Loading [MathJax]/jax/output/SVG/jax.js
Review

Sustainable packaging materials for fermented probiotic dairy or non-dairy food and beverage products: challenges and innovations

  • Received: 06 January 2024 Revised: 14 April 2024 Accepted: 28 April 2024 Published: 08 May 2024
  • 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

    Related Papers:

    [1] Chen Liang, Hai-Feng Huo, Hong Xiang . Modelling mosquito population suppression based on competition system with strong and weak Allee effect. Mathematical Biosciences and Engineering, 2024, 21(4): 5227-5249. doi: 10.3934/mbe.2024231
    [2] Liming Cai, Shangbing Ai, Guihong Fan . Dynamics of delayed mosquitoes populations models with two different strategies of releasing sterile mosquitoes. Mathematical Biosciences and Engineering, 2018, 15(5): 1181-1202. doi: 10.3934/mbe.2018054
    [3] Yang Li, Jia Li . Stage-structured discrete-time models for interacting wild and sterile mosquitoes with beverton-holt survivability. Mathematical Biosciences and Engineering, 2019, 16(2): 572-602. doi: 10.3934/mbe.2019028
    [4] Mugen Huang, Moxun Tang, Jianshe Yu, Bo Zheng . The impact of mating competitiveness and incomplete cytoplasmic incompatibility on Wolbachia-driven mosquito population suppressio. Mathematical Biosciences and Engineering, 2019, 16(5): 4741-4757. doi: 10.3934/mbe.2019238
    [5] Yuanxian Hui, Genghong Lin, Qiwen Sun . Oscillation threshold for a mosquito population suppression model with time delay. Mathematical Biosciences and Engineering, 2019, 16(6): 7362-7374. doi: 10.3934/mbe.2019367
    [6] Rajivganthi Chinnathambi, Fathalla A. Rihan . Analysis and control of Aedes Aegypti mosquitoes using sterile-insect techniques with Wolbachia. Mathematical Biosciences and Engineering, 2022, 19(11): 11154-11171. doi: 10.3934/mbe.2022520
    [7] Bo Zheng, Lihong Chen, Qiwen Sun . Analyzing the control of dengue by releasing Wolbachia-infected male mosquitoes through a delay differential equation model. Mathematical Biosciences and Engineering, 2019, 16(5): 5531-5550. doi: 10.3934/mbe.2019275
    [8] Mugen Huang, Zifeng Wang, Zixin Nie . A stage structured model for mosquito suppression with immigration. Mathematical Biosciences and Engineering, 2024, 21(11): 7454-7479. doi: 10.3934/mbe.2024328
    [9] Daiver Cardona-Salgado, Doris Elena Campo-Duarte, Lilian Sofia Sepulveda-Salcedo, Olga Vasilieva, Mikhail Svinin . Optimal release programs for dengue prevention using Aedes aegypti mosquitoes transinfected with wMel or wMelPop Wolbachia strains. Mathematical Biosciences and Engineering, 2021, 18(3): 2952-2990. doi: 10.3934/mbe.2021149
    [10] Hui Wan, Huaiping Zhu . A new model with delay for mosquito population dynamics. Mathematical Biosciences and Engineering, 2014, 11(6): 1395-1410. doi: 10.3934/mbe.2014.11.1395
  • 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.



    1. Introduction

    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 R0: if R0<1 the disease-free equilibrium is globally asymptotically stable; if R0>1, a unique endemic equilibrium is globally asymptotically stable.

    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 R0>1. In Section 5, we again use a Lyapunov function to derive the global stability of the epidemic equilibrium. Finally, a brief discussion is given in Section 6.


    2. The vector-borne disease model with two ages of infection and the local stabilities

    To introduce the model, we divide the host population under consideration into four groups: susceptible hosts at time t, denoted by Sh(t), infected but not infectious individuals Eh(τ,t), infected and infectious individuals Ih(a,t), and the number of recovered or immune individuals, denoted by Rh(t). The vector population, on the other hand, is divided into three compartmental classes: susceptible vector at time t, denoted by Sv(t), the number of recovered or immune vectors, denoted by Rv(t), and infected/infectious vectors Iv(t).

    With the above notation, we study the following infection-age-structured vector-borne epidemic model:

    {Sv(t)=ΛvSv(t)0βv(a)Ih(a,t)daμvSv(t),Iv(t)=Sv(t)0βv(a)Ih(a,t)da(μv+αv)Iv(t),Rv(t)=αvIv(t)μvRv(t),Sh(t)=ΛhβhSh(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,Rh(t)=0rh(a)Ih(a,t)daμhRh(t). (1)

    In equation (1), Λh is the birth /recruitment rate of the host population. Let μv,μh be the natural death rate of the vectors and the host, respectively. m(τ) denotes the removal rate of the infected hosts with age of incubation τ from the latent period. αh(a) gives the additional disease induced death rate due to vector-borne disease at age of infection a. αv denotes the recovery rate of the infected vectors. rh(a) denotes the recovery rate of the infected hosts with age of infection a. Furthermore, βv(a) is the transmission coefficient of the infected host individuals at age of infection a, and βh is the transmission coefficient from infected vectors to healthy host individuals.

    To understand the model, notice that susceptible host individuals are recruited at a rate Λh. Susceptible host individuals can become infected by a bite of an infected mosquito with disease. Upon infection through biting by infected mosquitoes, the newly infected individuals move to the latent class, then progress into the infectious class with the progression rate m(τ). The non-infectious and infectious individuals infected by disease with age-since-infection equal to zero move to the boundary condition. The number total recovery rate from the infected class Ih(a,t) is given by the integral over all ages-since-infection. The susceptible vectors are recruited at a rate Λv. Susceptible mosquitos can become infected through biting on an infected individual of any age-since-infection at a specific age-infection transmission rate. As a consequence, the force of infection of susceptible vectors is given by the integral over all ages-since-infection. The total recovery rate from the infected vector class Iv(t) is given by αvIv(t).

    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

    {Sv(t)=ΛvSv(t)0βv(a)Ih(a,t)daμvSv(t),Iv(t)=Sv(t)0βv(a)Ih(a,t)da(μv+αv)Iv(t),Sh(t)=ΛhβhSh(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, Λv>0, Λh>0, and βh>0, μv>0, μh>0. We make the following assumptions on the parameter-functions.

    Assumption 2.1 The parameter-functions satisfy the following.

    1. The functions βv(a) is bounded and uniformly continuous. When βv(a) is of compact support, the support has non-zero Lebesgue measure;

    2. The functions m(τ), αh(a), rh(a) belong to L(0,);

    3. The functions φ(τ), ψ(a) are integrable.

    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 t0. Furthermore, adding the first and the second equations we have

    ddt(Sv(t)+Iv(t))Λvμv(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)Λhμh(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 μh+m(τ), then the probability of still being latent after τ time units is given by

    π1(τ)=eμhτeτ0m(σ)dσ. (3)

    The exit rate of infected individuals from the infective compartment is given by μh+αh(a)+rh(a), thus the probability of still being infectious after a time units is given by

    π2(a)=eμhaea0(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)dτ0βv(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. R0 gives the strength of vector-borne disease to invade when rare and alone. In particular, we notice that the reproduction number for vector-borne diseases is a product of the reproduction numbers of the two transmission processes: human-to-vector Rh and vector-to-human Rv,

    Rh=Λvμv0βv(a)π2(a)da,Rv=βhΛhμh(μv+αv)0m(τ)π1(τ)dτ,

    that is R0=RvRh. In the next section we compute explicit expressions for the equilibria and establish their local stability.

    System (2) always has a unique disease-free equilibrium E0, which is given by

    E0=(Sv0, 0, Sh0, 0, 0),

    where

    Sv0=Λvμv,Sh0=Λhμh.

    In addition, for Dengue virus there is a corresponding endemic equilibrium E1 given by

    E1=(Sv, Iv, Sh, Eh(τ), Ih(a)).

    We denote by

    Λ=βhΛhΛvμhμv(μv+αv),b=0m(τ)π1(τ)dτ0βv(a)π2(a)da,b(λ)=0m(τ)eλτπ1(τ)dτ0βv(a)eλaπ2(a)da. (6)

    The non-zero components of the equilibrium E1 are given by

    Iv=μvμh(R01)βh(Λhb+μv),Sv=Λv(μv+αv)Ivμv,Sh=ΛhβhIv+μh,Eh(τ)=Eh(0)π1(τ),Eh(0)=βhShIv,Ih(a)=Ih(0)π2(a),Ih(0)=Eh(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 E0, we let Sv(t)=Sv0+xv(t), Iv(t)=yv(t), Sh(t)=Sh0+xh(t), Eh(τ,t)=zh(τ,t), Ih(a,t)=yh(a,t). The linearized system becomes

    {dxv(t)dt=Sv00βv(a)yh(a,t)daμvxv(t),dyv(t)dt=Sv00βv(a)yh(a,t)da(μv+αv)yv(t),dxh(t)dt=βhSh0yv(t)μhxh(t),zh(τ,t)τ+zh(τ,t)t=(μh+m(τ))zh(τ,t),zh(0,t)=βhSh0yv(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 xv(t)=ˉxveλt, yv(t)=ˉyveλt, xh(t)=ˉxheλt, zh(τ,t)=ˉzh(τ)eλt and yh(a,t)=ˉyh(a)eλt. We obtain the following eigenvalue problem

    {λˉxv=Sv00βv(a)ˉyh(a)daμvˉxv,λˉyv=Sv00βv(a)ˉyh(a)da(μv+αv)ˉyv,λˉxh=βhSh0ˉyvμhˉxh,dˉzh(τ)dτ=(λ+μh+m(τ))ˉzh(τ),ˉzh(0)=βhSh0ˉyv,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 ˉxv and ˉxh are decoupled from the equation for ˉyv, ˉzh, ˉyh. Hence, the equations for ˉxv and ˉxh are independent from the equations for ˉyv, ˉzh, ˉyh. Solving the differential equations for ˉzh, ˉyh, we have

    ˉzh(τ)=ˉzh(0) eλτπ1(τ)=βhSh0ˉyv eλτπ1(τ),ˉyh(a)=ˉyh(0) eλaπ2(a)=βhSh0ˉyv eλaπ2(a)0m(τ) eλτπ1(τ)dτ.  (10)

    Substituting for ˉyh(a) in the second equation of (9), we can obtain the following equation

    λ+μv+αv=βhSv0Sh00m(τ)eλτπ1(τ)dτ0βv(a)eλaπ2(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 R0>1, it is unstable.

