∂τ+∂Eh(τ,t)∂t=−(μh+m(τ))Eh(τ,t),Eh(0,t)=βhSh(t)Iv(t),∂Ih(a,t)∂a+∂Ih(a,t)∂t=−(μh+αh(a)+rh(a))Ih(a,t),Ih(0,t)=∫∞0m(τ)Eh(τ,t)dτ,R′h(t)=∫∞0rh(a)Ih(a,t)da−μhRh(t). | (1) |
In equation (1),
To understand the model, notice that susceptible host individuals are recruited at a rate
We notice that the equations for the recovered individuals and the recovered vectors are decoupled from the system and the analysis of system (1) is equivalent to the analysis of the system
{S′v(t)=Λv−Sv(t)∫∞0βv(a)Ih(a,t)da−μvSv(t),I′v(t)=Sv(t)∫∞0βv(a)Ih(a,t)da−(μv+αv)Iv(t),S′h(t)=Λh−βhSh(t)Iv(t)−μhSh(t),∂Eh(τ,t)∂τ+∂Eh(τ,t)∂t=−(μh+m(τ))Eh(τ,t),Eh(0,t)=βhSh(t)Iv(t),∂Ih(a,t)∂a+∂Ih(a,t)∂t=−(μh+αh(a)+rh(a))Ih(a,t),Ih(0,t)=∫∞0m(τ)Eh(τ,t)dτ. | (2) |
Model (2) is equipped with the following initial conditions:
Sv(0)=Sv0,Iv(0)=Iv0,Sh(0)=Sh0,Eh(τ,0)=φ(τ),Ih(a,0)=ψ(a). |
All parameters are nonnegative,
Assumption 2.1 The parameter-functions satisfy the following.
1. The functions
2. The functions
3. The functions
Define the space of functions
X=R×R×R×(L1(0,∞))×(L1(0,∞)). |
It can be verified that solutions of (2) with nonnegative initial conditions belong to the positive cone for
ddt(Sv(t)+Iv(t))≤Λv−μv(Sv(t)+Iv(t)). |
Hence,
lim supt(Sv(t)+Iv(t))≤Λvμv. |
The number of the hosts can be bounded as follows:
ddt(Sh(t)+∫∞0Eh(τ,t)dτ+∫∞0Ih(a,t)da)≤Λh−μh(Sh(t)+∫∞0Eh(τ,t)dτ+∫∞0Ih(a,t)da). |
Hence,
lim supt(Sh(t)+∫∞0Eh(τ,t)dτ+∫∞0Ih(a,t)da)≤Λhμh. |
Therefore, the following set is positively invariant for system
Ω={(Sv,Iv,Sh,Eh,Ih)∈X+|(Sv(t)+Iv(t))≤Λvμv,(Sh(t)+∫∞0Eh(τ,t)dτ+∫∞0Ih(a,t)da)≤Λhμh}. |
Finally, since the exit rate of exposed host individuals from the incubation compartment is given by
π1(τ)=e−μhτe−∫τ0m(σ)dσ. | (3) |
The exit rate of infected individuals from the infective compartment is given by
π2(a)=e−μhae−∫a0(αh(σ)+rh(σ))dσ. | (4) |
The reproduction number of disease in system (2) is given by the following expression
R0=βhΛvΛhμvμh(μv+αv)∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da. | (5) |
The reproduction number of disease gives the number of secondary infections produced in an entirely susceptible population by a typical infected individual during its entire infectious period.
Rh=Λvμv∫∞0βv(a)π2(a)da,Rv=βhΛhμh(μv+αv)∫∞0m(τ)π1(τ)dτ, |
that is
System (2) always has a unique disease-free equilibrium
E0=(S∗v0, 0, S∗h0, 0, 0), |
where
S∗v0=Λvμv,S∗h0=Λhμh. |
In addition, for Dengue virus there is a corresponding endemic equilibrium
E1=(S∗v, I∗v, S∗h, E∗h(τ), I∗h(a)). |
We denote by
Λ=βhΛhΛvμhμv(μv+αv),b=∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da,b(λ)=∫∞0m(τ)e−λτπ1(τ)dτ∫∞0βv(a)e−λaπ2(a)da. | (6) |
The non-zero components of the equilibrium
I∗v=μvμh(R0−1)βh(Λhb+μv),S∗v=Λv−(μv+αv)I∗vμv,S∗h=ΛhβhI∗v+μh,E∗h(τ)=E∗h(0)π1(τ),E∗h(0)=βhS∗hI∗v,I∗h(a)=I∗h(0)π2(a),I∗h(0)=E∗h(0)∫∞0m(τ)π1(τ)dτ. | (7) |
Next, we turn to the linearized equations for the disease-free equilibrium. To introduce the linearization at the disease-free equilibrium
{dxv(t)dt=−S∗v0∫∞0βv(a)yh(a,t)da−μvxv(t),dyv(t)dt=S∗v0∫∞0βv(a)yh(a,t)da−(μv+αv)yv(t),dxh(t)dt=−βhS∗h0yv(t)−μhxh(t),∂zh(τ,t)∂τ+∂zh(τ,t)∂t=−(μh+m(τ))zh(τ,t),zh(0,t)=βhS∗h0yv(t),∂yh(a,t)∂a+∂yh(a,t)∂t=−(μh+αh(a)+rh(a))yh(a,t),yh(0,t)=∫∞0m(τ)zh(τ,t)dτ. | (8) |
To study system (2), we look for solutions of the form
{λˉxv=−S∗v0∫∞0βv(a)ˉyh(a)da−μvˉxv,λˉyv=S∗v0∫∞0βv(a)ˉyh(a)da−(μv+αv)ˉyv,λˉxh=−βhS∗h0ˉyv−μhˉxh,dˉzh(τ)dτ=−(λ+μh+m(τ))ˉzh(τ),ˉzh(0)=βhS∗h0ˉyv,dˉyh(a)da=−(λ+μh+αh(a)+rh(a))ˉyh(a),ˉyh(0)=∫∞0m(τ)ˉzh(τ)dτ. | (9) |
We notice that the two equations for
ˉzh(τ)=ˉzh(0) e−λτπ1(τ)=βhS∗h0ˉyv e−λτπ1(τ),ˉyh(a)=ˉyh(0) e−λaπ2(a)=βhS∗h0ˉyv e−λaπ2(a)∫∞0m(τ) e−λτπ1(τ)dτ. | (10) |
Substituting for
λ+μv+αv=βhS∗v0S∗h0∫∞0m(τ)e−λτπ1(τ)dτ∫∞0βv(a)e−λaπ2(a)da. | (11) |
Now we are ready to establish the following result.