    Proof. Assume

    R0<1.

    We set

    LHSdef=λ+μv+αv,RHSdef=G1(λ)=βhSv0Sh00m(τ)eλτπ1(τ)dτ0βv(a)eλaπ2(a)da. (12)

    Consider λ with λ0. For such λ, following from (12), we have that

    |LHS|μv+αv,|RHS|G1(λ)G1(0)=βhSv0Sh00m(τ)π1(τ)dτ0βv(a)π2(a)da=βhΛvΛhμvμh0m(τ)π1(τ)dτ0βv(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 E0 depends on the eigenvalues of the equations for xv and xh. It is evident that λ=μv and λ=μh, so the disease-free equilibrium E0 is locally asymptotically stable if R0<1.

    Now assume

    R0>1.

    We rewrite the characteristic equation (11) in the form

    (λ+μv+αv)βhSv0Sh00m(τ)eλτπ1(τ)dτ0βv(a)eλaπ2(a)da=0. (13)

    We denote

    G2(λ)=(λ+μv+αv)βhSv0Sh00m(τ)eλτπ1(τ)dτ0βv(a)eλaπ2(a)da. (14)

    Thus equation (13) has turned into the following characteristic equation

    G2(λ)=0. (15)

    For λ real we have

    G2(0)=(μv+αv)βhSv0Sh00m(τ)π1(τ)dτ0βv(a)π2(a)da=(μv+αv)(1R0)<0.

    Furthermore, limλG2(λ)=+. Hence, the characteristic equation (15) has a real positive root. Therefore, the endemic equilibrium E0 is unstable. This concludes the proof.

    Now we turn to the local stability of the endemic equilibrium E1 if R0>1. The result on local stability of the equilibrium E1 is summarized below

    Proposition 2. Assume R0>1, then the endemic equilibrium E1 is locally asymptotically stable.

    Proof. We study the linearized equation around the endemic equilibrium E1. We introduce the following notation for the perturbations Sv(t)=Sv+xv(t), Iv(t)=Iv+yv(t),  Sh(t)=Sh+xh(t), Eh(τ,t)=Eh(τ)+zh(τ,t), Ih(a,t)=Ih(a)+yh(a,t). The system for the perturbations becomes (16)

    {dxv(t)dt=Sv0βv(a)yh(a,t)daxv(t)0βv(a)Ih(a)daμvxv(t),dyv(t)dt=Sv0βv(a)yh(a,t)da+xv(t)0βv(a)Ih(a)da(μv+αv)yv(t),dxh(t)dt=βhShyv(t)βhxh(t)Ivμhxh(t),dzh(τ)dτ=(λ+μh+m(τ))zh(τ,t),zh(0,t)=βhShyv(t)+βhxh(t)Iv,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=Sv0βv(a)yh(a)daxv0βv(a)Ih(a)daμvxv,λyv=Sv0βv(a)yh(a)da+xv0βv(a)Ih(a)da(μv+αv)yv,λxh=zh(0)μhxh,dzh(τ)dτ=(λ+μh+m(τ))zh(τ),zh(0)=βhShyv+βhIvxh,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) eλτπ1(τ),yh(a)=yh(0) eλaπ2(a)=zh(0) eλaπ2(a)0m(τ) eλτπ1(τ)dτ.

    Substituting for yh in the second equation of (17), we can obtain the following equation

    {(λ+μv+0βv(a)Ih(a)da)xv+Svb(λ)zh(0)=0,xv0βv(a)Ih(a)da+(λ+μv+αv)yvSvb(λ)zh(0)=0,(λ+μh)xh+zh(0)=0,βhIvxhβhShyv+zh(0)=0. (18)

    By direct calculation, we obtain the following characteristic equation:

    (λ+μv+0βv(a)Ih(a)da)(λ+μv+αv)(λ+μh+βhIv)=βhShSvb(λ)(λ+μv)(λ+μh). (19)

    We divide both sides by (λ+μv)(λ+μh), then we introduce the following notation.

    G3(λ)=(λ+μv+0βv(a)Ih(a)da)(λ+μv+αv)(λ+μh+βhIv)(λ+μv)(λ+μh),G4(λ)=βhShSvb(λ)=βhShSv0m(τ)eλτπ1(τ)dτ0βv(a)eλaπ2(a)da. (20)

    Thus (19) can be expressed as the the equation

    G3(λ)=G4(λ). (21)

    If λ is a root with λ0, it follows from equation (20) that

    |G3(λ)|>|λ+μv+αv|μv+αv. (22)

    From system (2), we have

    βhSvSh0m(τ)π1(τ)dτ0βv(a)π2(a)da=μv+αv.

    Hence,

    |G4(λ)||G4(λ)|G4(0)=βhSvSh0m(τ)π1(τ)dτ0βv(a)π2(a)da=μv+αv<|G3(λ)|. (23)

    This leads to contradiction. Hence, for λ0, (21) has no solutions. Thus, the characteristic equation (19) has only solutions with negative real parts. Therefore, the endemic equilibrium E1 is locally asymptotically stable if R0>1. This concludes the proof.


    3. Global stability of the disease-free equilibrium

    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), BI(t):

    BE(t)=Eh(0,t),BI(t)=Ih(0,t).

    Integrating along the characteristic lines, we obtain

    Eh(τ,t)={BE(tτ)π1(τ), t>τ,φ(τt)π1(τ)π1(τt), t<τ,Ih(a,t)={BI(ta)π2(a), t>a,ψ(at)π2(a)π2(at), t<a. (24)

    Theorem 3.1. Assume

    R01.

    Then the disease-free equilibrium E0 is globally asymptotically stable.

    Proof. We will use a Lyapunov function. We adopt the Volterra-type function used in [7,10,13]. Define

    f(x)=x1lnx.

    We note that f(x)0 for all x>0. f(x) achieves its global minimum at one, with f(1)=0. Let

    q(a)=aβv(s)esa(μh+αh(σ)+rh(σ))dσds,p(τ)=βhΛhΛvμhμv(μv+αv)q(0)τm(s)esτ(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 Λ=βhΛhΛvμhμv(μv+αv). So we define the following Lyapunov function:

    U1(t)=U11(t)+U12(t)+U13(t)+U14(t)+U15(t), (27)

    where

    U11(t)=Λf(SvSv0),U12(t)=ΛSv0Iv(t),U13(t)=Sh0f(ShSh0),U14(t)=0p(τ)Eh(τ,t)dτ,U15(t)=Λ0q(a)Ih(a,t)da..

    Because of the complexity of the expressions, we take the derivative of each component of the Lyapunov function separately

    U11(t)=ΛSv0(1Sv0Sv)(ΛvSv0βv(a)Ih(a,t)daμvSv)=ΛSv0(1Sv0Sv)(μvSv0μvSvSv0βv(a)Ih(a,t)da)=Λμv(SvSv0)2SvSv0ΛSv0Sv0βv(a)Ih(a,t)da+Λ0βv(a)Ih(a,t)da. (28)
    U12(t)=ΛSv0[Sv0βv(a)Ih(a,t)da(μv+αv)Iv]=ΛSv0Sv0βv(a)Ih(a,t)daβhSh0Iv. (29)

    Noting that Eh(0,t)=βhShIv, we have

    U13(t)=(1Sh0Sh)(ΛhβhShIvμhSh)=(1Sh0Sh)(μhSh0μhShβhShIv)=μh(ShSh0)2ShEh(0,t)+βhSh0Iv. (30)
    U14(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)|00Eh(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

    U15(t)=Λ0q(a)[Ih(a,t)a+(μh+αh(a)+rh(a))Ih(a,t)]da=Λq(0)Ih(0,t)Λ0βv(a)Ih(a,t)da. (32)

    Now differentiating (27) we have

    U1(t)=Λμv(SvSv0)2SvSv0ΛSv0Sv0βv(a)Ih(a,t)da+Λ0βv(a)Ih(a,t)da+ΛSv0Sv0βv(a)Ih(a,t)daβhSh0Ivμh(ShSh0)2ShEh(0,t)+βhSh0Iv+R0Eh(0,t)Λq(0)Ih(0,t)+Λq(0)Ih(0,t)Λ0βv(a)Ih(a,t)da. (33)

    Canceling all terms that cancel, we simplify the above expression:

    U1(t)=Λμv(SvSv0)2SvSv0μh(ShSh0)2Sh+(R01)Eh(0,t). (34)

    The last inequality follows from the fact that R01. Notice that U1 equals zero implies that Sv=Sv0, Sh=Sh0, Eh(0,t)=0. We define a set

    Θ1={(Sv,Iv,Sh,Eh,Ih)Ω|U1(t)=0}.