Proposition 1. If
R0<1, |
then the disease-free equilibrium is locally asymptotically stable. If
Proof. Assume
R0<1. |
We set
LHSdef=λ+μv+αv,RHSdef=G1(λ)=βhS∗v0S∗h0∫∞0m(τ)e−λτπ1(τ)dτ∫∞0βv(a)e−λaπ2(a)da. | (12) |
Consider
|LHS|≥μv+αv,|RHS|≤G1(ℜλ)≤G1(0)=βhS∗v0S∗h0∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da=βhΛvΛhμvμh∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da=R0(μv+αv)<|LHS|. |
This gives a contradiction. Hence, we have shown that equation (11) cannot have any roots with non-negative real parts. Therefore, the disease-free equilibrium
Now assume
R0>1. |
We rewrite the characteristic equation (11) in the form
(λ+μv+αv)−βhS∗v0S∗h0∫∞0m(τ)e−λτπ1(τ)dτ∫∞0βv(a)e−λaπ2(a)da=0. | (13) |
We denote
G2(λ)=(λ+μv+αv)−βhS∗v0S∗h0∫∞0m(τ)e−λτπ1(τ)dτ∫∞0βv(a)e−λaπ2(a)da. | (14) |
Thus equation (13) has turned into the following characteristic equation
G2(λ)=0. | (15) |
For
G2(0)=(μv+αv)−βhS∗v0S∗h0∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da=(μv+αv)(1−R0)<0. |
Furthermore,
Now we turn to the local stability of the endemic equilibrium
Proposition 2. Assume
Proof. We study the linearized equation around the endemic equilibrium
{dxv(t)dt=−S∗v∫∞0βv(a)yh(a,t)da−xv(t)∫∞0βv(a)I∗h(a)da−μvxv(t),dyv(t)dt=S∗v∫∞0βv(a)yh(a,t)da+xv(t)∫∞0βv(a)I∗h(a)da−(μv+αv)yv(t),dxh(t)dt=−βhS∗hyv(t)−βhxh(t)I∗v−μhxh(t),dzh(τ)dτ=−(λ+μh+m(τ))zh(τ,t),zh(0,t)=βhS∗hyv(t)+βhxh(t)I∗v,dyh(a)da=−(λ+μh+αh(a)+rh(a))yh(a,t),yh(0,t)=∫∞0m(τ)zh(τ,t)dτ. | (16) |
An approach similar to [8] (see Appendix B in [8]) can show that the linear stability of the system is in fact determined by the eigenvalues of the linearized system (16). To investigate the point spectrum, we look for exponential solutions (see the case of the disease-free equilibrium) and obtain a linear eigenvalue problem.
{λxv=−S∗v∫∞0βv(a)yh(a)da−xv∫∞0βv(a)I∗h(a)da−μvxv,λyv=S∗v∫∞0βv(a)yh(a)da+xv∫∞0βv(a)I∗h(a)da−(μv+αv)yv,λxh=−zh(0)−μhxh,dzh(τ)dτ=−(λ+μh+m(τ))zh(τ),zh(0)=βhS∗hyv+βhI∗vxh,dyh(a)da=−(λ+μh+αh(a)+rh(a))yh(a),yh(0)=∫∞0m(τ)zh(τ)dτ. | (17) |
Solving the differential equation, we have
zh(τ)=zh(0) e−λτπ1(τ),yh(a)=yh(0) e−λaπ2(a)=zh(0) e−λaπ2(a)∫∞0m(τ) e−λτπ1(τ)dτ. |
Substituting for
{(λ+μv+∫∞0βv(a)I∗h(a)da)xv+S∗vb(λ)zh(0)=0,−xv∫∞0βv(a)I∗h(a)da+(λ+μv+αv)yv−S∗vb(λ)zh(0)=0,(λ+μh)xh+zh(0)=0,−βhI∗vxh−βhS∗hyv+zh(0)=0. | (18) |
By direct calculation, we obtain the following characteristic equation:
(λ+μv+∫∞0βv(a)I∗h(a)da)(λ+μv+αv)(λ+μh+βhI∗v)=βhS∗hS∗vb(λ)(λ+μv)(λ+μh). | (19) |
We divide both sides by
G3(λ)=(λ+μv+∫∞0βv(a)I∗h(a)da)(λ+μv+αv)(λ+μh+βhI∗v)(λ+μv)(λ+μh),G4(λ)=βhS∗hS∗vb(λ)=βhS∗hS∗v∫∞0m(τ)e−λτπ1(τ)dτ∫∞0βv(a)e−λaπ2(a)da. | (20) |
Thus (19) can be expressed as the the equation
G3(λ)=G4(λ). | (21) |
If
|G3(λ)|>|λ+μv+αv|≥μv+αv. | (22) |
From system (2), we have
βhS∗vS∗h∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da=μv+αv. |
Hence,
|G4(λ)|≤|G4(ℜλ)|≤G4(0)=βhS∗vS∗h∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da=μv+αv<|G3(λ)|. | (23) |
This leads to contradiction. Hence, for
In the previous section, we have established that equilibria are locally stable, that is, given the conditions on the parameters, if the initial conditions are close enough to the equilibrium, the solution will converge to that equilibrium. In this section our objective is to extend these results to global results. That is, given the conditions on the parameters, convergence to the equilibrium occurs independently of the initial conditions.
As a first step, we establish the global stability of the disease-free equilibrium. We will use a Lyapunov function to approach the problem. We need to integrate the differential equation along the characteristic lines. Denote the initial condition by
BE(t)=Eh(0,t),BI(t)=Ih(0,t). |
Integrating along the characteristic lines, we obtain
Eh(τ,t)={BE(t−τ)π1(τ), t>τ,φ(τ−t)π1(τ)π1(τ−t), t<τ,Ih(a,t)={BI(t−a)π2(a), t>a,ψ(a−t)π2(a)π2(a−t), t<a. | (24) |
Theorem 3.1. Assume
R0≤1. |
Then the disease-free equilibrium
Proof. We will use a Lyapunov function. We adopt the Volterra-type function used in [7,10,13]. Define
f(x)=x−1−lnx. |
We note that
q(a)=∫∞aβv(s)e−∫sa(μh+αh(σ)+rh(σ))dσds,p(τ)=βhΛhΛvμhμv(μv+αv)q(0)∫∞τm(s)e−∫sτ(μh+m(σ))dσds. | (25) |
We notice that
p(0)=R0. |
Differentiating (25) first, we obtain
q′(a)=−βv(a)+(μh+αh(a)+rh(a))q(a),p′(τ)=−βhΛhΛvμhμv(μv+αv)q(0)m(τ)+(μh+m(τ))p(τ). | (26) |
According to (26), we have
U1(t)=U11(t)+U12(t)+U13(t)+U14(t)+U15(t), | (27) |
where
U11(t)=Λf(SvS∗v0),U12(t)=ΛS∗v0Iv(t),U13(t)=S∗h0f(ShS∗h0),U14(t)=∫∞0p(τ)Eh(τ,t)dτ,U15(t)=Λ∫∞0q(a)Ih(a,t)da.. |
Because of the complexity of the expressions, we take the derivative of each component of the Lyapunov function separately
U′11(t)=ΛS∗v0(1−S∗v0Sv)(Λv−Sv∫∞0βv(a)Ih(a,t)da−μvSv)=ΛS∗v0(1−S∗v0Sv)(μvS∗v0−μvSv−Sv∫∞0βv(a)Ih(a,t)da)=−Λμv(Sv−S∗v0)2SvS∗v0−ΛS∗v0Sv∫∞0βv(a)Ih(a,t)da+Λ∫∞0βv(a)Ih(a,t)da. | (28) |
U′12(t)=ΛS∗v0[Sv∫∞0βv(a)Ih(a,t)da−(μv+αv)Iv]=ΛS∗v0Sv∫∞0βv(a)Ih(a,t)da−βhS∗h0Iv. | (29) |
Noting that
U′13(t)=(1−S∗h0Sh)(Λh−βhShIv−μhSh)=(1−S∗h0Sh)(μhS∗h0−μhSh−βhShIv)=−μh(Sh−S∗h0)2Sh−Eh(0,t)+βhS∗h0Iv. | (30) |
U′14(t)=∫∞0p(τ)∂Eh(τ,t)∂tdτ=−∫∞0p(τ)[∂Eh(τ,t)∂τ+(μh+m(τ))Eh(τ,t)]dτ=−[∫∞0p(τ)dEh(τ,t)+∫∞0(μh+m(τ))p(τ)Eh(τ,t)dτ]=−[p(τ)Eh(τ,t)|∞0−∫∞0Eh(τ,t)dp(τ)+∫∞0(μh+m(τ))p(τ)Eh(τ,t)dτ]=p(0)Eh(0,t)−Λq(0)∫∞0m(τ)Eh(τ,t)dτ=R0Eh(0,t)−Λq(0)Ih(0,t). | (31) |
Similarly to (31), we obtain
U′15(t)=−Λ∫∞0q(a)[∂Ih(a,t)∂a+(μh+αh(a)+rh(a))Ih(a,t)]da=Λq(0)Ih(0,t)−Λ∫∞0βv(a)Ih(a,t)da. | (32) |
Now differentiating (27) we have
U′1(t)=−Λμv(Sv−S∗v0)2SvS∗v0−ΛS∗v0Sv∫∞0βv(a)Ih(a,t)da+Λ∫∞0βv(a)Ih(a,t)da+ΛS∗v0Sv∫∞0βv(a)Ih(a,t)da−βhS∗h0Iv−μh(Sh−S∗h0)2Sh−Eh(0,t)+βhS∗h0Iv+R0Eh(0,t)−Λq(0)Ih(0,t)+Λq(0)Ih(0,t)−Λ∫∞0βv(a)Ih(a,t)da. | (33) |
Canceling all terms that cancel, we simplify the above expression:
U′1(t)=−Λμv(Sv−S∗v0)2SvS∗v0−μh(Sh−S∗h0)2Sh+(R0−1)Eh(0,t). | (34) |
The last inequality follows from the fact that
Θ1={(Sv,Iv,Sh,Eh,Ih)∈Ω|U′1(t)=0}. |
LaSalle's Invariance Principle [9] implies that the bounded solutions of (2) converge to the largest compact invariant set of
Ih(0,t)=∫∞0m(τ)E(τ,t)dτ. |
So we have
limt→∞Ih(a,t)=0, t>a. |
Therefore, we conclude that the disease-free equilibrium is globally stable. This completes the proof.