    LaSalle's Invariance Principle [9] implies that the bounded solutions of (2) converge to the largest compact invariant set of Θ1. We will show that this largest compact invariant set is the singleton given by the disease-free equilibrium. First, we notice that equality in (34) occurs if and only if Sv=Sv0, Sh=Sh0, Eh(0,t)=0. Thus, from the solution for the equation along the characteristic line (24), we have that Eh(τ,t)=Eh(0,tτ)π1(τ)=0 for all t>τ. Hence, limtEh(τ,t)=0 for t>τ. Noting that

    Ih(0,t)=0m(τ)E(τ,t)dτ.

    So we have limtIh(0,t)=0. Thus, we have

    limtIh(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)


    4. The uniform strong persistence of the vector-borne disease

    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 R0>1, we will show that the vector-borne disease persists.

    From Proposition 2 we know that under the specified conditions the equilibrium E1 is locally asymptotically stable. It remains to be established that E1 is globally stable. We expect to show this result using a Lyapunov function, similar to the one used in [7,10,13]. With f(x)=x1lnx, we define the following Lyapunov function

    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(SvSv),U22(t)=1Svq(0)0m(τ)π1(τ)dτIvf(IvIv),U23(t)=Shf(ShSh),U24(t)=1R00p(τ)Eh(τ)f(Eh(τ,t)Eh(τ))dτ,U25(t)=1q(0)0m(τ)π1(τ)dτ0q(a)Ih(a)f(Ih(a,t)Ih(a))da,U26(t)=tShSh(s)Eh(0,s)ds,U27(t)=tSh(s)Sh(Eh(0))2Eh(0,s)ds,U28(t)=2Eh(0)t. (36)

    One difficulty with the Lyapunov function U2 above is that the component U21 is not defined if Sv=0, the component U22 is not defined if  Iv=0, the component U23,U26 is not defined if Sh=0, the component U24 is not defined if Eh(τ,t)=0, and the component U25 is not defined if Ih(a,t)=0. To show that the Lyapunov function above is valid, we need to show that the vector borne disease persists both in the hosts and in the vectors. For this to be the case, we need to guarantee that the initial conditions we start from are non-trivial, that is, the initial conditions are such that they lead to new infections of individuals and vectors either initially or at some future point. Mathematically speaking this means that the support of the initial density of latent individuals φ(τ) intersects the support of m(τ) or the support of the initial density of infectious individuals ψ(a) intersects the support of βv(a) either initially or at some future point. Thus, we define the following set

    ˆΩ1={φL1+(0,)|s0: 0m(τ+s)φ(τ)dτ>0},
    ˆΩ2={ψL1+(0,)|s0: 0βv(a+s)ψ(a)da>0}.

    Define

    Ω0=R+×R+×R+׈Ω1׈Ω2.

    Finally, define X0=ΩΩ0. We notice that X0 is forward invariant. It is not hard to see that Ω is a forward invariant. To see that ˆΩ2 is forward invariant, let us assume that the inequality holds for the initial condition. The inequality says that the condition is such that if the support of βv(a) is transferred s units to the right, it will intersect the support of the initial condition. But if that happens for the initial time, it will happen for any other time since the support of the initial condition only moves to the right. Similarly, ˆΩ1 is also forward invariant.

    We want to formulate the persistence result for the vector-borne disease which on one side will justify the use of the Lyapunov functional U2(t), and on the other, will show that when R0>1 the disease persists in the form of the endemic equilibrium. Consequently, we identify conditions which lead to the prevalence in individuals and vectors being bounded away from zero. There are many different types of persistence [21]. We identify here the two that we will be working with.

    Definition 4.1. We call the vector-borne disease uniformly weakly persistent if there exists some γ>0 independent of the initial conditions such that

    lim supt0Eh(τ,t)dτ>γwhenever0φ(τ)dτ>0,
    lim supt0Ih(a,t)da>γwhenever0ψ(a)da>0,

    and

    lim suptIv(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 γ>0 independent of the initial conditions such that

    lim inft0Eh(τ,t)dτ>γwhenever0φ(τ)dτ>0,
    lim inft0Ih(a,t)da>γwhenever0ψ(a)da>0,

    and

    lim inftIv(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 T.

    First, we show uniform weak persistence of the vector-borne disease. The following proposition states that result.

    Proposition 3. Assume R0>1. Then, for all initial conditions that belong to X0, the vector-borne disease is uniformly weakly persistent, that is, there exists γ>0 such that

    lim suptβhIv(t)γ,lim supt0m(τ)Eh(τ,t)dτγ,
    lim supt0βv(a)Ih(a,t)daγ.

    Proof. We argue by contradiction. Assume that the vector-borne disease dies out. In particular, assume that for every ε>0 and an initial condition in X0 we have

    lim suptβhIv(t)<ε,lim supt0m(τ)Eh(τ,t)dτ<ε,lim supt0βv(a)Ih(a,t)da<ε.

    Hence, there exist T>0 such that for all t>T, we have

    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 t0. From the first equation in (2), and taking into account the above inequality, we have

    Sv(t)ΛvεSvμvSv,Sh(t)ΛhεShμhSh.

    Therefore,

    limsuptβhIv(t)ε,limsupt0m(τ)Eh(τ,t)dτε,limsupt0βv(a)Ih(a,t)daε.

    Recall that we are using the following notation BE(t)=Eh(0,t), BI(t)=Ih(0,t). Using the inequality above we obtain

    {BE(t)=Eh(0,t)=βhShIvβhΛhε+μhIv,dIv(t)dtΛvε+μv0βv(a)Ih(a,t)da(μv+αv)Iv. (37)

    Now, we apply expression (24) to obtain the following system of inequalities in BE(t), BI(t) and Iv(t):

    {BE(t)βhΛhε+μhIv,BI(t)=0m(τ)Eh(τ,t)dτt0m(τ)BE(tτ)π1(τ)dτ,dIv(t)dtΛvε+μvt0βv(a)BI(ta)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 λ>0. We denote by ˆBE(λ) the Laplace transform of BE(t), by ˆBI(λ) the Laplace transform of BI(t), and by ˆIv(λ) the Laplace transform of Iv(t). Furthermore,

    ˆK1(λ)=0m(τ)π1(τ)eλτdτ,ˆK2(λ)=0βv(a)π2(a)eλada. (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), ˆBI(λ) and ˆIv(λ).

    {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 ˆBI(λ) and ˆIv(λ) from the system above, we obtain

    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 ε0 and for any λ>0. But this is impossible since for ε0 and λ0, the coefficient in front ˆBE(λ) on the right hand side is approximately R0>1, that is,

    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 supt0m(τ)Eh(τ,t)dτ<ε,
    lim supt0βv(a)Ih(a,t)da<ε. (41)

    Therefore, there exists at least one limit supremum which is bounded below by γ for any initial condition in X0 and some γ>0.

    Note that

    Eh(0,t)=ShβhIv(t)ΛhμhβhIv(t)Ih(0,t)=0m(τ)Eh(τ,t)dτ=t0m(τ)Eh(0,tτ)π1(τ)dτ+tm(τ)φ(τt)π1(τ)π1(τt)dτdIv(t)dt=0βv(a)Ih(a,t)da(μv+αv)Iv(t)=t0βv(a)Ih(0,ta)π2(a)da+tβv(a)ψ(at)π2(a)π2(at)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)ˉm0eμhτdτlim suptEh(0,t)=ˉmμhlim suptEh(0,t)lim suptdIv(t)dt0βv(a)π2(a)dalim suptIh(0,t)(μv+αv)lim suptIv(t)m00eμhadalim suptIh(0,t)(μv+αv)lim suptIv(t)=m0μhlim suptIh(0,t)(μv+αv)lim suptIv(t), (43)

    where ˉm=supτ{m(τ)}, m0=supa{βv(a)}. The last inequality means that

    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 ×ε. There is another contradiction with the above result that there exists at least one limit supremum which is bounded below by γ. As a result, there exists γ>0 such that for any initial condition in X0, we have

    lim suptβhIv(t)γ,lim supt0m(τ)Eh(τ,t)dτγ,lim supt0βv(a)Ih(a,t)daγ.

    In addition, the differential equation for Iv can be rewritten in the form

    dIvdtΛvγγ+μv(μv+αv)Iv,

    which in turn, implies a lower bound for Iv. This concludes the proof.

    Our next goal is to prove that system (2) has a global compact attractor T. As a first step, we define the semiflow Ψ of the solutions of system (2)

    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 Ψ:[0,)×X0X0. A set T in X0 is called a global compact attractor for Ψ, if T is a maximal compact invariant set and if for all open sets U containing T and all bounded sets B of X0 there exists some T>0 such that Ψ(t,B)U, for all t>T.

    The following proposition establishes the presence of a global compact attractor.