Our next step is to show the global asymptotic stability of the epidemic equilibrium in system (2)
In the previous section, we saw that if the reproduction number is less or equal to one, The vector-borne disease dies out. In this section, we assume that for
From Proposition 2 we know that under the specified conditions the equilibrium
U2(t)=U21(t)+U22(t)+U23(t)+U24(t)+U25(t)+U26(t)+U27(t)+U28(t), | (35) |
where
{U21(t)=1q(0)∫∞0m(τ)π1(τ)dτf(SvS∗v),U22(t)=1S∗vq(0)∫∞0m(τ)π1(τ)dτI∗vf(IvI∗v),U23(t)=S∗hf(ShS∗h),U24(t)=1R0∫∞0p(τ)E∗h(τ)f(Eh(τ,t)E∗h(τ))dτ,U25(t)=1q(0)∫∞0m(τ)π1(τ)dτ∫∞0q(a)I∗h(a)f(Ih(a,t)I∗h(a))da,U26(t)=∫∞tS∗hSh(s)Eh(0,s)ds,U27(t)=∫∞tSh(s)S∗h(E∗h(0))2Eh(0,s)ds,U28(t)=2E∗h(0)t. | (36) |
One difficulty with the Lyapunov function
ˆΩ1={φ∈L1+(0,∞)|∃s≥0: ∫∞0m(τ+s)φ(τ)dτ>0}, |
ˆΩ2={ψ∈L1+(0,∞)|∃s≥0: ∫∞0βv(a+s)ψ(a)da>0}. |
Define
Ω0=R+×R+×R+׈Ω1׈Ω2. |
Finally, define
We want to formulate the persistence result for the vector-borne disease which on one side will justify the use of the Lyapunov functional
Definition 4.1. We call the vector-borne disease uniformly weakly persistent if there exists some
lim supt→∞∫∞0Eh(τ,t)dτ>γwhenever∫∞0φ(τ)dτ>0, |
lim supt→∞∫∞0Ih(a,t)da>γwhenever∫∞0ψ(a)da>0, |
and
lim supt→∞Iv(t)>γwheneverIv0>0. |
for all solutions of model (2).
One of the important implications of uniform weak persistence of the disease is that the disease-free equilibrium is unstable.
Definition 4.2. We call the vector borne diease uniformly strongly persistent if there exists some
lim inft→∞∫∞0Eh(τ,t)dτ>γwhenever∫∞0φ(τ)dτ>0, |
lim inft→∞∫∞0Ih(a,t)da>γwhenever∫∞0ψ(a)da>0, |
and
lim inft→∞Iv(t)>γwheneverIv0>0. |
for all solutions of model (2).
It is evident from the definitions that, if the disease is uniformly strongly persistent, it is also uniformly weakly persistent. To show uniform strong persistence for the vector-borne disease, we need to show two components.
1. We have to show that the vector-borne disease is uniformly weakly persistent.
2. We need to show that the solution semiflow of system (2.2) has a global compact attractor
First, we show uniform weak persistence of the vector-borne disease. The following proposition states that result.
Proposition 3. Assume
lim suptβhIv(t)≥γ,lim supt∫∞0m(τ)Eh(τ,t)dτ≥γ, |
lim supt∫∞0βv(a)Ih(a,t)da≥γ. |
Proof. We argue by contradiction. Assume that the vector-borne disease dies out. In particular, assume that for every
lim suptβhIv(t)<ε,lim supt∫∞0m(τ)Eh(τ,t)dτ<ε,lim supt∫∞0βv(a)Ih(a,t)da<ε. |
Hence, there exist
βhIv(t)<ε,∫∞0m(τ)Eh(τ,t)dτ<ε,∫∞0βv(a)Ih(a,t)da<ε. |
By shifting the dynamical system we may assume that the above inequality holds for all
S′v(t)≥Λv−εSv−μvSv,S′h(t)≥Λh−εSh−μhSh. |
Therefore,
limsuptβhIv(t)<ε,limsupt∞∫0m(τ)Eh(τ,t)dτ<ε,limsupt∞∫0βv(a)Ih(a,t)da<ε. |
Recall that we are using the following notation
{BE(t)=Eh(0,t)=βhShIv≥βhΛhε+μhIv,dIv(t)dt≥Λvε+μv∫∞0βv(a)Ih(a,t)da−(μv+αv)Iv. | (37) |
Now, we apply expression (24) to obtain the following system of inequalities in
{BE(t)≥βhΛhε+μhIv,BI(t)=∫∞0m(τ)Eh(τ,t)dτ≥∫t0m(τ)BE(t−τ)π1(τ)dτ,dIv(t)dt≥Λvε+μv∫t0βv(a)BI(t−a)π2(a)da−(μv+αv)Iv. | (38) |
We will take the Laplace transform of both sides of inequalities (38). Since all functions above are bounded, their Laplace transform exists for
ˆK1(λ)=∫∞0m(τ)π1(τ)e−λτdτ,ˆK2(λ)=∫∞0βv(a)π2(a)e−λada. | (39) |
Taking the Laplace transform of inequalities (38) and using the convolution property of the Laplace transform, we obtain the following system of inequalities for
{ˆBE(λ)≥βhΛhε+μhˆIv(λ),ˆBI(λ)≥ˆK1(λ)ˆBE(λ),λˆIv(λ)−Iv(0)≥Λvε+μvˆK2(λ)ˆBI(λ)−(μv+αv)ˆIv(λ). | (40) |
Eliminating
ˆBE(λ)≥βhΛvΛhˆK1(λ)ˆK2(λ)(ε+μv)(ε+μh)(λ+μv+αv)ˆBE(λ)+βhΛh(ε+μh)(λ+μv+αv)Iv(0). |
This last inequality should hold for the given
βhΛvΛhˆK1(λ)ˆK2(λ)(ε+μv)(ε+μh)(λ+μv+αv)≈R0>1. |
In addition, there is another positive term on the right side of this equality. This is a contradiction with our assumption that
lim suptβhIv(t)<ε,lim supt∫∞0m(τ)Eh(τ,t)dτ<ε, |
lim supt∫∞0βv(a)Ih(a,t)da<ε. | (41) |
Therefore, there exists at least one limit supremum which is bounded below by
Note that
Eh(0,t)=ShβhIv(t)≤ΛhμhβhIv(t)Ih(0,t)=∫∞0m(τ)Eh(τ,t)dτ=∫t0m(τ)Eh(0,t−τ)π1(τ)dτ+∫∞tm(τ)φ(τ−t)π1(τ)π1(τ−t)dτdIv(t)dt=∫∞0βv(a)Ih(a,t)da−(μv+αv)Iv(t)=∫t0βv(a)Ih(0,t−a)π2(a)da+∫∞tβv(a)ψ(a−t)π2(a)π2(a−t)da−(μv+αv)Iv(t). | (42) |
Following (42), we get
lim suptEh(0,t)≤Λhμhlim suptβhIv(t)lim suptIh(0,t)≤∫∞0m(τ)π1(τ)dτlim suptEh(0,t)≤ˉm∫∞0e−μhτdτlim suptEh(0,t)=ˉmμhlim suptEh(0,t)lim suptdIv(t)dt≤∫∞0βv(a)π2(a)dalim suptIh(0,t)−(μv+αv)lim suptIv(t)≤m0∫∞0e−μhadalim suptIh(0,t)−(μv+αv)lim suptIv(t)=m0μhlim suptIh(0,t)−(μv+αv)lim suptIv(t), | (43) |
where
lim suptIv(t)≤m0μh(μv+αv)lim suptIh(0,t). |
Thus we obtain that if any inequality in (41) holds, all the three inequalities are less than a constant
lim suptβhIv(t)≥γ,lim supt∫∞0m(τ)Eh(τ,t)dτ≥γ,lim supt∫∞0βv(a)Ih(a,t)da≥γ. |
In addition, the differential equation for
dIvdt≥Λvγγ+μv−(μv+αv)Iv, |
which in turn, implies a lower bound for
Our next goal is to prove that system (2) has a global compact attractor
Ψ(t:Sv0,Iv0,Sh0,φ(⋅),ψ(⋅))=(Sv(t),Iv(t),Sh(t),Eh(τ,t),Ih(a,t)). |
Definition 4.3. The semiflow is a mapping
The following proposition establishes the presence of a global compact attractor.
Proposition 4. Assume
Ψ(t,x0)⊆Tforeveryx0∈T, ∀t≥0. |
Proof. To establish this result, we will apply Lemma 3.1.3 and Theorem 3.4.6 in [22]. To show the assumptions of Lemma 3.1.3 and Theorem 3.4.6 in [22], we split the solution semiflow into two components. For an initial condition
ˆΨ(t:Sv0,Iv0,Sh0,φ(⋅),ψ(⋅))=(0,0,0,ˆEh(⋅,t),ˆIh(⋅,t))˜Ψ(t:Sv0,Iv0,Sh0,φ(⋅),ψ(⋅))=(Sv(t),Iv(t),Sh(t),˜Eh(⋅,t),˜Ih(⋅,t)), | (44) |
where
{∂ˆEh∂t+∂ˆEh∂τ=−(μh+m(τ))ˆEh(τ,t),ˆEh(0,t)=0,ˆEh(τ,0)=φ(τ), | (45) |
{∂ˆIh∂t+∂ˆIh∂a=−(μh+αh(a)+rh(a))ˆIh(τ,t),ˆIh(0,t)=0,ˆIh(a,0)=ψ(a), | (46) |
and
{∂˜Eh∂t+∂˜Eh∂τ=−(μ+m(τ))˜Eh(τ,t),˜Eh(0,t)=βhShIv,˜Eh(τ,0)=0, | (47) |
{∂˜Ih∂t+∂˜Ih∂a=−(μh+αh(a)+rh(a))˜Ih(τ,t),˜Ih(0,t)=∫∞0m(τ)˜Eh(τ,t)dτ,˜Ih(τ,0)=0. | (48) |
System (45) is decoupled from the remaining equations. Using the formula (24) to integrate along the characteristic lines, we obtain
ˆEh(τ,t)={0, t>τ,φ(τ−t)π1(τ)π1(τ−t), t<τ, | (49) |
ˆIh(a,t)={0, t>a,ψ(a−t)π2(a)π2(a−t), t<a. | (50) |
Integrating