    Proposition 4. Assume R0>1. Then, there exists T, a compact subset of X0, which is a global attractor for the solution semiflow Ψ of (2) in X0. Moreover, T is invariant under the solution semiflow, that is

    Ψ(t,x0)Tforeveryx0T, t0.

    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 x0X0 we have Ψ(t,x0)=ˆΨ(t,x0)+˜Ψ(t,x0). The splitting is done in such a way that ˆΨ(t,x0)0 as t for every x0X0, and for a fixed t and any bounded set B in X0, the set {˜Ψ(t,x0): x0B} is precompact. The two components of the semiflow are defined as follows:

    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 Eh(τ,t)=ˆEh(τ,t)+˜Eh(τ,t), Ih(a,t)=ˆIh(a,t)+˜Ih(a,t) and ˆEh(τ,t),ˆIh(a,t),

    ˜Eh(τ,t),˜Ih(a,t) are the solutions of the following equations (the remaining equations are as in system (2)

    {ˆEht+ˆEhτ=(μh+m(τ))ˆEh(τ,t),ˆEh(0,t)=0,ˆEh(τ,0)=φ(τ), (45)
    {ˆIht+ˆIha=(μh+αh(a)+rh(a))ˆIh(τ,t),ˆIh(0,t)=0,ˆIh(a,0)=ψ(a), (46)

    and

    {˜Eht+˜Ehτ=(μ+m(τ))˜Eh(τ,t),˜Eh(0,t)=βhShIv,˜Eh(τ,0)=0, (47)
    {˜Iht+˜Iha=(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(τt)π1(τ)π1(τt), t<τ, (49)
    ˆIh(a,t)={0, t>a,ψ(at)π2(a)π2(at), t<a. (50)

    Integrating ˆEh with respect to τ, we obtain:

    tφ(τt)π1(τ)π1(τt)dτ=0φ(τ)π1(t+τ)π1(τ)dτeμht0φ(τ)dτ0,

    as t+. Integrating ˆIh with respect to a, we obtain:

    tψ(at)π2(a)π2(at)da=0ψ(a)π2(t+a)π2(a)daeμht0ψ(a)da0,

    as t+. This shows the first claim, that is, it shows that ˆΨ(t,x0)0 as t+ uniformly for every x0BX0, where B is a ball of a given radius.

    To show the second claim, we need to show compactness. We fix t and let x0X0. Note that X0 is bounded. We have to show that for that fixed t the family of functions defined by

    ˜Ψ(t,x0)=(Sv(t),Iv(t),Sh(t),˜Eh(τ,t),˜Ih(a,t)),

    obtained by taking different initial conditions in X0 is a compact family of functions. The family

    {˜Ψ(t,x0)|x0X0,tfixed}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 L1 is trivially satisfied since ˜Eh(τ,t)=0 for τ>t and ˜Ih(a,t)=0 for a>t. To see the second condition of that Theorem, we have to bound by two constants the L1-norms of Eh/τ and Ih/a. To derive that bound, first notice that

    ˜Eh(τ,t)={˜BE(tτ)π1(τ), t>τ,0, t<τ,˜Ih(a,t)={˜BI(ta)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(tτ)π1(τ)dτ. (52)

    First, we notice that for x0X0, ˜BE(t) is bounded. We can see that by recalling that Sh and Iv are bounded. Hence, the ˜BE(t) satisfies

    ˜BE(t)k1.

    Then, we obtain

    ˜BI(t)=t0m(τ)˜BE(tτ)π1(τ)dτk2t0˜BE(tτ)dτ=k2t0˜BE(τ)dτk1k2t.

    Next, we differentiate (51) with respect to τ and a:

    |˜Eh(τ,t)τ|{|˜BE(tτ)|π1(τ)+˜BE(tτ)|π1(τ)|, t>τ,0, t<τ,|˜Ih(a,t)a|{|˜BI(ta)|π2(a)+˜BI(ta)|π2(a)|, t>a,0, t<a.

    We have to see that |˜BE(tτ)|, |˜BI(ta)| are bounded. Differentiating (52), we obtain

    ˜BE(t)=βh(Sh(t)Iv(t)+Sh(t)Iv(t)),˜BI(t)=m(t)˜BE(0)π1(t)+t0m(τ)˜BE(tτ)π1(τ)dτ. (53)

    Taking an absolute value and bounding all terms, we can rewrite the above equality as the following inequality:

    |˜BE(t)|k3,|˜BI(t)|k4.

    Putting all these bounds together, we have

    τ˜Ehk30π1(τ)dτ+k1(μh+ˉm)0π1(τ)dτ<b1,a˜Ihk40π2(a)da+k1k2(μh+ˉαh+ˉrh)t0π2(a)da<b2,

    where ˉm=supτ{m(τ)}, ˉαh=supa{αh(a)}, ˉrh=supa{rh(a)}. To complete the proof, we notice that

    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 Iv, Eh and Ih.

    Proposition 5. Assume R0>1. Then, for all initial conditions that belong to X0, The vector-borne disease persists, that is, there exists γ>0 such that

    lim inftβhIv(t)γ,lim inft0m(τ)Eh(τ,t)dτγ,lim inft0βv(a)Ih(a,t)daγ.

    Proof. We apply Theorem 2.6 in [29]. We consider the solution semiflow Ψ on X0. We define three functionals ρj:X0R+, j=1,2,3 as follows:

    {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 ρ-persistent. Proposition 4 shows that the solution semiflow has a global compact attractor T. Total orbits are solutions to the system (2) defined for all times tR. Since the solution semiflow is nonnegative, we have that for any s and any t>s

    βhIv(t)βhIv(s)e(μv+αv)(ts),0m(τ)˜Eh(τ,t)dτ=˜BI(t)=t0m(τ)˜BE(tτ)π1(τ)dτk1t0˜BE(tτ)dτ=k1t0˜BE(τ)dτ=k1t0βhSh(τ)Iv(τ)dτk2t0Iv(τ)dτ=k2t0Iv(s)e(μv+αv)(τs)dτ=k2Iv(s)μv+αve(μv+αv)s(1e(μv+αv)t),0βv(a)˜Ih(a,t)da=t0βv(a)˜BI(ta)π2(a)dak3t0˜BI(ta)da=k3t0˜BI(a)dak2k3Iv(s)μv+αve(μv+αv)st0(1e(μv+αv)a)da.

    Therefore, βhIv(t)>0, 0m(τ)˜Eh(τ,t)dτ>0, 0βv(a)˜Ih(a,t)da>0 for all t>s, provided Iv(s)>0. Theorem 2.6 in [29] now implies that the semiflow is uniformly strongly ρ-persistent. Hence, there exists γ such that

    lim inftβhIv(t)γ,lim inft0m(τ)Eh(τ,t)dτγ,lim inft0βv(a)Ih(a,t)daγ.

    Corollary 1. Assume R0>1. There exists constants ϑ>0 and M>0 such that for each orbit (Sv(t),Iv,Sh(t),Eh(τ,t),Ih(a,t)) of Ψ in T, we have

    ϑSv(t)M,ϑSh(t)M,  tR,

    and

    ϑβhIv(t)M,ϑ0m(τ)Eh(τ,t)dτM,ϑ0βv(a)Ih(a,t)daM,tR.

    In the next section we show that the endemic equilibrium E1 is globally stable.


    5. Global stability of the endemic equilibrium

    Now we are ready to establish the global stability of the equilibrium E1. To demonstrate that with the Lyapunov function defined in (35) we have to establish that U2(t)0 along the solution curves of system (2). The following Theorem summarizes the result.

    Theorem 5.1. Assume R0>1. Then, equilibrium E1 is globally asymptotically stable, that is, for any initial condition x0X0 the solution semiflow converges to E1.

    Proof. Since R0>1, for any initial condition x0X0 we can find a complete orbit (Sv(t),Iv(t), Sh(t),Eh(τ,t),Ih(a,t)) of Ψ in T (similarly to the proof of Proposition 4) for which the inequalities in Corollary 1 hold and, consequently, there exist ε1>0 and M1>0 such that

    ε1IvIvM1,ε1Eh(τ,t)Eh(τ)M1,ε1Ih(a,t)Ih(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)).

    U21(t)=(1SvSv)(ΛvSv0βv(a)Ih(a,t)daμvSv)Svq(0)0m(τ)π1(τ)dτ=(1SvSv)[Sv0βv(a)Ih(a)da+μvSvSv0βv(a)Ih(a,t)daμvSv]Svq(0)0m(τ)π1(τ)dτ=μv(SvSv)2SvSvq(0)0m(τ)π1(τ)dτ+0βv(a)Ih(a)(1SvSvSvIh(a,t)SvIh(a)+Ih(a,t)Ih(a))daq(0)0m(τ)π1(τ)dτ. (54)

    Next, we need to take the time derivative of U22.

    U22(t)=(1IvIv)[Sv0βv(a)Ih(a,t)da(μv+αv)Iv]Svq(0)0m(τ)π1(τ)dτ=(1IvIv)(Sv0βv(a)Ih(a,t)daSv0βv(a)Ih(a)daIvIv)Svq(0)0m(τ)π1(τ)dτ=(1IvIv)Sv0βv(a)Ih(a)(SvIh(a,t)SvIh(a)IvIv)daSvq(0)0m(τ)π1(τ)dτ=0βv(a)Ih(a)(SvIh(a,t)SvIh(a)IvIvSvIh(a,t)IvSvIh(a)Iv+1)daq(0)0m(τ)π1(τ)dτ, (55)

    and

    U23(t)=(1ShSh)(ΛhβhShIvμhSh)=(1ShSh)(Eh(0)+μhShEh(0,t)μhSh)=μh(ShSh)2Sh+(Eh(0)Eh(0,t)ShShEh(0)+ShShEh(0,t)). (56)

    Differentiating U24(t), we have

    U24(t)=1R00p(τ)Eh(τ)f(Eh(τ,t)Eh(τ))1Eh(τ)Eh(τ,t)tdτ=1R00p(τ)Eh(τ)Eh(τ)f(Eh(τ,t)Eh(τ))(Eh(τ,t)τ+(μh+m(τ))Eh(τ,t))dτ=1R00p(τ)Eh(τ)df(Eh(τ,t)Eh(τ))=1R0[p(τ)Eh(τ)f(Eh(τ,t)Eh(τ))|00f(Eh(τ,t)Eh(τ))d(p(τ)Eh(τ))]=1R0[p(0)Eh(0)f(Eh(0,t)Eh(0))Λq(0)0m(τ)Eh(τ)f(Eh(τ,t)Eh(τ))dτ]=Eh(0)f(Eh(0,t)Eh(0))0m(τ)Eh(τ)f(Eh(τ,t)Eh(τ))dτ0m(τ)π1(τ)dτ=Eh(0,t)Eh(0)Eh(0)lnEh(0,t)Eh(0)0m(τ)Eh(τ)f(Eh(τ,t)Eh(τ))dτ0m(τ)π1(τ)dτ. (57)

    The above equality follows from (35) and the fact

    p(τ)Eh(τ)+p(τ)Eh(τ)=[Λq(0)m(τ)+(μh+m(τ))p(τ)]Eh(τ)p(τ)(μh+m(τ))Eh(τ)=Λq(0)m(τ)Eh(τ).

    We also have

    q(τ)Ih(a)+q(a)Ih(a)=[βv(a)+(μh+αh(a)+rh(a))q(a)]Ih(a)q(a)(μh+αh(a)+rh(a))Ih(a)=βv(a)Ih(a).

    Similar to the differentiation of U24(t), we have

    U25(t)=1q(0)0m(τ)π1(τ)dτ0q(a)Ih(a)f(Ih(a,t)Ih(a))1Ih(a)Ih(a,t)tda=1q(0)0m(τ)π1(τ)dτ0q(a)Ih(a)df(Ih(a,t)Ih(a))=q(0)Ih(0)f(Ih(0,t)Ih(0))0βv(a)Ih(a)f(Ih(a,t)Ih(a))daq(0)0m(τ)π1(τ)dτ=0m(τ)Eh(τ)(Ih(0,t)Ih(0)1lnIh(0,t)Ih(0))dτ0m(τ)π1(τ)dτ0βv(a)Ih(a)f(Ih(a,t)Ih(a))daq(0)0m(τ)π1(τ)dτ. (58)

    Finally, we differentiate U26(t), U27(t) with respect to t, and we have

    U26(t)=ShShEh(0,t),U27(t)=ShSh(Eh(0))2Eh(0,t). (59)

    Adding all five components of the Lyapunov function, we have

    U2(t)=μv(SvSv)2SvSvq(0)0m(τ)π1(τ)dτ+1q(0)0m(τ)π1(τ)dτ0βv(a)Ih(a)(1SvSvSvIh(a,t)SvIh(a)+Ih(a,t)Ih(a))da+0βv(a)Ih(a)(SvIh(a,t)SvIh(a)IvIvSvIh(a,t)IvSvIh(a)Iv+1)daq(0)0m(τ)π1(τ)dτμh(ShSh)2Sh+(Eh(0)Eh(0,t)ShShEh(0)+ShShEh(0,t))+Eh(0,t)Eh(0)Eh(0)lnEh(0,t)Eh(0)0m(τ)Eh(τ)f(Eh(τ,t)Eh(τ))dτ0m(τ)π1(τ)dτ+0m(τ)Eh(τ)(Ih(0,t)Ih(0)1lnIh(0,t)Ih(0))dτ0m(τ)π1(τ)dτ0βv(a)Ih(a)f(Ih(a,t)Ih(a))daq(0)0m(τ)π1(τ)dτShShEh(0,t)ShSh(Eh(0))2Eh(0,t)+2Eh(0). (60)

    Canceling all terms that cancel, we simplify (60):

    U2(t)=μv(SvSv)2SvSvq(0)0m(τ)π1(τ)dτμh(ShSh)2Sh+0βv(a)Ih(a)(3SvSvIvIvSvIh(a,t)IvSvIh(a)Iv+lnIh(a,t)Ih(a))daq(0)0m(τ)π1(τ)dτShShEh(0)ShSh(Eh(0))2Eh(0,t)Eh(0)lnEh(0,t)Eh(0)+2Eh(0)+0m(τ)Eh(τ)(Ih(0,t)Ih(0)Eh(τ,t)Eh(τ)+lnEh(τ,t)Eh(τ)Ih(0)Ih(0,t))dτ0m(τ)π1(τ)dτ. (61)

    Noting that

    0m(τ)Eh(τ)(Ih(0,t)Ih(0)Eh(τ,t)Eh(τ))dτ=0,0m(τ)Eh(τ)(Eh(τ,t)Eh(τ)Ih(0)Ih(0,t)1)=0. (62)

    Indeed,

    0m(τ)Eh(τ)(Ih(0,t)Ih(0)Eh(τ,t)Eh(τ))dτ=Ih(0,t)Ih(0)0m(τ)Eh(τ)dτ0m(τ)Eh(τ,t)dτ,=Ih(0,t)Ih(0)Ih(0)Ih(0,t)=0,0m(τ)Eh(τ)(Eh(τ,t)Eh(τ)Ih(0)Ih(0,t)1)=Ih(0)Ih(0,t)0m(τ)Eh(τ,t)dτ0m(τ)Eh(τ)dτ=Ih(0)Ih(0,t)Ih(0,t)Ih(0)=0. (63)

    Using (62) to simplify (61) we obtain

    U2(t)=μv(SvSv)2SvSvq(0)0m(τ)π1(τ)dτμh(ShSh)2Sh0βv(a)Ih(a)[f(SvSv)+f(IvIv)+f(SvIh(a,t)IvSvIh(a)Iv)]daq(0)0m(τ)π1(τ)dτEh(0)[f(ShSh)+f(ShShEh(0)Eh(0,t))]10m(τ)π1(τ)dτ0m(τ)Eh(τ)f(Eh(τ,t)Ih(0)Eh(τ)Ih(0,t))dτ. (64)

    Hence, U2(t)0. Define,

    Θ2={(Sv,Iv,Sh,Eh,Ih)X0|U2(t)=0}.

    We want to show that the largest invariant set in Θ2 is the singleton E1. First, we notice that equality in (64) occurs if and only if Sv(t)=Sv, Sh(t)=Sh, Iv(t)=Iv, and

    Ih(a,t)Ih(a)=1,Eh(0)Eh(0,t)=1,Eh(τ,t)Ih(0)Eh(τ)Ih(0,t)=1. (65)

    Thus, we obtain

    Ih(a,t)=Ih(a),Eh(0,t)=Eh(0).

    According to (35),

    Eh(τ,t)=BE(tτ)π1(τ)=Eh(0,tτ)π1(τ)=Eh(0)π1(τ)=Eh(τ), t>τ.

    Furthermore, we obtain Eh(τ,t)=Eh(τ). We conclude that the largest invariant set in Θ2 is the singleton E1. Reasoning similarly to [7] can show that the compact global attractor T={E1}.


    6. Discussion

    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 R0 is obtained for the infection-age structured vector-host epidemic model. We show that if R0 of system (2) is less or equal to one, the disease-free equilibrium is locally and globally asymptotically stable. That means the disease dies out while the endemic equilibrium is not feasible. On the other hand, we show that if R0 is greater than one, system (2) is permanent and the endemic equilibrium is globally asymptotically stable. Therefore the disease becomes endemic. As a result, the global stability of the equilibria of system (2) is completely determined by its basic reproductive number R0. Hence, to control the disease, a strategy should be devised to reduce the reproduction number to below one.

    Examining the reproduction number more closely reveals that the relative impact of the recruitment rate of susceptible vectors Λv, the transmission rate βh and the specific age-since-infection transmission coefficient βv(a) of the infected host individuals increases R0. It is easy to see that R0 is an decreasing function of the death rate of the vector individuals μv and the recovery rate of the infected vector individuals αv. It is also evident that R0 decreases with the rates rh(a) and αh(a) that give recovery and disease-induced mortality of infected hosts.

    Furthermore, to see the link between R0 and the removal rate of the exposed host individuals with the incubation age τ, we first need to transform the reproduction number R0. We will use the representation of R0 given in (3) and (5).

    R0=βhΛvΛhμvμh(μv+αv)0m(τ)π1(τ)dτ0βv(a)π2(a)da=βhΛvΛhμvμh(μv+αv)0m(τ)eμhτeτ0m(σ)dσdτ0βv(a)π2(a)da=βhΛvΛhμvμh(μv+αv)[0(μhμhm(τ))eμhτeτ0m(σ)dσdτ]0βv(a)π2(a)da=βhΛvΛhμvμh(μv+αv)[1μh0eμhτeτ0m(σ)dσdτ]0βv(a)π2(a)da.