∫∞tφ(τ−t)π1(τ)π1(τ−t)dτ=∫∞0φ(τ)π1(t+τ)π1(τ)dτ≤e−μht∫∞0φ(τ)dτ→0, |
as
∫∞tψ(a−t)π2(a)π2(a−t)da=∫∞0ψ(a)π2(t+a)π2(a)da≤e−μht∫∞0ψ(a)da→0, |
as
To show the second claim, we need to show compactness. We fix
˜Ψ(t,x0)=(Sv(t),Iv(t),Sh(t),˜Eh(τ,t),˜Ih(a,t)), |
obtained by taking different initial conditions in
{˜Ψ(t,x0)|x0∈X0,t−fixed}⊆X0, |
and, therefore, it is bounded. Thus, we have established the boundedness of the set. To show compactness we first see that the remaining conditions of the Frechet-Kolmogorov Theorem [19]. The third condition in the Frechet-Kolmogorov Theorem for compactness in L
˜Eh(τ,t)={˜BE(t−τ)π1(τ), t>τ,0, t<τ,˜Ih(a,t)={˜BI(t−a)π2(a), t>a,0, t<a, | (51) |
where
˜BE(t)=βhSh(t)Iv(t),˜BI(t)=∫∞0m(τ)˜Eh(τ,t)dτ=∫t0m(τ)˜BE(t−τ)π1(τ)dτ. | (52) |
First, we notice that for
˜BE(t)≤k1. |
Then, we obtain
˜BI(t)=∫t0m(τ)˜BE(t−τ)π1(τ)dτ≤k2∫t0˜BE(t−τ)dτ=k2∫t0˜BE(τ)dτ≤k1k2t. |
Next, we differentiate (51) with respect to
|∂˜Eh(τ,t)∂τ|≤{|˜B′E(t−τ)|π1(τ)+˜BE(t−τ)|π′1(τ)|, t>τ,0, t<τ,|∂˜Ih(a,t)∂a|≤{|˜B′I(t−a)|π2(a)+˜BI(t−a)|π′2(a)|, t>a,0, t<a. |
We have to see that
˜B′E(t)=βh(S′h(t)Iv(t)+Sh(t)I′v(t)),˜B′I(t)=m(t)˜BE(0)π1(t)+∫t0m(τ)˜B′E(t−τ)π1(τ)dτ. | (53) |
Taking an absolute value and bounding all terms, we can rewrite the above equality as the following inequality:
|˜B′E(t)|≤k3,|˜B′I(t)|≤k4. |
Putting all these bounds together, we have
∥∂τ˜Eh∥≤k3∫∞0π1(τ)dτ+k1(μh+ˉm)∫∞0π1(τ)dτ<b1,∥∂a˜Ih∥≤k4∫∞0π2(a)da+k1k2(μh+ˉαh+ˉrh)t∫∞0π2(a)da<b2, |
where
∫∞0|˜Eh(τ+h,t)−˜Eh(τ,t)|dτ≤∥∂τ˜Eh∥|h|≤b1|h|,∫∞0|˜Ih(a+h,t)−˜Ih(a,t)|dτ≤∥∂a˜Ih∥|h|≤b2|h|. |
Thus, the integral can be made arbitrary small uniformly in the family of functions. That establishes the second requirement of the Frechét-Kolmogorov Theorem. We conclude that the family is compact.
Now we have all components to establish the uniform strong persistence. The next proposition states the uniform strong persistence of
Proposition 5. Assume
lim inftβhIv(t)≥γ,lim inft∫∞0m(τ)Eh(τ,t)dτ≥γ,lim inft∫∞0βv(a)Ih(a,t)da≥γ. |
Proof. We apply Theorem 2.6 in [29]. We consider the solution semiflow
{ρ1(Ψ(t,x0))=βhIv(t),ρ2(Ψ(t,x0))=∫∞0m(τ)˜Eh(τ,t)dτ,ρ3(Ψ(t,x0))=∫∞0βv(a)˜Ih(a,t)da. |
Proposition 3 implies that the semiflow is uniformly weakly
βhIv(t)≥βhIv(s)e−(μv+αv)(t−s),∫∞0m(τ)˜Eh(τ,t)dτ=˜BI(t)=∫t0m(τ)˜BE(t−τ)π1(τ)dτ≥k1∫t0˜BE(t−τ)dτ=k1∫t0˜BE(τ)dτ=k1∫t0βhSh(τ)Iv(τ)dτ≥k2∫t0Iv(τ)dτ=k2∫t0Iv(s)e−(μv+αv)(τ−s)dτ=k2Iv(s)μv+αve(μv+αv)s(1−e−(μv+αv)t),∫∞0βv(a)˜Ih(a,t)da=∫t0βv(a)˜BI(t−a)π2(a)da≥k3∫t0˜BI(t−a)da=k3∫t0˜BI(a)da≥k2k3Iv(s)μv+αve(μv+αv)s∫t0(1−e−(μv+αv)a)da. |
Therefore,
lim inftβhIv(t)≥γ,lim inft∫∞0m(τ)Eh(τ,t)dτ≥γ,lim inft∫∞0βv(a)Ih(a,t)da≥γ. |
Corollary 1. Assume
ϑ≤Sv(t)≤M,ϑ≤Sh(t)≤M, ∀t∈R, |
and
ϑ≤βhIv(t)≤M,ϑ≤∫∞0m(τ)Eh(τ,t)dτ≤M,ϑ≤∫∞0βv(a)Ih(a,t)da≤M,∀t∈R. |
In the next section we show that the endemic equilibrium
Now we are ready to establish the global stability of the equilibrium
Theorem 5.1. Assume
Proof. Since
ε1≤IvI∗v≤M1,ε1≤Eh(τ,t)E∗h(τ)≤M1,ε1≤Ih(a,t)I∗h(a)≤M1. |
This makes the Lyapunov function defined in (35) well defined.
Because of the complexity of the expressions, we make the derivative of each component of the Lyapunov function separately (see (35)).