    Denoting by

    ρ=0eμhτeτ0m(σ)dσdτ.

    We obtain

    R0=βhΛvΛhμvμh(μv+αv)0βv(a)π2(a)da(1μhρ).

    Taking the ρ derivatives of R0

    dR0dρ=μhβhΛvΛhμvμh(μv+αv)0βv(a)π2(a)da<0.

    We have that ρ decrease with the increase of m(τ) and R0 decreases with increase of ρ. Thus we have that increasing m(τ) increases the reproduction number R0.

    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 αh(a) at the age of infection a.


    Acknowledgments

    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.



    Acknowledgments



    DVF, TG and PSN: writing—review and editing. All authors have read and agreed to the published version of the manuscript. The writing of this review did not receive any grant from funding agencies in the public, commercial, or not-for-profit sectors.

    Conflicts of interest



    The authors declare no conflict of interest.

    [1] Ganatsios V, Nigam P, Plessas S, et al. (2021) Kefir as a functional beverage gaining momentum towards its health promoting attributes. Beverages 7: 1-15. https://doi.org/10.3390/beverages7030048
    [2] Dahiya D, Nigam P (2022) Use of characterized microorganisms in fermentation of non-dairy-based substrates to produce probiotic food for gut-health and nutrition. Fermentation 9: 1-12. https://doi.org/10.3390/fermentation9010001
    [3] Dahiya D, Nigam P (2023) Nutraceuticals prepared with specific strains of probiotics for supplementing gut microbiota in hosts allergic to certain foods or their additives. Nutrients 15: 2979. https://doi.org/10.3390/nu15132979
    [4] Terpou A, Bekatorou A, Kanellaki M, et al. (2017) Enhanced probiotic viability and aromatic profile of yogurts produced using wheat bran (Triticum aestivum) as cell immobilization carrier. Process Biochem 55: 1-10. https://doi.org/10.1016/j.procbio.2017.01.013
    [5] Dahiya D, Nigam P (2023) Therapeutic and dietary support for gastrointestinal tract using kefir as a nutraceutical beverage: dairy-milk-based or plant-sourced kefir probiotic products for vegan and lactose-intolerant populations. Fermentation 9: 388. https://doi.org/10.3390/fermentation9040388
    [6] Vasiliki S, Terpou A, Bosnea L, et al. (2018) Entrapment of Lactobacillus casei ATCC393 in the viscus matrix of Pistacia terebinthus resin for functional myzithra cheese manufacture. LWT Food Sci Technol 89: 441-448. https://doi.org/10.1016/j.lwt.2017.11.015
    [7] Terpou A, Nigam P, Bosnea L, et al. (2018) Evaluation of Chios mastic gum as antimicrobial agent and matrix forming material targeting probiotic cell encapsulation for functional fermented milk production. LWT Food Sci Technol 97: 109-116. https://doi.org/10.1016/j.lwt.2018.06.045
    [8] Dahiya D, Nigam P (2022) Probiotics, prebiotics, synbiotics, and fermented foods as potential biotics in nutrition improving health via microbiome-gut-brain axis. Fermentation 8: 1-16. https://doi.org/10.3390/fermentation8070303
    [9] Dahiya D, Nigam P (2023) Inclusion of dietary-fibers in nutrition provides prebiotic substrates to probiotics for the synthesis of beneficial metabolites SCFA to sustain gut health minimizing risk of IBS, IBD, CRC. Recent Prog Nutr 3: 017. https://doi.org/10.21926/rpn.2303017
    [10] Dahiya D, Nigam P (2022) Nutrition and health through the use of probiotic strains in fermentation to produce non-dairy functional beverage products supporting gut microbiota. Foods 11: 2760-2773. https://doi.org/10.3390/foods11182760
    [11] Tamang JP (2015) Functionality and therapeutic values of fermented foods. Health Benefits of Fermented Foods and Beverages. Boca Raton: CRC Press 126-183.
    [12] Kakadellis S, Harris ZM (2020) Don't scrap the waste: The need for broader system boundaries in bioplastic food packaging life-cycle assessment–A critical review. J Clean Prod 274: 122831. https://doi.org/10.1016/j.jclepro.2020.122831
    [13] Borghesi G, Stefanini R, Vignali G (2022) Life cycle assessment of packaged organic dairy product: A comparison of different methods for the environmental assessment of alternative scenarios. J Food Eng 318: 110902. https://doi.org/10.1016/j.jfoodeng.2021.110902
    [14] Murtas G, Pedeliento G, Andreini D (2022) To pack sustainably or not to pack sustainably? A review of the relationship between consumer behaviour and sustainable packaging. Managing Sustainability. Berlin: Springer International Publishing 147-168. https://doi.org/10.1007/978-3-031-12027-5_9
    [15] Mirza Alizadeh A, Masoomian M, Shakooie M, et al. (2021) Trends and applications of intelligent packaging in dairy products: a review. Crit Rev Food Sci Nutr 62: 383-397. https://doi.org/10.1080/10408398.2020.1817847
    [16] Cooper TA (2013) Developments in plastic materials and recycling systems for packaging food, beverages and other fast-moving consumer goods. Trends in Packaging of Food, Beverages and Other Fast-Moving Consumer Goods [FMCG]. Cambridge: Woodhead publisher 58-107. https://doi.org/10.1533/9780857098979.58
    [17] Teck Kim Y, Min B, Won Kim K (2014) General characteristics of packaging materials for food system. Innovations in Food Packaging. Cambridge: Academic Press 13-35. https://doi.org/10.1016/B978-0-12-394601-0.00002-3
    [18] Alfei S, Marengo B, Zuccari G (2020) Nanotechnology application in food packaging: A plethora of opportunities versus pending risks assessment and public concerns. Food Res Int 137: 109664. https://doi.org/10.1016/j.foodres.2020.109664
    [19] Hay C, De Matos AD, Low J, et al. (2021) Comparing cross-cultural differences in perception of drinkable yoghurt by Chinese and New Zealand European consumers. Int Dairy J 113: 104901. https://doi.org/10.1016/j.idairyj.2020.104901
    [20] Karaman AD, Özer B, Pascall MA, et al. (2015) Recent advances in dairy packaging. Food Rev Int 31: 295-318. https://doi.org/10.1080/87559129.2015.1015138
    [21] Hersh J (2021) Yoghurt: A Global History. London: Reaktion Books 1-160. https://reaktionbooks.co.uk/work/yoghurt
    [22] Whelan K, Jones N (2022) Fermented foods: Availability, cost, ingredients, nutritional content and on-pack claims. J Hum Nutr Diet 35: 396-405. https://doi.org/10.1111/jhn.12905
    [23] Biegańska M (2022) Packaging of dairy products: Emerging strategies. Food Packaging: The Smarter Way. Singapore: Springer Nature Singapore 127-164. https://doi.org/10.1007/978-981-16-7196-8_6
    [24] Lal R, Yambrach F, McProud L (2015) Consumer perceptions towards package designs: A cross cultural study. J Appl Packag Res 7: 61-94. https://doi.org/10.14448/japr.04.0004
    [25] Schiano AN, Harwood WS, Gerard PD, et al. (2020) Consumer perception of the sustainability of dairy products and plant-based dairy alternatives. J Dairy Sci 103: 11228-11243. https://doi.org/10.3168/jds.2020-18406
    [26] Nguyen AT, Parker L, Brennan L, et al. (2020) A consumer definition of eco-friendly packaging. J Clean Prod 252: 119792. https://doi.org/10.1016/j.jclepro.2019.119792
    [27] Ncube LK, Ude AU, Ogunmuyiwa EN, et al. (2021) An overview of plastic waste generation and management in food packaging industries. Recycling 6: 12. https://doi.org/10.3390/recycling6010012
    [28] Helmes RJK, Goglio P, Salomoni S, et al. (2022) Environmental impacts of end-of-life options of biobased and fossil-based polyethylene terephthalate and high-density polyethylene packaging. Sustainability 14: 11550. https://doi.org/10.3390/su141811550
    [29] De Oliveira J, de Souza Vandenberghe LP, et al. (2021) Bioconversion of potato-processing wastes into an industrially-important chemical lactic acid. Bioresour Technol Rep 15: 100698. https://doi.org/10.1016/j.biteb.2021.100698
    [30] Boura K, Dima A, Nigam P, et al. (2022) A critical review for advances on industrialization of immobilized cell bioreactors: economic evaluation on cellulose hydrolysis for PHB production. Bioresour Technol 349: 126757. https://doi.org/10.1016/j.biortech.2022.126757
    [31] Zhuo Y, He J, Li W, et al. (2023) A review on takeaway packaging waste: Types, ecological impact, and disposal route. Environ Pollut 337: 122518. https://doi.org/10.1016/j.envpol.2023.122518
    [32] Boesen S, Bey N, Niero M (2019) Environmental sustainability of liquid food packaging: Is there a gap between Danish consumers' perception and learnings from life cycle assessment?. J Clean Prod 210: 1193-1206. https://doi.org/10.1016/j.jclepro.2018.11.055
    [33] Otto S, Strenger M, Maier-Nöth A, et al. (2021) Food packaging and sustainability–Consumer perception vs. correlated scientific facts: A review. J Clean Prod 298: 126733. https://doi.org/10.1016/j.jclepro.2021.126733
    [34] Dahiya D, Nigam P (2023) Nutraceutical combinational therapy for diarrhoea control with probiotic beverages from fermented fruits, vegetables and cereals to regain lost hydration, nutrition and gut microbiota. Microorganisms 11: 2190. https://doi.org/10.3390/microorganisms11092190
    [35] Sohail M, Sun DW, Zhu Z (2018) Recent developments in intelligent packaging for enhancing food quality and safety. Crit Rev Food Sci Nutr 58: 2650-2662. https://doi.org/10.1080/10408398.2018.1449731
    [36] Manzoor A, Yousuf B, Pandith JA, et al. (2023) Plant-derived active substances incorporated as antioxidant, antibacterial or antifungal components in coatings/films for food packaging applications. Food Biosci 53: 102717. https://doi.org/10.1016/j.fbio.2023.102717
    [37] Drago E, Campardelli R, Pettinato M, et al. (2020) Innovations in smart packaging concepts for food: an extensive review. Foods 9: 1628. https://doi.org/10.3390/foods9111628
    [38] Bontzolis C, Plioni I, Dimitrellou D, et al. (2022) Isolation of antimicrobial compounds from aniseed and techno-economic feasibility report for industrial-scale application. Int J Food Sci Tech 57: 1-26. https://doi.org/10.1111/ijfs.15824
    [39] Manzoor A, Khan S, Dar AH, et al. (2023) Recent insights into green antimicrobial packaging towards food safety reinforcement: A review. J Food Saf 43: e13046. https://doi.org/10.1111/jfs.13046
    [40] Fernandez CM, Alves J, Gaspar PD, et al. (2023) Innovative processes in smart packaging. A systematic review. J Sci Food Agric 103: 986-1003. https://doi.org/10.1002/jsfa.11863
    [41] Tan A, Ngan PT (2020) A proposed framework model for dairy supply chain traceability. Sustain Futur 2: 100034. https://doi.org/10.1016/j.sftr.2020.100034
    [42] Wang X, Guo J, Ren H, et al. (2023) Research progress of nanocellulose-based food packaging. Trends Food Sci Technol 143: 104289. https://doi.org/10.1016/j.tifs.2023.104289
    [43] Zhu X, Cheng JH, Han Z (2024) Construction of a sustainable and hydrophobic high-performance all-green pineapple peel cellulose nanocomposite film for food packaging. Int J Biol Macromol 256: 128396. https://doi.org/10.1016/j.ijbiomac.2023.128396
    [44] Chadha U, Bhardwaj P, Selvaraj SK, et al. (2022) Current trends and future perspectives of nanomaterials in food packaging application. J Nanomater 2022. https://doi.org/10.1155/2022/2745416
    [45] Chausali N, Saxena J, Prasad R (2022) Recent trends in nanotechnology applications of bio-based packaging. J Agric Food Res 7: 100257. https://doi.org/10.1016/j.jafr.2021.100257
    [46] He Y, Li H, Fei X, et al. (2021) Carboxymethyl cellulose/cellulose nanocrystals immobilized silver nanoparticles as an effective coating to improve barrier and antibacterial properties of paper for food packaging applications. Carbohydr Polym 252: 100257. https://doi.org/10.1016/j.jafr.2021.100257
    [47] Francis DV, Thaliyakattil S, Cherian L, et al. (2022) Metallic nanoparticle integrated ternary polymer blend of pva/starch/glycerol: a promising antimicrobial food packaging material. Polymers 14: 1379. https://doi.org/10.3390/polym14071379
    [48] McCarthy B, Wang P (2022) Shades of Sustainability: Who are the buyers and non-buyers of sustainable packaging?. J Food Prod Mark 28: 153-178. https://doi.org/10.1080/10454446.2022.2064202
    [49] Singh N, Singhania RR, Nigam P, et al. (2022) Global status of lignocellulosic biorefinery: challenges and perspectives. Bioresou. Technol 344: 126415. https://doi.org/10.1016/j.biortech.2021.126415
    [50] Diyana ZN, Jumaidin R, Selamat MZ, et al. (2021) Physical properties of thermoplastic starch derived from natural resources and its blends: A Review. Polymers 13: 1396. https://doi.org/10.3390/polym13091396
    [51] Rezić I, Haramina T, Rezić T (2017) Metal nanoparticles and carbon nanotubes—perfect antimicrobial nano-fillers in polymer-based food packaging materials. Food Packaging. Cambridge: Academic Press 497-532. https://doi.org/10.1016/B978-0-12-804302-8.00015-7
    [52] Ncube LK, Ude AU, Ogunmuyiwa EN, et al. (2020) Environmental impact of food packaging materials: a review of contemporary development from conventional plastics to polylactic acid based materials. Materials 13: 4994. https://doi.org/10.3390/ma13214994
    [53] Chu R, Tang T, Hetherington MM (2022) Attention to detail: A photo-elicitation study of salience and packaging design for portion control and healthy eating. Nutr Bull 47: 501-515. https://doi.org/10.1111/nbu.12588
    [54] Zhu Y, Guillemat B, Vitrac O (2019) Rational design of packaging: toward safer and eco designed food packaging systems. Front Chem 7: 349. https://doi.org/10.3389/fchem.2019.00349
    [55] Shin J, Selke SEM (2014) Food packaging. Food Processing: Principles and Applications. New York: Wiley 249-273. https://doi.org/10.1002/9781118846315.ch11
    [56] Phelan A, Meissner K, Humphrey J, et al. (2022) Plastic pollution and packaging: Corporate commitments and actions from the food and beverage sector. J Clean Prod 331: 129827. https://doi.org/10.1016/j.jclepro.2021.129827
    [57] Andreasi Bassi S, Boldrin A, Faraca G, et al. (2020) Extended producer responsibility: How to unlock the environmental and economic potential of plastic packaging waste?. Resour Conserv Recycl 162: 105030. https://doi.org/10.1016/j.resconrec.2020.105030
    [58] Boz Z, Korhonen V, Koelsch Sand C (2020) Consumer considerations for the implementation of sustainable packaging: A review. Sustainability 12: 2192. https://doi.org/10.3390/su12062192
    [59] Dahiya D, Nigam P (2022) The gut microbiota influenced by the intake of probiotics and functional foods with prebiotics can sustain wellness and alleviate certain ailments like gut-inflammation and colon-cancer. Microorganisms 10: 665. https://doi.org/10.3390/microorganisms10030665
    [60] Dahiya D, Nigam P (2022) Clinical potential of microbial strains, used in fermentation for probiotic food, beverages and in synbiotic supplements, as psychobiotics for cognitive treatment through gut-brain signaling. Microorganisms 10: 1687. https://doi.org/10.3390/microorganisms10091687
    [61] Dahiya D, Nigam P (2023) Biotherapy using probiotics as therapeutic agents to restore the gut microbiota to relieve gastrointestinal tract inflammation, IBD, IBS and prevent induction of cancer. Int J Mol Sci 24: 5748. https://doi.org/10.3390/ijms24065748
    [62] Dahiya D, Nigam P (2023) Antibiotic-therapy-induced gut dysbiosis affecting gut microbiota—brain axis and cognition: restoration by intake of probiotics and synbiotics. Int J Mol Sci 24: 3074. https://doi.org/10.3390/ijms24043074
    [63] Yang B, Yin SN, Bian XF, et al. (2022) Preparation and properties of monomethoxyl polyethylene glycol grafted O-carboxymethyl chitosan for edible, fresh-keeping packaging materials. Food Packag Shelf Life 33: 100874. https://doi.org/10.1016/j.fpsl.2022.100874
    [64] Liu ZQ, Qin ZH, Jia HX, et al. (2023) Dual-crosslinked starch–poly(ester urethane)–oligochitosan films with high starch content: Application as biodegradable food packaging. Food Packag Shelf Life 37: 101064. https://doi.org/10.1016/j.fpsl.2023.101064
    [65] Plasek B, Lakner Z, Temesi Á (2021) I believe it is healthy-impact of extrinsic product attributes in demonstrating healthiness of functional food products. Nutrients 13: 3518. https://doi.org/10.3390/nu13103518
    [66] Marone PA (2017) Food safety: marketing trends intended for consumer awareness and partnership. Developing New Functional Food and Nutraceutical Products. Cambridge: Academic press 85-108. https://doi.org/10.1016/B978-0-12-802780-6.00005-5
    [67] Deng X, Srinivasan R (2013) When do transparent packages increase [or decrease] food consumption?. J Mark 77: 104-117. https://doi.org/10.1509/jm.11.0610
    [68] Kaur B, Gangwar V, Dash G (2022) Green marketing strategies, environmental attitude, and green buying intention: a multi-group analysis in an emerging economy context. Sustainability 14: 6107. https://doi.org/10.3390/su14106107
    [69] Esmerino EA, Ferraz JP, Filho ERT, et al. (2017) Consumers' perceptions toward 3 different fermented dairy products: Insights from focus groups, word association, and projective mapping. J Dairy Sci 100: 8849-8860. https://doi.org/10.3168/jds.2016-12533
    [70] Speight KC, Schiano AN, Harwood WS, et al. (2019) Consumer insights on prepackaged Cheddar cheese shreds using focus groups, conjoint analysis, and qualitative multivariate analysis. J Dairy Sci 102: 6971-6986. https://doi.org/10.3168/jds.2018-16209