U′21(t)=(1−S∗vSv)(Λv−Sv∫∞0βv(a)Ih(a,t)da−μvSv)S∗vq(0)∫∞0m(τ)π1(τ)dτ=(1−S∗vSv)[S∗v∫∞0βv(a)I∗h(a)da+μvS∗v−Sv∫∞0βv(a)Ih(a,t)da−μvSv]S∗vq(0)∫∞0m(τ)π1(τ)dτ=−μv(Sv−S∗v)2S∗vSvq(0)∫∞0m(τ)π1(τ)dτ+∫∞0βv(a)I∗h(a)(1−S∗vSv−SvIh(a,t)S∗vI∗h(a)+Ih(a,t)I∗h(a))daq(0)∫∞0m(τ)π1(τ)dτ. | (54) |
Next, we need to take the time derivative of
U′22(t)=(1−I∗vIv)[Sv∫∞0βv(a)Ih(a,t)da−(μv+αv)Iv]S∗vq(0)∫∞0m(τ)π1(τ)dτ=(1−I∗vIv)(Sv∫∞0βv(a)Ih(a,t)da−S∗v∫∞0βv(a)I∗h(a)daI∗vIv)S∗vq(0)∫∞0m(τ)π1(τ)dτ=(1−I∗vIv)S∗v∫∞0βv(a)I∗h(a)(SvIh(a,t)S∗vI∗h(a)−IvI∗v)daS∗vq(0)∫∞0m(τ)π1(τ)dτ=∫∞0βv(a)I∗h(a)(SvIh(a,t)S∗vI∗h(a)−IvI∗v−SvIh(a,t)I∗vS∗vI∗h(a)Iv+1)daq(0)∫∞0m(τ)π1(τ)dτ, | (55) |
and
U′23(t)=(1−S∗hSh)(Λh−βhShIv−μhSh)=(1−S∗hSh)(E∗h(0)+μhS∗h−Eh(0,t)−μhSh)=−μh(Sh−S∗h)2Sh+(E∗h(0)−Eh(0,t)−S∗hShE∗h(0)+S∗hShEh(0,t)). | (56) |
Differentiating
U′24(t)=1R0∫∞0p(τ)E∗h(τ)f′(Eh(τ,t)E∗h(τ))1E∗h(τ)∂Eh(τ,t)∂tdτ=−1R0∫∞0p(τ)E∗h(τ)E∗h(τ)f′(Eh(τ,t)E∗h(τ))(∂Eh(τ,t)∂τ+(μh+m(τ))Eh(τ,t))dτ=−1R0∫∞0p(τ)E∗h(τ)df(Eh(τ,t)E∗h(τ))=−1R0[p(τ)E∗h(τ)f(Eh(τ,t)E∗h(τ))|∞0−∫∞0f(Eh(τ,t)E∗h(τ))d(p(τ)E∗h(τ))]=1R0[p(0)E∗h(0)f(Eh(0,t)E∗h(0))−Λq(0)∫∞0m(τ)E∗h(τ)f(Eh(τ,t)E∗h(τ))dτ]=E∗h(0)f(Eh(0,t)E∗h(0))−∫∞0m(τ)E∗h(τ)f(Eh(τ,t)E∗h(τ))dτ∫∞0m(τ)π1(τ)dτ=Eh(0,t)−E∗h(0)−E∗h(0)lnEh(0,t)E∗h(0)−∫∞0m(τ)E∗h(τ)f(Eh(τ,t)E∗h(τ))dτ∫∞0m(τ)π1(τ)dτ. | (57) |
The above equality follows from (35) and the fact
p′(τ)E∗h(τ)+p(τ)E′∗h(τ)=[−Λq(0)m(τ)+(μh+m(τ))p(τ)]E∗h(τ)−p(τ)(μh+m(τ))E∗h(τ)=−Λq(0)m(τ)E∗h(τ). |
We also have
q′(τ)I∗h(a)+q(a)I′∗h(a)=[−βv(a)+(μh+αh(a)+rh(a))q(a)]I∗h(a)−q(a)(μh+αh(a)+rh(a))I∗h(a)=−βv(a)I∗h(a). |
Similar to the differentiation of
U′25(t)=1q(0)∫∞0m(τ)π1(τ)dτ∫∞0q(a)I∗h(a)f′(Ih(a,t)I∗h(a))1I∗h(a)∂Ih(a,t)∂tda=−1q(0)∫∞0m(τ)π1(τ)dτ∫∞0q(a)I∗h(a)df(Ih(a,t)I∗h(a))=q(0)I∗h(0)f(Ih(0,t)I∗h(0))−∫∞0βv(a)I∗h(a)f(Ih(a,t)I∗h(a))daq(0)∫∞0m(τ)π1(τ)dτ=∫∞0m(τ)E∗h(τ)(Ih(0,t)I∗h(0)−1−lnIh(0,t)I∗h(0))dτ∫∞0m(τ)π1(τ)dτ−∫∞0βv(a)I∗h(a)f(Ih(a,t)I∗h(a))daq(0)∫∞0m(τ)π1(τ)dτ. | (58) |
Finally, we differentiate
U′26(t)=−S∗hShEh(0,t),U′27(t)=−ShS∗h(E∗h(0))2Eh(0,t). | (59) |
Adding all five components of the Lyapunov function, we have
U′2(t)=−μv(Sv−S∗v)2S∗vSvq(0)∫∞0m(τ)π1(τ)dτ+1q(0)∫∞0m(τ)π1(τ)dτ∫∞0βv(a)I∗h(a)(1−S∗vSv−SvIh(a,t)S∗vI∗h(a)+Ih(a,t)I∗h(a))da+∫∞0βv(a)I∗h(a)(SvIh(a,t)S∗vI∗h(a)−IvI∗v−SvIh(a,t)I∗vS∗vI∗h(a)Iv+1)daq(0)∫∞0m(τ)π1(τ)dτ−μh(Sh−S∗h)2Sh+(E∗h(0)−Eh(0,t)−S∗hShE∗h(0)+S∗hShEh(0,t))+Eh(0,t)−E∗h(0)−E∗h(0)lnEh(0,t)E∗h(0)−∫∞0m(τ)E∗h(τ)f(Eh(τ,t)E∗h(τ))dτ∫∞0m(τ)π1(τ)dτ+∫∞0m(τ)E∗h(τ)(Ih(0,t)I∗h(0)−1−lnIh(0,t)I∗h(0))dτ∫∞0m(τ)π1(τ)dτ−∫∞0βv(a)I∗h(a)f(Ih(a,t)I∗h(a))daq(0)∫∞0m(τ)π1(τ)dτ−S∗hShEh(0,t)−ShS∗h(E∗h(0))2Eh(0,t)+2E∗h(0). | (60) |
Canceling all terms that cancel, we simplify (60):
U′2(t)=−μv(Sv−S∗v)2S∗vSvq(0)∫∞0m(τ)π1(τ)dτ−μh(Sh−S∗h)2Sh+∫∞0βv(a)I∗h(a)(3−S∗vSv−IvI∗v−SvIh(a,t)I∗vS∗vI∗h(a)Iv+lnIh(a,t)I∗h(a))daq(0)∫∞0m(τ)π1(τ)dτ−S∗hShE∗h(0)−ShS∗h(E∗h(0))2Eh(0,t)−E∗h(0)lnEh(0,t)E∗h(0)+2E∗h(0)+∫∞0m(τ)E∗h(τ)(Ih(0,t)I∗h(0)−Eh(τ,t)E∗h(τ)+lnEh(τ,t)E∗h(τ)I∗h(0)Ih(0,t))dτ∫∞0m(τ)π1(τ)dτ. | (61) |
Noting that
∫∞0m(τ)E∗h(τ)(Ih(0,t)I∗h(0)−Eh(τ,t)E∗h(τ))dτ=0,∫∞0m(τ)E∗h(τ)(Eh(τ,t)E∗h(τ)I∗h(0)Ih(0,t)−1)=0. | (62) |
Indeed,
∫∞0m(τ)E∗h(τ)(Ih(0,t)I∗h(0)−Eh(τ,t)E∗h(τ))dτ=Ih(0,t)I∗h(0)∫∞0m(τ)E∗h(τ)dτ−∫∞0m(τ)Eh(τ,t)dτ,=Ih(0,t)I∗h(0)I∗h(0)−Ih(0,t)=0,∫∞0m(τ)E∗h(τ)(Eh(τ,t)E∗h(τ)I∗h(0)Ih(0,t)−1)=I∗h(0)Ih(0,t)∫∞0m(τ)Eh(τ,t)dτ−∫∞0m(τ)E∗h(τ)dτ=I∗h(0)Ih(0,t)Ih(0,t)−I∗h(0)=0. | (63) |
Using (62) to simplify (61) we obtain
U′2(t)=−μv(Sv−S∗v)2S∗vSvq(0)∫∞0m(τ)π1(τ)dτ−μh(Sh−S∗h)2Sh−∫∞0βv(a)I∗h(a)[f(S∗vSv)+f(IvI∗v)+f(SvIh(a,t)I∗vS∗vI∗h(a)Iv)]daq(0)∫∞0m(τ)π1(τ)dτ−E∗h(0)[f(S∗hSh)+f(ShS∗hE∗h(0)Eh(0,t))]−1∫∞0m(τ)π1(τ)dτ∫∞0m(τ)E∗h(τ)f(Eh(τ,t)I∗h(0)E∗h(τ)Ih(0,t))dτ. | (64) |
Hence,
Θ2={(Sv,Iv,Sh,Eh,Ih)∈X0|U′2(t)=0}. |
We want to show that the largest invariant set in
Ih(a,t)I∗h(a)=1,E∗h(0)Eh(0,t)=1,Eh(τ,t)I∗h(0)E∗h(τ)Ih(0,t)=1. | (65) |
Thus, we obtain
Ih(a,t)=I∗h(a),Eh(0,t)=E∗h(0). |
According to (35),
Eh(τ,t)=BE(t−τ)π1(τ)=Eh(0,t−τ)π1(τ)=E∗h(0)π1(τ)=E∗h(τ), t>τ. |
Furthermore, we obtain
In this paper, we formulate a partial differential equation (PDE) model describing the transmission dynamics of a vector-borne disease that incorporates both incubation age of the exposed hosts and infection age of the infectious hosts. An explicit formula for the basic reproduction number
Examining the reproduction number more closely reveals that the relative impact of the recruitment rate of susceptible vectors
Furthermore, to see the link between
R0=βhΛvΛhμvμh(μv+αv)∫∞0m(τ)π1(τ)dτ∫∞0βv(a)π2(a)da=βhΛvΛhμvμh(μv+αv)∫∞0m(τ)e−μhτe−∫τ0m(σ)dσdτ∫∞0βv(a)π2(a)da=βhΛvΛhμvμh(μv+αv)[−∫∞0(μh−μh−m(τ))e−μhτe−∫τ0m(σ)dσdτ]∫∞0βv(a)π2(a)da=βhΛvΛhμvμh(μv+αv)[1−μh∫∞0e−μhτe−∫τ0m(σ)dσdτ]∫∞0βv(a)π2(a)da. |
Denoting by
ρ=∫∞0e−μhτe−∫τ0m(σ)dσdτ. |
We obtain
R0=βhΛvΛhμvμh(μv+αv)∫∞0βv(a)π2(a)da(1−μhρ). |
Taking the
dR0dρ=−μhβhΛvΛhμvμh(μv+αv)∫∞0βv(a)π2(a)da<0. |
We have that
In conclusion, our model and its analysis suggest that a better strategy of beginning mosquito control is to remove possible breeding grounds, because the larvae and pupae cycle of the mosquito is aquatic. Mosquitoes lay eggs in stagnant water, that is to say, larvae need standing water to prosper, so we must remove items that retain standing water or construct ways to keep the water moving. Furthermore, we can look for shaded rest areas used by adult mosquitoes and eliminate them. When we are outside during the day and evening hours, we can wear long sleeves and pants to prevent the bites of mosquitoes and the transmission of disease. If the infected host individuals who are in the latent period take an active drug therapy in time, the total number of the infected hosts with the virus may become small. At last it is interesting that the disease prevalence will decrease with the increase of the disease induced death rate
Y. Dang is supported by NSF of Henan Province No.142300 \break 410350, Z. Qiu's research is supported by NSFC grants No. 11671206 and No. 11271190, X. Li is supported by NSF of China grant No.11271314 and Plan For Scientific Innovation Talent of Henan Province No.144200510021, and M. Martcheva is supported partially through grant NSF DMS-1220342. We are very grateful to the anonymous referees for their careful reading, valuable comments and helpful suggestions, which help us to improve the presentation of this work significantly.
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