    [71] Chirilli C, Martina M, Torri L (2022) Consumers' awareness, behavior and expectations for food packaging environmental sustainability: influence of socio-demographic characteristics. Foods 11: 2388. https://doi.org/10.3390/foods11162388
    [72] Keener L (2022) Food safety and regulatory survey of food additives and other substances in human food. Ensuring Global Food Safety. Cambridge: Academic Press 259-273. https://doi.org/10.1016/B978-0-12-816011-4.00005-7
    [73] Schonrock FT (2023) The role of international, regional, and national organizations in the development of standards. Food Safety Management. Cambridge: Academic Press 1005-1017. https://doi.org/10.1016/B978-0-12-820013-1.00050-4
    [74] Pomeranz JL, Romo Palafox MJ, Harris JL (2018) Toddler drinks, formulas, and milks: Labeling practices and policy implications. Prev Med 109: 11-16. https://doi.org/10.1016/j.ypmed.2018.01.009
    [75] Gibson KM, Temple NJ (2022) Food labels and sources of nutrients: sorting the wheat from the chaff. Nutrition Guide for Physicians and Related Healthcare Professions. Berlin: Springer International Publishing 425-432. https://doi.org/10.1007/978-3-030-82515-7_41
    [76] Kasapila W, Shaarani SMd (2016) Legislation-impact and trends in nutrition labeling: a global overview. Crit Rev Food Sci Nutr 56: 56-64. https://doi.org/10.1080/10408398.2012.710277
    [77] Koirala S, Anal AK (2021) Probiotics-based foods and beverages as future foods and their overall safety and regulatory claims. Future Foods 3: 100013. https://doi.org/10.1016/j.fufo.2021.100013
    [78] Negowetti N, Ambwani S, Karr S (2022) Digging up the dirt on “clean” dietary labels: Public health considerations and opportunities for increased Federal oversight. Int J Eat Disord 55: 39-48. https://doi.org/10.1002/eat.23585
    [79] Hattimare D, Shakya S, Patyal A, et al. (2022) Occurrence and exposure assessment of Aflatoxin M1 in milk and milk products in India. J Food Sci Technol 59: 2460-2468. https://doi.org/10.1007/s13197-021-05265-4
    [80] Misra SK, Pathak K (2023) Legislation on active and intelligent packaging. Green Sustainable Process For Chemical and Environmental Engineering ad Science. Cambridge: Academic Press 97-113. https://doi.org/10.1016/B978-0-323-95644-4.00012-7
    [81] Galimova A, Smolnikova F, Kosheleva Y, et al. (2022) Food safety research and improvement of the technology of cottage cheese product with the use of green buckwheat. J Environ Sci Health Part B 57: 848-857. https://doi.org/10.1080/03601234.2022.2127297
    [82] Okpala COR, Korzeniowska M (2023) Understanding the relevance of quality management in agro-food product industry: from ethical considerations to assuring food hygiene quality safety standards and its associated processes. Food Rev Int 39: 1879-1952. https://doi.org/10.1080/87559129.2021.1938600
    [83] Padmanabhan SC, Cruz-Romero MC, Kerry JP, et al. (2018) Food packaging: surface engineering and commercialization. Nanomaterials For Food Packaging. Cambridge: Academic Press 301-328. https://doi.org/10.1016/B978-0-323-51271-8.00011-5
    [84] King T, Cole M, Farber JM, et al. (2017) Food safety for food security: Relationship between global megatrends and developments in food safety. Trends Food Sci Technol 68: 160-175. https://doi.org/10.1016/j.tifs.2017.08.014
    [85] Garcia Martinez M, Fearne A, Caswell JA, et al. (2007) Co-regulation as a possible model for food safety governance: Opportunities for public-private partnerships. Food Policy 32: 299-314. https://doi.org/10.1016/j.foodpol.2006.07.005
    [86] Marucheck A, Greis N, Mena C, et al. (2011) Product safety and security in the global supply chain: issues, challenges and research opportunities. J Oper Manag 29: 707-720. https://doi.org/10.1016/j.jom.2011.06.007
    [87] Olsson A (2017) Managing packaging design for sustainable development: A compass for strategic directions. New York: John Wiley & Sons 1-216. https://doi.org/10.1002/9781119151036
    [88] Ismail A, Wan Ismail, Kaliappen N (2020) Tastiway's Export Strategy. Malaysia: UUM Press 73. http://cdr.uum.edu.my/jspui/handle/123456789/155
    [89] Lopez-Rubio A, Gavara R, Lagaron JM (2006) Bioactive packaging: turning foods into healthier foods through biomaterials. Trends Food Sci Technol 17: 567-575. https://doi.org/10.1016/j.tifs.2006.04.012
    [90] Deshwal GKr, Panjagari NR (2020) Review on metal packaging: materials, forms, food applications, safety and recyclability. J Food Sci Technol 57: 2377-2392. https://doi.org/10.1007/s13197-019-04172-z
    [91] National Advisory Committee on Microbiological Criteria for Foods.Parameters for determining inoculated pack/challenge study protocols. J Food Prot (2020) 73: 140-202. https://doi.org/10.4315/0362-028X-73.1.140
    [92] Owolabi IO, Akinmosin BO, Kupoluyi AO, et al. (2023) Packaging and packaging technology for indigenous fermented foods in the tropics: challenges and opportunities. Indigenous Fermented Foods for the Tropics. Cambridge: Academic Press 563-575. https://doi.org/10.1016/B978-0-323-98341-9.00022-0
    [93] Pilevar Z, Bahrami A, Beikzadeh S, et al. (2019) Migration of styrene monomer from polystyrene packaging materials into foods: Characterization and safety evaluation. Trends Food Sci Technol 91: 248-261. https://doi.org/10.1016/j.tifs.2019.07.020
    [94] Bumbudsanpharoke N, Ko S (2015) Nano-food packaging: An overview of market, migration research, and safety regulations: An overview of nano-food packaging. J Food Sci 80: R910-R923. https://doi.org/10.1111/1750-3841.12861
    [95] Khalid MY, Arif ZU (2022) Novel biopolymer-based sustainable composites for food packaging applications: A narrative review. Food Packag Shelf Life 33: 100892. https://doi.org/10.1016/j.fpsl.2022.100892
    [96] Guillard V, Gaucel S, Fornaciari C, et al. (2018) The next generation of sustainable food packaging to preserve our environment in a circular economy context. Front Nutr 5: 121. https://doi.org/10.3389/fnut.2018.00121
    [97] Meherishi L, Narayana SA, Ranjani KS (2019) Sustainable packaging for supply chain management in the circular economy: A review. J Clean Prod 237: 117582. https://doi.org/10.1016/j.jclepro.2019.07.057
    [98] Victor Ntuli, Thulani Sibanda, James A, et al. (2023) Dairy production: microbial safety of raw milk and processed milk products. Present Knowledge in Food Safety. Cambridge: Academic Press 439-454. https://doi.org/10.1016/B978-0-12-819470-6.00076-7
    [99] Riccaboni A, Neri E, Trovarelli F, et al. (2021) Sustainability-oriented research and innovation in ‘farm to fork’ value chains. Curr Opin Food Sci 42: 102-112. https://doi.org/10.1016/j.cofs.2021.04.006
    [100] Rejeesh CR, Anto T (2023) Packaging of milk and dairy products: Approaches to sustainable packaging. Mater Today Proc 72: 2946-2951. https://doi.org/10.1016/j.matpr.2022.07.467
    [101] Teixeira LV, Bomtempo JV, Oroski FDA, et al. (2023) The diffusion of bioplastics: What can we learn from poly [Lactic Acid]. Sustainability 15: 4699. https://doi.org/10.3390/su15064699
    [102] David JRD, Coronel PM, Simunovic J (2022) Handbook of Aseptic Processing and Packaging. Third edition. Boca Raton: CRC Press 1-702. https://doi.org/10.1201/9781003158653
    [103] Vodnar DC, Călinoiu LF, Mitrea L, et al. (2019) A new generation of probiotic functional beverages using bioactive compounds from agro-industrial waste. Functional and Medicinal Beverages. Cambridge: Academic press 483-528. https://doi.org/10.1016/B978-0-12-816397-9.00015-7
    [104] Chen A, Moradi S, Hort J (2022) On-the-pack voluntary well-being messaging for milks targeting chinese older adults: a content analysis. Foods 11: 2212. https://doi.org/10.3390/foods11152212
    [105] Wei W, Kim G, Miao L, et al. (2018) Consumer inferences of corporate social responsibility [CSR] claims on packaged foods. J Bus Res 83: 186-201. https://doi.org/10.1016/j.jbusres.2017.10.046
    [106] Verma M, Rout PK (2022) Probiotics: promising opportunity for future functional foods. Recent Advances in Food Biotechnology. Singapore: Springer Nature 75-96. https://doi.org/10.1007/978-981-16-8125-7_5
    [107] Miller KB, Eckberg JO, Decker EA, et al. (2021) Role of food industry in promoting healthy and sustainable diets. Nutrients 13: 2740. https://doi.org/10.3390/nu13082740
  • Reader Comments
  • © 2024 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(1879) PDF downloads(119) Cited by(3)

Article outline

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog