1 Introduction
Cholera, a waterborne disease caused by V. cholerae, can be found in diverse aquatic environments, such as the ocean, estuaries, rivers, and lakes [Reference Garay, Arnau and Amaro11, Reference Perez-Rosas and Hazen33, Reference Yamazaki, Yang and Wang59]. It is characterised by severe vomiting and diarrhoea, and if not promptly treated, the disease can lead to severe dehydration and death [Reference Codeço7, Reference Hove-Musekwa, Nyabadza, Chiyaka, Das, Tripathi and Mukandavire16, Reference Kierek and Watnick22]. This is attributed to the ability of V. cholerae to produce cholera toxin, which stimulates water and electrolyte secretion by intestinal endothelial cells [Reference Mari, Bertuzzo, Righetto, Casagrandi, Gatto, Rodriguez-Iturbe and Rinaldo27]. The primary symptoms of cholera include diarrhoea, dehydration, abdominal cramps, a drop in blood pressure and kidney failure [Reference Cai, Modnak and Wang5]. Besides, the dynamics of cholera epidemics involve a complex web of interactions between human hosts, pathogens and environments [Reference Wang and Wang51]. The disease is primarily transmitted to humans by ingesting water or food contaminated with toxigenic forms of V. cholerae O1 and O139 from the environment [Reference Colwell and Huq8, Reference Hartley, Morris and Smith14, Reference Kaper, Morris and Levine21]. Cholera outbreaks frequently arise in regions lacking access to antibiotics and adequate public health infrastructure, especially in developing countries with limited healthcare resources, such as the Indian subcontinent, parts of Asia, Africa and Latin America. Cholera remains a persistent health challenge [Reference Kong, Davis and Wang23, Reference Safi, Melesse and Gumel35].
Research on mathematical models of cholera can be traced back to 1973, when Capasso and Paveri-Fontana [Reference Capasso and Paveri-Fontana6] introduced an ordinary differential equation (ODE) model to study the spread of cholera in the Mediterranean region. The model described compartments for V. cholerae and infected individuals, investigating the transmission of cholera in the European Mediterranean region. Joh et al. first proposed an iSIR model describing indirectly transmitted infectious diseases with immunological threshold [Reference Joh, Wang, Weiss and Weitz20], with a follow up work [Reference Luo, Wang and Wang25] studying a seasonal forcing iSIR model with a smoothing immunological threshold. Tien and Earn [Reference Tien and Earn43] proposed a waterborne disease model incorporating both direct transmission and indirect transmission with bilinear incidence. Wu and Zou [Reference Wu and Zou58] examined a diffusive host-pathogen model that incorporates distinct dispersal rates for susceptible and infected hosts. They analysed the asymptotic profiles of the positive steady state as the dispersal rate of the susceptible or infected hosts tends to zero. The findings indicate that the infected hosts concentrate at certain points, which can be characterised as the pathogen’s most favoured sites when the mobility of the infected host is limited. Wang et al. [Reference Wang, Zhao and Wang52] proposed a new reaction-convection-diffusion model to investigate the spatiotemporal dynamics of cholera transmission. The model incorporates time-periodic parameters to describe the seasonality of the disease transmission and bacterial growth rates. Wang and Wang [Reference Wang and Wang45] proposed a reaction-diffusion cholera model incorporating the different dispersal rates of the susceptible and infected hosts in the absence of diffusion term for the cholera equation.
Recent laboratory findings in [Reference Andrews and Basu3, Reference Hartley, Morris and Smith14] suggested that the V. cholerae induces a short-lived, hyperinfectious (HI) state through the gastrointestinal tract and decays into a lower infectiousness (LI) state within hours [Reference Hartley, Morris and Smith14, Reference Nelson, Chowdhury, Flynn, Schild, Bourassa, Shao, LaRocque, Calderwood, Qadri, Camilli and Ausubel30]. Moreover, the infectivity of freshly shed V. cholerae greatly out-competes bacteria grown in vitro, exhibiting infectivity levels up to 700 times higher [Reference Nelson, Harris, Glenn Morris, Calderwood and Camilli31, Reference Wang and Wang51]. HI vibrios, being closer to human hosts than environmental vibrios, are more likely to come into contact with human susceptible individuals [Reference Hartley, Morris and Smith14]. To investigate hyperinfectious state of V. cholerae is crucial and also holds substantial practical significance. Furthermore, incorporating these hyperinfectious states and lower infectiousness states of V. cholerae into cholera disease models may lead to a better understanding of the observed cholera epidemic patterns.
Research on hyperinfectivity of V. cholerae has received increasing attention in recent years. Hartley et al. [Reference Hartley, Morris and Smith14] incorporated hyperinfectivity vibrios into the mathematical model. The results suggest that for minimising the epidemic spread of cholera, intervention measures should focus on minimising the transmission risk of short-lived, highly infectious cholera vibrios. Shuai et al. [Reference Shuai, Tien and van den Driessche39] investigated cholera dynamics with both hyperinfectivity and temporary immunity. Wang and Wang [Reference Wang and Wang51] introduced a novel modelling framework to investigate the impact of bacterial hyperinfectivity on cholera epidemics in a spatially heterogeneous environment. Specifically, this model categorised V. cholerae into HI vibrios compartment and LI vibrios compartment. Wang and Wu [Reference Wang and Wu46] extended the work in [Reference Wang and Wang45] by incorporating bacterial hyperinfectivity and saturation mechanism for indirect transmission pathway. Wang et al. [Reference Wang, Wu, Wang and Feng49] developed a reaction-advection-diffusion model with a general boundary conditions, considering HI and LI vibrio strains, convection factors, and human behaviour change, to establish the threshold-type results of cholera transmission in spatial–temporal heterogeneous environment (see also [Reference Wang, Wang and Fan53]). Wang et al. [Reference Wang, Wang and Wang48] formulated a generalised cholera model incorporating nonlocal time delays to investigate the effects of bacterial hyperinfectivity on cholera outbreaks and to derive the detailed classifications of global dynamics in a spatially heterogeneous environment.
Phages, viruses that specifically infect and destroy bacteria, have been characterised as bacterial parasites, with each phage type exhibiting a distinct ability to replicate within specific strains of host bacteria [Reference Wang and Wang55]. The interaction mechanism between bacteriophages and bacteria begins when a lytic phage inserts its genetic material into a bacterial cell, where it proliferates, leading to cell lysis and the release of new phages into the environment [Reference Botelho, Kong, Lucien, Shuai and Wang4]. This process can significantly impact the severity of cholera outbreaks. For example, the investigation of the cholera epidemic in Dhaka, Bangladesh, indicates that lytic bacteriophages may mitigate epidemic severity by eliminating bacteria in both reservoirs and infected individuals [Reference Faruque, Naser, Islam, Faruque, Ghosh, Nair, Sack and Mekalanos10, Reference Jensen, Faruque, Mekalanos and Levin19].
Phages (viruses of bacteria) play a pivotal role in shaping both the evolution and dynamics of bacterial species, especially for V. cholerae [Reference Jensen, Faruque, Mekalanos and Levin19, Reference Kong, Davis and Wang23, Reference Nelson, Chowdhury, Flynn, Schild, Bourassa, Shao, LaRocque, Calderwood, Qadri, Camilli and Ausubel30, Reference Netter, Dunham and Seed32]. Kong et al. [Reference Kong, Davis and Wang23] proposed an ODE model incorporating a Holling II response function to depict the interaction between V. cholerae and bacteriophages. Misra et al. [Reference Misra and Gupta29] investigated a reaction-diffusion system for the biological control of cholera epidemics. They focused on temporal evolution of cholera within a region and explored its control using lytic bacteriophage in aquatic reservoirs. Botelho et al. [Reference Botelho, Kong, Lucien, Shuai and Wang4] proposed an ODE model with the bacteria-phage interaction of Holling type I. This model includes human populations (SIRS), bacteria population (B) and phage population (p) to represent these interactions. In their study, they derived threshold parameters to characterise the stability of equilibria. The findings suggest that the reservoir environment might contribute to the periodicity of cholera outbreaks. Hu et al. [Reference Hu, Wang and Nie18] proposed a cholera model comprising coupled reaction-diffusion equations and ODEs to discuss the effects of spatial heterogeneity, horizontal transmission, environmental viruses and phages on the spread of V. cholerae.
The aim of the paper is to investigate multiple effects of the interaction between V. cholerae and phage on cholera transmission, thereby improving our understanding of the transmission mechanism of cholera diseases and proposing targeted disease control measures. Generally speaking, it is very challenging to discuss the threshold-type results in the case of multi-class steady states. Fortunately, in this paper, we derive the existence and stability analysis of multi-class steady states for some special cases.
The remainder of the paper is organised as follows. In Section 2, we propose a degenerate reaction-diffusion model with different dispersal rates, which incorporates short-lived hyperinfectious (HI vibrios) state of V. cholerae and lower-infectious (LI vibrios) state of V. cholerae simultaneously in a heterogeneous environment. In Section 3, we present the main results of this paper, including the well-posedness, dynamics of the disease-free steady state, dynamics of the phage-free steady state and dynamics of the phage-present steady state. In Section 4, we give the proofs of the main results. A brief discussion of this paper is given in Section 5.
2 Mathematical model

Figure 1. Schematic diagram of model (2.1). The green solid line represents the recruitment and mortality rates of human hosts and V. cholerae, and the blue solid line denotes the direct development of cholera. The purple dashed line represents the infection process and the interaction between phages and V. cholerae.
Building upon the model presented by Jensen et al. [Reference Jensen, Faruque, Mekalanos and Levin19], which integrates cholera epidemiology with bacterial and bacteriophage population dynamics, we examine the interaction between HI vibrios and LI vibrios with bacteriophages, as well as the intrinsic growth rate of V. cholerae, and divide the infected human hosts into two parts, one consists of human hosts infected only with V. cholerae, denoted as
$I_{1}$
, while the other consists of human hosts that are simultaneously infected with V. cholerae and bacteriophages, indicating the parasitism of bacteriophages within the host cells (bacteria), denoted as
$I_{2}$
. Based on the above considerations, we propose a degenerate reaction-diffusion cholera model:

The population density of susceptible individuals at location
$x$
and time
$t$
is denoted by
$S(x,t)$
. The population densities of phage-negative and phage-positive infected individuals at location
$x$
and time
$t$
are denoted by
$I_{1}(x,t),I_{2}(x,t)$
, respectively. Let
$ I(x,t)=I_{1}(x,t)+I_{2}(x,t)$
, where
$ I(x,t)$
denotes all human hosts infected with V. cholerae. The concentrations of HI and LI vibrios in the water environment at location
$x$
and time
$t$
are denoted by
$ B_{1}(x,t), B_{2}(x,t)$
, respectively. The concentration of phage in the water environment at location
$x$
and time
$t$
is denoted by
$P(x,t)$
. The recruitment rate of susceptible human hosts is represented by
$\Lambda (x)$
. The parameters
$\alpha _{1}(x)$
and
$\alpha _{2}(x)$
can be interpreted as the rates of HI and LI vibrios consumption.
$L(x)$
represents the half-saturation concentration of phage. For simplicity, we consider only natural deaths by
$\mu (x)$
and disregard deaths caused by the disease. The functions
$ h_{1}(x,B_{1})$
and
$ h_{2}(x,B_{2})$
are the intrinsic growth rates of HI and LI vibrios, respectively. The rate of bacterial shedding is represented by
$\eta (x)$
, while
$\delta _{1}(x), \delta _{2}(x)$
denote the natural death rate of HI and LI vibrios, respectively. Phage interacts with both HI and LI vibrios, resulting in bacterial death rates of
$ b_{1}(x)$
and
$b_{2}(x)$
, respectively. Meanwhile, the phage has a gain from two vibrios’ deaths represented by
$\chi _{1}(x)$
and
$ \chi _{2}(x)$
. The mean phage shed rate is denoted as
$\alpha (x)$
, and
$m(x)$
represents the phage decay rate. The cholera transmission process is shown in Figure 1. In model (2.1), we choose

where
$H_{i}(x)$
denotes the half-saturation concentration of bacteria.
$ d_{S}, d_{I}$
represent the dispersal rates of susceptible and infected human hosts, respectively. Here, we assume that the dispersal rate
$d_{I}$
for both phage-negative and phage-positive infections are equal. We also consider an isolated habitat
$\Omega$
, which is characterised by the homogeneous Neumann boundary condition.

and the initial conditions are

for
$ x\in \bar {\Omega }$
, and where
$ S^{0}(x),I_{1}^{0}(x),I_{2}^{0}(x),B_{1}^{0}(x),B_{2}^{0}(x),P^{0}(x)$
are nonnegative continuous functions. Furthermore, if spatial heterogeneity is not considered, model (2.1) degenerates to the homogeneous model:

In the following, we make some basic assumptions:
-
(H1 )
$ d_{S}, d_{I}$ are positive
$ C^{1}$ -function on
$\bar {\Omega }$ ;
-
(H2 )
$ (I_{1}^{0},I_{2}^{0},B_{1}^{0},B_{2}^{0},P^{0})\not \equiv 0$ on
$\bar {\Omega }$ ;
-
(H3 )
$ h_{1}(x,v), h_{2}(x,v) \in C^{0,1}(\bar {\Omega }\times \mathbb{R}_{+})$ are nonnegative and strictly concave down in relation to the second variable, and
$ h_{i}(x,v)=0, i= 1, 2,$ if and only if
$ v=0$ , then
(2.5)\begin{equation} \lim \limits _{v\to \infty }\dfrac {h_{i}(x,v)}{v}\lt \delta _{i}(x), \ i=1,2, \ x\in \Omega . \end{equation}
For the assumption (
$ \mathbf{H}_{\mathbf{3}}$
), we also refer to [Reference Botelho, Kong, Lucien, Shuai and Wang4, Reference Wang and Wang51], these general incidence functions are set to be

where
$\theta (x)$
is the intrinsic growth rate of bacteria, and
$H_{B_{i}}(x)$
denotes the maximum capacity of the bacteria.
It should be pointed out that since multiple effects of the interaction between V. cholerae and phages on cholera transmission, the complexity of model (2.1)–(2.3) leads to several mathematical difficulties:
-
(i) We prove the global asymptotic stability of the disease-free steady state for the critical case when
$\mathscr{R}_{0}=1$ for the high-dimensional system, which is instituted by six equations.
-
(ii) Generally speaking, it is very challenging to discuss the threshold-type results in the case of multi-class steady states. Fortunately, in this paper, we derive the existence and stability analysis of multi-class steady states for some special cases. We show the existence of phage-free steady state in a heterogeneous environment. An appropriate Lyapunov function is constructed to discuss the global stability of the phage-free steady state in a homogeneous environment.
3 Main results
In this section, we state the main results of this paper, whose proofs are given in Section 4.
3.1 Well-posedness of the model
Define
$\mathit{H}=C(\bar {\Omega },\mathbb{R}^{6})$
, which is assigned the following supremum norm:

with
$ \varphi =(\varphi _{1},\varphi _{2},\varphi _{3},\varphi _{4},\varphi _{5},\varphi _{6})\in \mathit{H}.$
Define
$H^{+}=C(\bar {\Omega },\mathbb{R}^{6}_{+})$
as the positive cone of
$\mathit{H}$
. Let
$L_{p}(\Omega )$
be the Banach space of function
$y$
whose
$p$
-th power of absolution value is integrable on
$\Omega$
for
$1 \leq p\leq \infty$
with

Define

where
$ z(x)\in C(\bar {\Omega },\mathbb{R})$
. Define
$ \mathbb{B}_{i} : D(\mathbb{B}_{i})\to C(\bar {\Omega },\mathbb{R})$
as the linear operator with

where
$ D(\mathbb{B}_{i}) :=\left \{\phi \in \cap _{y\ge 1}W^{2,y}(\Omega ):\ \frac {\partial \phi }{\partial \nu }=0\ \text{on}\ \partial \Omega \ \text{and}\ \mathbb{B}_{i}\phi \in C(\bar {\Omega },\mathbb{R}) \right \}$
. By [Reference Webb56], we know that the operator
$ \mathbb{B}_{i}$
is the infinitesimal generator of the strongly continuous semigroup
$\left \{e^{t\mathbb{B}_{i}}\right \}_{t\ge 0}, i=1,2$
. The operator
$ \mathscr{B}\,:\, \mathit{H}\to \mathit{H}$
defined by

is also the infinitesimal generator of the strongly continuous semigroup
$\left \{e^{t\mathscr{B}}\right \}_{t\ge 0}$
in
$\mathit{H}$
. Moreover, we define the nonlinear operator
$ \mathscr{L}\,\,:\,\mathit{H}\to \mathit{H}$
as

Thus, model (2.1) can be expressed as

Theorem 3.1. For any
$c^{0}(x)= (S^{0}(x),I_{1}^{0}(x),I_{2}^{0}(x),B_{1}^{0}(x),B_{2}^{0}(x),P^{0}(x))\in \mathit{H^{+}}$
, model (2.1)–(2.3) admits a unique global nonnegative classical solution defined on
$\bar {\Omega }\times [0,\infty )$
. Moreover, model (2.1)–(2.3) has a connected global attractor in
$\mathit{H}^{+}$
.
3.2 Dynamics of the disease-free steady state
A steady state of model (2.1)–(2.3) is a solution of the following model

for
$ t\gt 0$
. Model (2.1)–(2.3) admits a unique disease-free steady state
$F_{0}=(S^{*}(x),0,0,0,0,0)$
, where
$ S^{*}(x)$
is the unique positive solution of

Define

Linearising model (2.1)–(2.3) at
$F_{0}$
and adding the equations for
$ I_{1}(x,t)$
and
$I_{2}(x,t)$
, we obtain

Let
$J(t)$
be the solution semiflow associated with model (3.6), where
$ J(t)\varphi =(I(\cdot ,t,\varphi ),B_{1}(\cdot ,t,\varphi ),B_{2}(\cdot ,t,\varphi ))$
for
$\varphi \in C(\bar {\Omega },\mathbb{R}^{3})$
. Since model (3.6) is cooperative,
$ J(t)$
is a
$ C_{0}$
-semigroup with generator

To ensure the well-definedness of
$\mathscr{A}$
, we impose the following assumption on
$ \,\hat{\!h}_{i}(x)$
for the remainder of this paper:

Following [Reference Thieme42, Reference Wang and Zhao50], the basic reproduction number
$\mathscr{R}_{0}$
of model (2.1)–(2.3) is defined as the spectral radius of
$-FV^{-1}$
, which is denoted by
$ r(\!-FV^{-1})$
, namely

From the similar results in [Reference Thieme42, Reference Wang and Zhao50], we can assert the following statement.
Lemma 3.2.
$\mathscr{R}_{0}-1$
has the same sign as
$s(\mathscr{A} \, )$
, where
$s(\mathscr{A} \, )$
denotes the spectrum bound of
$\mathscr{A}$
with
$s(\mathscr{A} \, )=\sup \{Re\lambda , \lambda \in \sigma (\mathscr{A} \, )\}$
.
To derive an equivalent formula for the basic reproduction number
$\mathscr{R}_0$
, similar to the proof in [Reference Shu, Ma and Wang38, Reference Wang and Feng47], we introduce the following result involving the next generation operators
$D_H$
and
$D_L$
for HI vibrios and LI vibrios infections, respectively.
Lemma 3.3. Let

be a positive operator, and

be a resolvent-positive operator with
$s(V)\lt 0$
, where
$s(V)$
denotes the spectral bound of
$V$
, then we obtain

where
$D_{H}=F_{11}V_{22}^{-1}V_{21}(V_{11}-d_{I}\Delta )^{-1}$
and
$D_{L}=F_{12}V_{33}^{-1}V_{32}V_{22}^{-1}V_{21}(V_{11}-d_{I}\Delta )^{-1}.$
In addition, based on Lemma 3.3, we can derive a specific form for
$\mathscr{R}_{0}$
as follows:

where

is the next generation operator for HI vibrios transmission to human hosts, and

is the next generation operator for LI vibrios transmission to human hosts.
If considering exclusively the infection of human hosts by HI vibrios, the basic reproduction number
$\mathscr{R}_{0}^{\,H}$
can be represented as

On the other hand, if considering exclusively the infection of human hosts by LI vibrios, the basic reproduction number
$\mathscr{R}_{0}^{\,L}$
can be represented as

By [Reference Allen, Bolker and Lou2, Theorem 2] and the expressions of
$\mathscr{R}_{0}^{\,H}$
and
$\mathscr{R}_{0}^{\,L}$
, we immediately get Theorems3.4 and 3.5.
Theorem 3.4. The following statements are valid:
-
(i)
$\mathscr{R}_{0}^{\,H}$ is decreasing in
$ d_{I}$ with
\begin{align*} \lim \limits _{d_{I}\to 0}\mathscr{R}_{0}^{\,H}=\max \left \{ \dfrac {\alpha _{1}\Lambda \eta }{\mu ^{2}H_{1}(\delta _{1}-\,\hat{\!h}_{1})}\,:\,x\in \bar {\Omega }\right \} \end{align*}
\begin{align*} \lim \limits _{d_{I}\to \infty }\mathscr{R}_{0}^{\,H}=\dfrac {\int _{\Omega }\alpha _{1}\Lambda \eta /\mu H_{1}(\delta _{1}-\,\hat{\!h}_{1})dx}{\int _{\Omega } \mu dx}. \end{align*}
-
(ii) If
$\Omega$ is a favourable environment for HI vibrios in the sense that
\begin{align*} \int _{\Omega }\dfrac {\alpha _{1}\Lambda \eta }{\mu H_{1}(\delta _{1}-\,\hat{\!h}_{1})}dx\gt \int _{\Omega }\mu dx, \end{align*}
$\mathscr{R}_{0}^{\,H}\gt 1$ for all
$ d_{I}\gt 0$ .
-
(iii) If
$\Omega$ is a non-favourable environment for HI vibrios in the sense that
\begin{align*} \int _{\Omega }\dfrac {\alpha _{1}\Lambda \eta }{\mu H_{1}(\delta _{1}-\,\hat{\!h}_{1})}dx\lt \int _{\Omega }\mu dx, \end{align*}
$ x$ within the domain in the sense that
$ \alpha _{1}(x)\Lambda (x)\eta (x) \gt \mu ^{2}(x)H_{1}(\delta _{1}(x)-\,\hat{\!h}_{1}(x)),$ then there exists
$ \bar {d}_{I}$ such that
$\mathscr{R}_{0}^{\,H}\gt 1$ when
$d_{I}\lt \bar {d}_{I}$ , and
$\mathscr{R}_{0}^{\,H}\lt 1$ when
$d_{I}\gt \bar {d}_{I}$ .
Theorem 3.5. The following statements are valid:
-
(i)
$\mathscr{R}_{0}^{\,L}$ is decreasing in
$ d_{I}$ with
\begin{align*} \lim \limits _{d_{I}\to 0}\mathscr{R}_{0}^{\,L}=\max \left \{\dfrac {\alpha _{2}\Lambda \delta _{1}\eta }{\mu ^{2}H_{2}(\delta _{1}-\,\hat{\!h}_{1})(\delta _{2}-\,\hat{\!h}_{2})}\,:\,x\in \bar {\Omega }\right \} \end{align*}
\begin{align*} \lim \limits _{d_{I}\to \infty }\mathscr{R}_{0}^{\,L}=\dfrac {\int _{\Omega }\alpha _{2}\Lambda \delta _{1}\eta /\mu H_{2}(\delta _{1}-\,\hat{\!h}_{1})(\delta _{2}-\,\hat{\!h}_{2})dx}{\int _{\Omega } \mu dx}. \end{align*}
-
(ii) If
$\Omega$ is a favourable environment for LI vibrios in the sense that
\begin{align*} \int _{\Omega }\dfrac {\alpha _{2}\Lambda \delta _{1}\eta }{\mu H_{2}(\delta _{1}-\,\hat{\!h}_{1})(\delta _{2}-\,\hat{\!h}_{2})}dx\gt \int _{\Omega }\mu dx, \end{align*}
$\mathscr{R}_{0}^{\,L}\gt 1$ for all
$ d_{I}\gt 0$ .
-
(iii) If
$\Omega$ is a non-favourable environment for LI vibrios in the sense that
\begin{align*} \int _{\Omega }\dfrac {\alpha _{2}\Lambda \delta _{1}\eta }{\mu H_{2}(\delta _{1}-\,\hat{\!h}_{1})(\delta _{2}-\,\hat{\!h}_{2})}dx\lt \int _{\Omega }\mu dx, \end{align*}
$ x$ within the domain in the sense that
$ \alpha _{2}(x)\Lambda (x)\delta _{1}(x)\eta (x) \gt \mu ^{2}(x)H_{2}(\delta _{1}(x)-\,\hat{\!h}_{1}(x))(\delta _{2}(x)-\,\hat{\!h}_{2}(x)),$ then there exists
$ \,\hat{\!d}_{I}$ such that
$\mathscr{R}_{0}^{\,L}\gt 1$ when
$d_{I}\lt \,\hat{\!d}_{I}$ , and
$\mathscr{R}_{0}^{\,L}\lt1$ when
$d_{I}\gt \,\hat{\!d}_{I}$ .
Remark 3.6. For model (2.4), there exists a disease-free steady state
$ \tilde {F}_{0} = (S^{*},0,0,0,0,0)$
, where
$ S^{*}=\frac {\Lambda }{\mu }$
. By a simple computation, the basic reproduction number of model (2.4) is

The extinction of the disease for model (2.1)–(2.3) in terms of
$\mathscr{R}_{0}$
can be expressed as follows:
3.3 Dynamics of the phage-free steady state
In this subsection, we discuss the case that phages and phage-positive infected individuals are absent in model (2.1), and analyse the dynamics of the model under this case.
Theorem 3.8. If
$\mathscr{R}_{0}\gt 1$
, model (2.1) has at least one phage-free steady state
$ F_{1} =(S^{a}(x),I_{1}^{a}(x),0, B_{1}^{a}(x),B_{2}^{a}(x),0)$
.
Remark 3.9. Although we establish the existence of phage-free steady state for model (2.1), the problems of uniqueness and local/global stability are still unresolved. However, if the heterogeneous space degenerates to a homogeneous one, that is, model (2.1) degenerates to model (2.4), we can determine the uniqueness and stability of
$ F_{1}$
.
For model (2.4), if
$\ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
, there exists a phage-free steady state
$ \tilde {F}_{1}=(\tilde {S}^{a},\tilde {I}_{1}^{a},0,\tilde {B}_{1}^{a},\tilde {B}_{2}^{a},0)$
, where

and
$ \tilde {I}_{1}^{a}$
is the positive root of
$ f(I_{1}) =\tilde {A}I_{1}^{2}+\tilde {B}I_{1}+\tilde {C}$
, where


If
$ \, \ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
, we find that
$f(0)=\tilde {C}\gt 0$
. Additionally, since
$\tilde {A}\lt 0$
, it follows that
$ f(I_{1})=0$
has two real roots: one positive and one negative. Hence, model (2.4) has a unique phage-free positive steady state
$\tilde {F}_{1} =(\tilde {S}^{a}, \tilde {I}_{1}^{a},0,\tilde {B}_{1}^{a},\tilde {B}_{2}^{a},0)$
for
$\, \ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
. Assume that
$b_{2}=0$
, the following theorem presents a result regarding the global stability of the phage-free steady state
$\tilde {F}_{1}$
.
Theorem 3.10. If
$ \, \ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
,
$ \tilde {B}_{1}^{a}\leq \tilde {B}_{1}^{b}$
and
$l_{1}\leq \frac {\mu \chi _{1}}{\alpha \eta }$
hold, then the phage-free steady state
$\tilde {F}_{1}$
of model (2.4) is globally asymptotically stable.
3.4 Dynamics of phage-present steady state
In this section, the existence and uniform persistence of phage-present steady state of model (2.1) are difficult to obtain due to the spatial heterogeneity and other mathematical difficulties. Therefore, we focus on proving the existence and uniform persistence of the phage-present steady state for its homogeneous case. Assuming
$\alpha =b_{2}=0$
and
$ I=I_{1}+I_{2}$
in this subsection. From model (2.4), we assume that there exists the phage-present positive steady state
$\tilde {F}_{2}=(\tilde {S}^{b},\tilde {I}^{b},\tilde {B}_{1}^{b},\tilde {B}_{2}^{b},\tilde {P}^{b})$
. We have

One gets


We define the phage invasion reproduction number as

If
$ \ \;\widetilde{\!\!\!\mathscr{R}}_{0}^{\, b}\gt 1$
, then
$\tilde {P}^{b}\gt 0$
. Consequently, model (2.4) has a unique phage-present positive steady state
$\tilde {F}_{2}=( \tilde {S}^{b},\tilde {I}^{b},\tilde {B}_{1}^{b},\tilde {B}_{2}^{b},\tilde {P}^{b})$
. The following theorem demonstrates the uniform persistence of the disease for model (2.4) when
$\ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
.
Theorem 3.11. If
$\ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
, and
$\tilde {B}_{1}^{a}\gt \tilde {B}_{1}^{b}$
hold, there exists a
$\tilde {\vartheta }\gt 0$
such that for the initial condition
$ c^{0}(\!\cdot\!)=(S^{0},I_{1}^{0},I_{2}^{0},B_{1}^{0},B_{2}^{0},P^{0})(\!\cdot\!)\in \mathit{H^{+}}$
with
$ I_{1}^{0}(x)\not \equiv 0$
or
$ I_{2}^{0}(x)\not \equiv 0$
or
$ B_{1}^{0}(x)\not \equiv 0$
or
$ B_{2}^{0}(x)\not \equiv 0$
or
$ P^{0}(x)\not \equiv 0$
, the solution
$ \tilde {c}(x,t\,;\,c^{0})=(S(x,t),I_{1}(x,t),I_{2}(x,t),B_{1}(x,t),B_{2}(x,t),P(x,t))$
of model (2.4) satisfies
$ \lim _{t\to \infty }\inf \tilde {c}(x,t\,;\,c^{0})\ge \tilde {\vartheta }$
uniformly for
$x\in \bar {\Omega }.$
4 Proofs
4.1 Proof of Theorem3.1
In this section, we present a series of lemmas to prove Theorem3.1. The first lemma is just a consequence of applying the general results in [Reference Martin and Smith28].
Lemma 4.1. Let
$\mathscr{B}$
and
$\mathscr{L}\,$
be defined by (3.1)–(3.2). For any
$c^{0}\in D(\mathscr{B})\subset \mathit{H^{+}}$
, there exists a
$ T_{M} \gt 0$
satisfying that model (3.3) admits a unique nonnegative solution

where
$T_{M}\leq +\infty$
, then we have
$\lim \limits _{t\to T_{M}}\|c(\cdot ,t\,;\,c^{0})\|=\infty$
if
$T_{M}=\infty$
.
Lemma 4.2. For any
$c^{0}(x)= (S^{0}(x),I_{1}^{0}(x),I_{2}^{0}(x),B_{1}^{0}(x),B_{2}^{0}(x),P^{0}(x))\in \mathit{H^{+}}$
, model (2.1)–(2.3) admits a unique nonnegative global solution defined on
$\bar {\Omega }\times [0,\infty )$
.
Proof. Let
$c(x,t)=(S,I_{1},I_{2},B_{1},B_{2},P)$
be a solution associated with
$c^{0}(x)=(S^{0}(x),I_{1}^{0}(x),I_{2}^{0}(x), B_{1}^{0}(x),B_{2}^{0}(x),P^{0}(x))$
. The first equation of model (2.1) implies that
$\partial S/\partial t \leq d_{S}\Delta S+\Lambda (x)-\mu (x)S$
. By [Reference Lou and Zhao24, Lemma 1], we derive

has a unique positive steady state
$S^{*}(x)$
, which is globally asymptotically stable. According to the comparison principle, we have

Thus, there exists a
$ Q_{1} \gt 0$
satisfying

Let
$ \{J_{2}(t)\}_{t\ge 0}$
be the semigroup generated by the operator
$d_{I}\Delta -\mu (\!\cdot\!)$
, then from the second equation of model (2.1), we have

from (4.3), we derive

where
$\,\hat{\!\alpha }^{m}=\max _{x\in \bar {\Omega }}\{\alpha _{1}^{m}(x),\alpha _{2}^{m}(x)\}$
, and
$\lambda _{1}\gt 0$
is the principal eigenvalue of
$ -d_{I}\Delta +\mu (\!\cdot\!)$
. Similarly, from the third equation of model (2.1), we have

one gets

By [Reference Shu, Ma and Wang37, proof of Theorem 2.3] and assumption (
$ \mathbf{H}_{\mathbf{3}}$
), for
$v\ge 0$
, there exist
$C_{0}$
and
$C_{1}$
satisfying
$ h_{1}(x,v)-\delta _{1}v\leq C_{0}-C_{1}v$
, we derive

in which
$ \,\hat{\!B}_{1}(x,t)$
satisfies

For the first equation of model (4.7), applying the Gronwall’s inequality yields

based on (4.4)–(4.5), there exist
$Q_{2}\gt 0$
and
$Q_{3}\gt 0$
satisfying
$\|I_{1}(x,t)\|\leq Q_{2}$
and
$\|I_{2}(x,t)\|\leq Q_{3}$
, along with the comparison principle, we derive

Similarly, there exist
$ C_{2}\gt 0$
and
$ C_{3}\gt 0$
satisfying
$ h_{2}(x,v)-\delta _{2}v\leq C_{2}-C_{3}v$
, we derive

in which
$ \,\hat{\!B}_{2}(x,t)$
satisfies

For the first equation of model (4.10), applying the Gronwall’s inequality again yields

based on (4.8), there is a
$Q_{4}\gt 0$
satisfying
$\|B_{1}(x,t)\|\leq Q_{4}$
, along with the comparison principle, we derive

Considering the last equation of model (2.1), we have

Based on (4.11), there is a
$Q_{5}\gt 0$
satisfying
$\|B_{2}(x,t)\|\leq Q_{5}$
, then

where

By (4.3)–(4.5), (4.8), (4.11)–(4.12) and Lemma 4.1, the solution
$c(x,t)=(S,I_{1},I_{2},B_{1},B_{2},P)$
exists globally.
Lemma 4.3. There exists a constant
$ \,\hat{\!M}_{\infty }\gt 0$
independent of
$c^{0}=(S^{0}(x), I_{1}^{0}(x),I_{2}^{0}(x), B_{1}^{0}(x), B_{2}^{0}(x), P^{0}(x)) \in \mathit{H^{+}}$
satisfying

Proof. From the first equation of model (2.1), we derive

By the comparison principle, there exists
$ T_{1}\gt 0$
such that for all
$ t\ge T_{1}$
and
$x\in \bar {\Omega }$
,

The second equation
$ I_{1}(x,t)$
of model (2.1) yields

Applying the comparison principle, there exists
$ T_{2}\gt T_{1}$
such that for all
$ t\ge T_{2}$
and
$x\in \bar {\Omega }$
,

Similarly, one gets

From the fourth equation of models (2.1) and (4.6), we derive

By the comparison principle, there exists
$ T_{3}\gt T_{2}$
such that for all
$ t\ge T_{3}$
and
$x\in \bar {\Omega }$
,

Similarly, for equation
$ B_{2}(x,t)$
of models (2.1) and (4.9), one gets

The comparison principle yields
$ T_{4}\gt T_{3}$
such that for all
$ t\ge T_{4}$
and
$x\in \bar {\Omega }$
,

Let
$\bar {N}(x,t)=\chi _{1}(x)B_{1}(x,t)+\chi _{2}(x)B_{2}(x,t)+P(x,t)$
, we obtain

where
$\delta _{m}=\min _{x\in \bar {\Omega }}\{\delta _{1}(x),\delta _{2}(x), m(x)\}, h_{i}^{m}=\max _{x\in \bar {\Omega }}h_{i}(x,B_{i}),i=1,2$
. By the comparison principle, there exists a
$ T_{5}\gt T_{4}$
such that for all
$ t\ge T_{5}$
and
$x\in \bar {\Omega }$
,

Let
$ \,\hat{\!M}_{\infty }=M_{2}+\sum _{i=1}^{5}M_{i}$
. Then by (4.13)–(4.18), for all
$ t\ge T_{5}$
, the solution satisfies

This establishes Lemma 4.3.
Define
$\,\,\hat{\!\!J}(t)\,:\,\mathit{H}^{+}\to \mathit{H}^{+}$
as the semiflow generated by model (2.1)–(2.3), namely
$\,\,\hat{\!\!J}(t)c^{0}=c(x,t)$
for
$t\gt 0$
. We observe that the last three equations in model (2.1)–(2.3) lack diffusion terms; the solution semiflow
$\,\,\hat{\!\!J}(t)$
loses its compactness. We introduce the Kuratowski measure of noncompactness, denoted as
$ \kappa (\!\cdot\!)$
,

Denote

as the vector field associated with the last three equations of model (2.1). The Jacobian of
$K$
with
$(B_{1},B_{2},P)$
is defined as

Lemma 4.4.
$\,\,\hat{\!\!J}(t)$
is asymptotically smooth and
$ \kappa$
-contracting if there exists a
$ r^{*}\gt 0$
satisfying

Proof. By using similar proof in [Reference Sell and You36, Lemma 23.1(2)], we can derive that
$\,\,\hat{\!\!J}(t)$
is asymptotically compact on any closed bounded set
$\mathscr{P}$
for
$\,\,\hat{\!\!J}(t)\mathscr{P} \subset \mathscr{P}$
. Thus, the omega limit
$\omega (\mathscr{P})$
is nonempty, invariant and compact, and attracts
$\mathscr{P}$
. This proves the asymptotic smoothness of
$\,\,\hat{\!\!J}(t)$
. By [Reference Magal and Zhao26, Lemma 2.1(b)], we have

where
$ \bar {d}(\,\hat{\!J}(t)\mathscr{P},\omega (\mathscr{P}))$
denotes the distance from
$\,\,\hat{\!\!J}(t)\mathscr{P}$
to
$\omega (\mathscr{P})$
, which tends to zero as
$t\to + \infty$
. Consequently,
$\,\,\hat{\!\!J}(t)$
is
$\kappa$
-contracting.
Remark 4.5. A sufficient condition for (4.19) is that

Proof of Theorem
3.1
The global existence and uniqueness of solution of model (2.1)–(2.3) can be obtained from Lemmas 4.1–4.2. In view of Lemma 4.3,
$\,\,\hat{\!\!J}(t)$
is point dissipative. According to Lemma 4.4,
$\,\,\hat{\!\!J}(t)$
is asymptotically smooth. Thus, by [Reference Hale and Waltman13, Theorem 2.1], model (2.1)–(2.3) has a connected global attractor in
$\mathit{H}^{+}$
.
4.2 Proof of Lemma 3.3
Let
$\psi =Fw$
and
$w=-V^{-1}\varphi$
. Then,

we can easily derive



By a straightforward calculation, we get

and

where

It follows by iteration that

Then, we have

By applying the Gelfand’s formula and the squeeze theorem, we obtain
$ r(\!-FV^{-1}) = r(D_{H}+D_{L})$
. This establishes Lemma 3.3.
4.3 Proof of Theorem3.7
Before proving Theorem3.7, we first give some preliminaries.
Lemma 4.6. Define
$\lambda ^{0}$
as the principal eigenvalue of the eigenvalue problem

Then
$\mathscr{R}_{0}-1$
and
$ s(\mathscr{A} \, )$
have the same sign as
$\lambda ^{0}$
.
Proof. It is well-known that there exists a least eigenvalue
$\lambda ^{0}$
associated with the eigenvalue problem (4.20), its corresponding eigenfunction
$\bar {\varphi }$
can be chosen to be positive on
$\Omega$
, that is,

Next, we consider the following eigenvalue problem

By multiplying (4.21) with
$\varphi$
and (4.22) with
$\bar {\varphi }$
, and performing integration by parts on
$\Omega$
, subtracting the resulting equation, we get

Apparently,

and
$\int _{\Omega }\bar {\varphi }\varphi dx$
are both positive, it implies that
$\left (1-\frac {1}{\mathscr{R}_{0}}\right )$
and
$\lambda ^{0}$
have the same sign, namely
$\mathscr{R}_{0}$
and
$\lambda ^{0}$
have the same sign. This establishes Lemma 4.6.
Let
$I(x,t)=e^{\lambda t}\phi _{2},\ B_{1}(x,t)=e^{\lambda t}\phi _{3},\ B_{2}(x,t)=e^{\lambda t}\phi _{4}$
in model (3.6), then

Lemma 4.7. If
$\mathscr{R}_{0}\ge 1$
, then
$ s(\mathscr{A} \, )$
is the principal eigenvalue of problem (4.23) with respect to a strongly positive eigenfunction.
Proof. Let

be a family of linear operators on
$ C(\bar {\Omega })$
. Notice that
$ s(T_{\lambda })$
is decreasing and continuously dependent on
$\lambda$
, where
$\lambda$
denotes the principal eigenvalue of
$T_{\lambda }c=\lambda c$
. As a result, it has the following variational characterisation:

Clearly, we have
$ s(T_{\lambda })\lt 0$
if
$\lambda$
is large enough. From
$\mathscr{R}_{0}\ge 1$
and Lemma 4.6, the following equation holds
$s(T_{0})=\lambda ^{0}\ge 0.$
Therefore, we duduce that there exists a unique
$\bar {\lambda }$
satisfying
$ s(T_{\bar {\lambda }})= \bar {\lambda }$
. Let
$\tilde {\phi }\gt 0$
be an eigenvector with respect to
$ s(T_{\bar {\lambda }})$
, we get
$ T_{\bar {\lambda }}\tilde {\phi }=\bar {\lambda }\tilde {\phi }.$
Similar to the results in [Reference Wang and Zhao50, Theorem 2.3], we have
$\bar {\lambda }=s(\mathscr{A} \, )$
. This establishes Lemma 4.7.
Proof of Theorem
3.7 (i) The locally asymptotically stability of
$ F_{0}$
for model (2.1)–(2.3) follows from [Reference Wang and Zhao50, Theorem3.1]. Next, we only need to establish the global attractivity of
$ F_{0}$
. Initially, we set
$\varepsilon _{0}\gt 0$
. From (4.2), we deduce that there exists a
$t_{1}\gt 0$
such that
$ 0\leq S(\cdot ,t) \leq S^{*}(x)+\varepsilon _{0}$
for all
$ t\gt t_{1}$
, and from the comparison principle for cooperative models, we get
$(I(x,t),B_{1}(x,t),B_{2}(x,t))\leq (\bar {I}(x,t),\bar {B}_{1}(x,t),\bar {B}_{2}(x,t))$
, where
$(\bar {I}(x,t),\bar {B}_{1}(x,t),\bar {B}_{2}(x,t))$
is the solution of the following model

Let
$J_{\varepsilon _{0}}(t)$
be the linear semigroup of model (4.24) with respect to
$C_{\varepsilon _{0}}$
, where
$C_{\varepsilon _{0}}$
is defined as the following generator

Next, we prove that
$ \|J_{\varepsilon _{0}}(t)\|\leq Ne^{\gamma _{\varepsilon _{0}}t} \text{ for some } N\gt 0,$
where
$\gamma _{\varepsilon _{0}}:=\lim _{t\to \infty }\frac {\ln \|J_{\varepsilon _{0}}(t)\|}{t}$
is the exponential growth bound of
$J_{\varepsilon _{0}}(t)$
. Note that

where
$ \gamma _{ess}(J_{\varepsilon _{0}}(t))$
:=
$\lim _{t\to \infty }\frac {n(J_{\varepsilon _{0}}(t))}{t}$
, and
$ n(\!\cdot\!)$
represents the measure of non-compactness. Similar to the arguments in [Reference Wu and Zou58, Lemma 3.5], there exists a
$\delta _{*}\gt 0$
such that
$\gamma _{ess}(J_{\varepsilon _{0}})\leq -\delta _{*}$
. Then we can choose
$\varepsilon _{0}$
small enough such that
$\gamma _{\varepsilon _{0}}\lt 0$
. To see this,
$\gamma _{\varepsilon _{0}}$
has the same sign as
$ s(C_{\varepsilon _{0}})$
. Moreover,
$ s(C_{\varepsilon _{0}})$
has the same sign as
$\lambda _{\varepsilon _{0}}$
, in which
$\lambda _{\varepsilon _{0}}$
represents the principal eigenvalue of the eigenvalue problem

According to Lemma 4.6,
$ \mathscr{R}_{0}\lt 1$
and the continuous dependence of
$\lambda _{\varepsilon _{0}}^{0}$
on
$\varepsilon _{0}$
, it can be inferred that
$ \lambda _{\varepsilon _{0}}^{0} \lt 0$
if
$\varepsilon _{0}$
is small enough. Then we get
$\gamma _{\varepsilon _{0}}\lt 0$
. It implies that
$(\bar {I}(x,t),\bar {B}_{1}(x,t),\bar {B}_{2}(x,t))\to (0,0,0)$
as
$ t\to \infty$
uniformly for
$x\in \bar {\Omega }$
. Clearly, we derive
$(I(x,t),B_{1}(x,t),B_{2}(x,t))\to (0,0,0)$
as
$ t\to \infty$
uniformly for
$x\in \bar {\Omega }$
. Then, we have
$(I_{1}(x,t),I_{2}(x,t),B_{1}(x,t),B_{2}(x,t))\to (0,0,0,0)$
as
$ t\to \infty$
uniformly for
$x\in \bar {\Omega }$
. Furthermore, it follows from model (4.2) that
$S(x,t)\to S^{*}(x)$
as
$ t\to \infty$
uniformly for
$x\in \bar {\Omega }$
. This establishes Theorem3.7 (i).
Proof of Theorem
3.7 (ii) First, we prove the local stability of
$F_{0}$
. For any given
$\varepsilon \gt 0$
, we assume that
$\vartheta \gt 0$
and initial conditions
$c^{0}=(S^{0},I_{1}^{0},I_{2}^{0},B_{1}^{0},B_{2}^{0},P^{0})$
with
$ \|c^{0}-F_{0}\|\leq \vartheta$
. Let

From model (3.5), we have
$ d_{S}\Delta S^{*} +\Lambda -\mu S^{*} =0,$
and by the first equation of model (2.1), we derive

Define
$\,\,\hat{\!\!J}_{1}(t)$
as the positive semigroup generated by the following operator

By [Reference Webb57, Proposition 2.3], there exists a
$z_{1}\gt 0$
satisfying
$\|\,\hat{\!J}_{1}(t)\|\leq \bar {M}e^{-z_{1}t}$
for some
$\bar {M}\gt 0$
. We derive

where
$v_{10}=\dfrac {S^{0}}{S^{*}}-1$
. In view of the positivity of
$\,\,\hat{\!\!J}_{1}(t)$
, one gets

where
$ S_{m}^{*}=\min _{x\in \bar {\Omega }}S^{*}(x).$
From
$\mathscr{R}_{0}=1$
and [Reference Wu and Zou58, Lemma 3.6], we obtain
$\|J(t)\|\leq \bar {M}$
for
$t\ge 0$
and
$\bar {M}\gt 0$
. Recall that
$ a(t)\leq \vartheta \bar {M}e^{-z_{1}t}/S^{*}_{m}$
, we derive

where
$I^{0}=I_{1}^{0}+I_{2}^{0}$
. Thus,

where
$\tilde {M}_{1}=\bar {M}^{2}\|\,\hat{\!\alpha }^{m}\|\|S^{*}\|/S^{*}_{m}$
. This yields that

Utilising Gronwall’s inequality, we derive

Moreover, we can also derive

The last equation in model (2.1) yields

Let
$ \tilde {M}_{2}=\alpha ^{m}\eta ^{m}\bar {M}\vartheta (1 + 2\tilde {M}_{1}\vartheta e^{2\tilde {M}_{1}\vartheta /z_{1}}/ z_{1}),\ \tilde {M}_{3}=\chi ^{m}b^{m}2\bar {M}\vartheta e^{2\tilde {M}_{1}\vartheta /z_{1}},$
we have

Applying Gronwall’s inequality, we obtain

By the first equation of models (2.1) and (4.28), we get

Let
$\,\hat{\!S}$
be the solution of the following model

The comparison principle yields that
$S(x,t)\ge \,\hat{\!S}(x,t)$
for
$x\in \bar {\Omega }$
and
$t\ge 0$
. Define
$ S^{*}_{\vartheta }$
as the positive steady state of model (4.32) and
$\,\hat{\!v}=\,\hat{\!S}-S^{*}_{\vartheta }$
,
$ \,\hat{\!v}(x,t)$
satisfies

Define
$ J_{1}(t)$
as the semigroup generated by
$ d_{S}\Delta -\mu$
, then we have
$ \|J_{1}(t)\|\leq \bar {M}e^{-\mu _{m}t}$
, where
$ \bar {M}\gt 0$
and large enough. From model (4.33), we derive

Then

Applying the Gronwall’s inequality again yields

where
$\tilde {M}_{4}=2\bar {M}^{2}\vartheta e^{2\tilde {M}_{1}\vartheta /z_{1}}\|\,\hat{\!\alpha }^{m}\|.$
Choosing
$\vartheta \gt 0$
small enough such that
$ \tilde {M}_{4}\lt \mu _{m}/2$
, (4.34) yields that

Inequality (4.35) implies that

Since
$ a(t)\leq \vartheta \bar {M} e^{-z_{1}t}/S^{*}_{m} \leq \vartheta \bar {M}/S^{*}_{m}$
, we have


Thus, from (4.28)–(4.31), (4.38) and
$\lim _{\vartheta \to 0}S_{\vartheta }^{*}=S^{*}$
, we choose
$\vartheta \gt 0$
small enough satisfying for
$ t\gt 0$
,

This proves the local stability of
$F_{0}=(S^{*},0,0,0,0,0)$
. Then we need to discuss the global attractivity of
$F_{0}$
. Theorem3.1 implies that
$\,\,\hat{\!\!J}(t)$
has a connected global attractor
$\mathscr{D}$
. From Lemma 4.7, the eigenvalue problem (4.23) has a positive eigenvector
$ (\phi _{2},\phi _{3},\phi _{4})$
with
$ s(\mathscr{A} \, )=0$
. Let

We present the following two claims.
Claim 1. For any
$ c^{0}=(S^{0},I_{1}^{0},I_{2}^{0},B_{1}^{0},B_{2}^{0},P^{0}) \in \mathscr{D}$
, the omega limit set
$\omega (c^{0})\subset \partial Y_{1}$
.
In view of (4.2), we have
$S^{0}\leq S^{*}$
. If
$ I_{1}^{0}=I_{2}^{0}=B_{1}^{0}=B_{2}^{0}=P^{0}=0$
, the claim easily follows from the fact that
$\partial Y_{1}$
is invariant for
$\,\,\hat{\!\!J}(t)$
. Hence, we assume that either
$ I_{1}^{0}\not =0$
or
$ I_{2}^{0}\not =0$
or
$ B_{1}^{0}\not =0$
or
$ B_{2}^{0}\not =0$
or
$ P^{0}\not =0$
. From the results in Theorem3.1, we easily know that
$c(x,t,c^{0})\gt 0$
for
$ x\in \bar {\Omega }$
and
$ t\gt 0$
.
$ S(x,t)$
satisfies

Applying the comparison principle, we have
$ S(x,t)\lt S^{*}(x)$
for
$ x\in \bar {\Omega }$
and
$t\gt 0$
. Motivated by [Reference Cui, Lam and Lou9], we assume

and
$ u(t\,;\,c^{0})\gt 0$
holds for all
$ t\gt 0$
, we also know that
$ u(t\,;\,c^{0})$
is strictly decreasing. Then we choose a
$ t_{2}\gt 0$
satisfying
$ \widetilde{I}(\cdot ,t)=u(t_{2}\,;\,c^{0})\phi _{2}, \widetilde{B}_{1}(\cdot ,t)=u(t_{2}\,;\,c^{0})\phi _{3}, \widetilde{B}_{2}(\cdot ,t)=u(t_{2}\,;\,c^{0})\phi _{4}$
for
$ t\ge t_{2}$
. Note that
$ S(x,t)\lt S^{*}$
, we have

Applying the comparison principle, we have
$ (\widetilde{I}(x,t),\widetilde{B}_{1}(x,t), \widetilde{B}_{2}(x,t))\ge (I(x,t),B_{1}(x,t), B_{2}(x,t))$
for
$ x\in \bar {\Omega }$
and
$ t\ge t_{2}$
. From model (4.39) and the strong comparison principle, we have
$u(t_{2}\,;\,c^{0})\phi _{2} =\widetilde{I}(x,t) \gt I(x,t)$
,
$u(t_{2}\,;\,c^{0})\phi _{3} =\widetilde{B}_{1}(x,t) \gt {B_{1}}(x,t),\ u(t_{2}\,;\,c^{0})\phi _{4} =\widetilde{B}_{2}(x,t) \gt B_{2}(x,t)$
for
$x\in \bar {\Omega }$
and
$ t\gt t_{2}$
. Due to
$ t_{2}\gt 0$
is arbitrary,
$ u(t\,;\,c^{0})$
is strictly decreasing function. Define
$ u_{*}=\lim _{t\to \infty }u(t\,;\,c^{0})$
, which implies
$ u_{*}=0$
, and define
$ \mathbb{T} =(\mathbb{T}_{1}, \mathbb{T}_{2},\mathbb{T}_{3},\mathbb{T}_{4},\mathbb{T}_{5},\mathbb{T}_{6})\in \omega (c^{0})$
. Then there exists a sequence
$ \{t_{k}\}$
with
$ t_{k}\to \infty$
satisfying
$\,\,\hat{\!\!J}(t_{k})c^{0}\to \mathbb{T}$
. We easily obtain
$u(t,\mathbb{T})=u_{*}$
for
$ t\ge 0$
. In view of
$\lim _{t_{k}\to \infty }\,\hat{\!J}(t+t_{k})c^{0}=\,\hat{\!J}(t)\lim _{t_{k}\to \infty }\,\hat{\!J}(t_{k})c^{0}=\,\hat{\!J}(t)\mathbb{T}.$
If
$ \mathbb{T}_{2}\not =0$
or
$ \mathbb{T}_{3}\not =0$
or
$ \mathbb{T}_{4}\not =0$
or
$ \mathbb{T}_{5}\not =0$
or
$ \mathbb{T}_{6}\not =0$
, it follows from [Reference Wu and Zou58, Theorem 3.12] that
$u(t\,;\,\mathbb{T})$
is strictly decreasing. This leads to a contradiction. Hence, we have
$ \mathbb{T}_{2}=\mathbb{T}_{3}=\mathbb{T}_{4}=\mathbb{T}_{5}=\mathbb{T}_{6}=0$
. By the theory of asymptotically autonomous semiflows in [Reference Thieme41], it follows that

Claim 2.
$\mathscr{D}=\{F_{0}\}$
.
Since
$ \{F_{0}\}$
is globally attractive in
$ \partial Y_{1}$
,
$ \{F_{0}\}$
is the unique invariant subset of model (2.1)–(2.3) in
$ \partial Y_{1}$
. In view of the fact that the omega limit set
$\omega (c^{0})$
is compact invariant and
$\omega (c^{0})\subset \partial Y_{1}$
, for any
$ c^{0}\in \mathscr{D}$
, we get
$\omega (c^{0})=\{F_{0}\}$
. Since the global attractor
$\mathscr{D}$
is compact invariant in
$H^+$
,
$F_0$
is stable, and according to [Reference Wu and Zou58, Lemma 3.11], one gets
$\mathscr{D}=\left \{F_{0}\right \}$
. Combining the global attractivity and local stability, we immediately obtain the globally asymptotical stability of
$F_0$
, completing the proof of Theorem3.7 (ii).
4.4 Proof of Theorem3.8
If
$ \mathscr{R}_{0}\gt 1$
, model (2.1) has a phage-free steady state
$ F_{1} = (S^{a}(x),I_{1}^{a}(x),0,B_{1}^{a}(x),B_{2}^{a}(x),0)$
. Let
$ I_{2}(x,t)=P(x,t)=0$
in model (2.1), we have

By applying a similar proof as in Theorem3.1, for model (4.40), we have the following corollary:
Corollary 4.8. Let
$ \mathbb{E}=C(\bar {\Omega },\mathbb{R}^{4})$
be the Banach space and its positive cone is denoted by
$ \mathbb{E}^{+}$
.
-
(i) For any
$ c^{0}(x) = (S^{0}(x),I_{1}^{0}(x),B_{1}^{0}(x),B_{2}^{0}(x))\in \mathbb{E}^{+}$ , model (4.40) admits a unique global nonnegative classical solution
$\bar {c}(\cdot ,t\,;\,c^{0})$ defined on
$\Omega \times [0,\infty )$ .
-
(ii) Let
$\tilde {J}_{1}(t): \mathbb{E}^{+}\to \mathbb{E}^{+}$ be the semiflow generated by model (4.40), namely
$ \tilde {J}_{1}(t)c^{0}=\bar {c}(x,t)$ for
$ t\gt 0$ . Moreover,
$ \tilde {J}_{1}(t)$ is point dissipative.
-
(iii) The semiflow
$ \tilde {J}_{1}(t)$ of model (4.40) has a connected global attractor in
$ \mathbb{E}^{+}$ .
Note that model (4.40) has a disease-free steady state
$ \bar {F}_{0}=(S^{*}(x),0,0,0)$
. Linearising model (4.40) at
$ \bar {F}_{0}$
yields

We continue the discussion on the threshold dynamics of model (4.40). The following theorem presents the uniform persistence and the existence of phage-free steady state for model (4.40) when
$\mathscr{R}_{0}\gt 1$
.
Theorem 4.9. If
$\mathscr{R}_{0}\gt 1$
, there exists
$\bar {\vartheta }\gt 0$
such that for any
$ c^{0}(\!\cdot\!)=(S^{0},I_{1}^{0},B_{1}^{0},B_{2}^{0})(\!\cdot\!)\in \mathbb{E}^{+}$
with
$ I_{1}^{0}(x)\not \equiv 0$
or
$ B_{1}^{0}(x)\not \equiv 0$
or
$ B_{2}^{0}(x)\not \equiv 0$
, the solution
$ \bar {c}(x,t\,;\,c^{0})=(S(x,t),I_{1}(x,t),B_{1}(x,t),B_{2}(x,t))$
of model (4.40) satisfies
$\lim _{t\to \infty }\inf \bar {c}(x,t)\ge \bar {\vartheta } \text{ uniformly for } x\in \bar {\Omega }.$
Moreover, model (4.40) has at least one positive steady state.
Before proving Theorem4.9, we first give some preliminaries. We define

and

Define

for
$t\ge 0$
, and
$\omega (\varphi )$
be the omega limit set of the orbit
$\mathit{G}^{+}\,:=\{\tilde {J}_{1}(t)\varphi\,:\,t\geq 0\}$
.
Claim 1.
$\mathbb{E}_{0}$
is positively invariant regarding
$\tilde {J}_{1}(t)$
, namely
$\tilde {J}_{1}(t)\mathbb{E}_{0}\subseteq \mathbb{E}_{0}$
for all
$t\ge 0$
.
Let
$c^{0}\in \mathbb{E}_{0}$
, which implies
$ I_{1}^{0}\not \equiv 0$
and
$ B_{1}^{0}\not \equiv 0$
and
$ B_{2}^{0}\not \equiv 0$
. We derive that
$\partial I_{1}/\partial t \ge d_{I}\Delta I_{1}-\mu (x)I_{1}$
from model (4.40). Thus,
$ I_{1}$
is an upper solution of the problem

It follows from the maximum principle and
$I_{1}^{0}\not \equiv 0$
that
$I_{1}^{*}(x,t)\gt 0$
for
$x\in \bar {\Omega }$
and
$t\gt 0$
. It holds that
$I_{1}(x,t)\ge I_{1}^{*}(x,t)\gt 0$
for
$x\in \bar {\Omega }$
and
$ t\gt 0$
. Assume that there exist
$ \tilde {t}\gt 0$
and
$ \tilde {x}\in \bar {\Omega }$
such that
$ B_{1}(\tilde {x},\tilde {t})=0$
, and from the third equation of model (4.40), along with
$(\mathbf{H}_{\mathbf{3}})$
, we derive

It implies that
$\eta (\tilde {x})I_{1}(\tilde {x},\tilde {t})=0$
, which leads to a contradiction. Hence, we get
$B_{1}(x,t)\gt 0$
for
$ x\in \bar {\Omega }$
and
$ t\gt 0$
. From the fourth equation of model (4.40), one gets

Similar to [Reference Hsu, Jiang and Wang17, Lemma 2.1] and [Reference Wang44, Proposition 3.1], by strong maximum principle [Reference Protter and Weinberger34, Theorem 4] and Hopf boundary theorem [Reference Protter and Weinberger34, Theorem 3], we derive
$ B_{2}(x,t)\gt 0$
for
$x\in \bar {\Omega }$
and
$ t\gt 0$
. Then
$\tilde {J}_{1}(t)c^{0}\in \mathbb{E}_{0}$
.
Claim 2. If
$\mathscr{R}_{0}\gt 1$
, there exists
$\bar {\delta }\gt 0$
such that the semiflow
$\tilde {J}_{1}(t)$
of model (4.40) satisfies
$\lim _{t\to \infty }\sup \|\tilde {J}_{1}(t)\varphi -\bar {F}_{0}\|\ge \bar {\delta }$
for all
$ \varphi \in \mathbb{E}_{0}$
.
By way of contradiction, assuming that there exists a
$\varphi _{0}\in \mathbb{E}_{0}$
satisfying

Thus, there exists
$ t^{*}\gt 0$
satisfying
$ S(x,t,\varphi _{0})\ge S^{*}(x)-\bar {\delta },\ \forall t\ge t^{*}.$
Therefore,
$ (I_{1}(x,t,\varphi _{0}), B_{1}(x,t,\varphi _{0}), B_{2}(x,t,\varphi _{0}))$
is an upper solution of the following linear model

Denote
$\lambda _{\bar {\delta }}^{0}$
as the principal eigenvalue of the following eigenvalue problem

Then
$\lambda _{\bar {\delta }}^{0}$
is continuous in
$\bar {\delta }$
. The following eigenvalue problem

has a principal eigenvalue
$\tilde {\lambda }_{\bar {\delta }}^{0}$
with respect to positive eigenvector
$ \left (\varphi _{2}^{\bar {\delta }}(x),\varphi _{3}^{\bar {\delta }}(x),\varphi _{4}^{\bar {\delta }}(x)\right )$
. We can choose a small enough
$ \rho _{1}\gt 0$
such that

Then the linear model (4.42) with initial conditions
$ (\tilde {I}_{1}(x,t^{*}), \tilde {B}_{1}(x,t^{*}), \tilde {B}_{2}(x,t^{*}))=\rho _{1}\left (\varphi _{2}^{\bar {\delta }}(x),\varphi _{3}^{\bar {\delta }}(x),\varphi _{4}^{\bar {\delta }}(x)\right )$
has a unique solution

By the comparison principle of quasimonotone model, we have

on
$\bar {\Omega }\,\times [t^{*},\infty )$
, which implies that
$\lim _{t\to \infty }\|(I_{1}(\cdot ,t\,;\,\varphi _{0}),B_{1}(x,t\,;\,\varphi _{0}), B_{2}(x,t\,;\,\varphi _{0}))\|=\infty$
, which contradicts the boundedness of
$ (I_{1}(\cdot ,t), B_{1}(\cdot ,t), B_{2}(\cdot ,t))$
by Corollary 4.8. This establishes Claim 2.
Proof of Theorem
4.9
First, we prove that
$\omega (\varphi )=\{\bar {F}_{0}\}, \varphi \in F_{\partial }$
. For any
$\varphi \in F_{\partial }$
, we have
$\tilde {J}_{1}(t)\varphi \in F_{\partial }$
,
$t\ge 0$
. Then,
$I_{1}(\cdot ,t)\equiv 0$
or
$B_{1}(\cdot ,t)\equiv 0$
or
$B_{2}(\cdot ,t)\equiv 0$
for
$ t\ge 0$
. In the case that
$I_{1}(\cdot ,t)\equiv 0$
, we can derive that
$B_{1}(\cdot ,t)\equiv 0$
and
$B_{2}(\cdot ,t)\equiv 0$
from the second equation of model (4.40). Therefore,
$ S(\cdot ,t)\to S^{*}(x)$
uniformly for
$x\in \bar {\Omega }.$
In the case that
$B_{1}(\cdot ,t)\equiv 0$
, we can derive that
$I_{1}(\cdot ,t)\equiv 0$
from the third equation of model (4.40), then
$B_{2}(\cdot ,t)\equiv 0$
and
$ S(\cdot ,t)\to S^{*}(x)$
uniformly for
$x\in \bar {\Omega }.$
In the case that
$B_{2}(\cdot ,t)\equiv 0$
, we can derive that
$B_{1}(\cdot ,t)\equiv 0$
from the fourth equation of model (4.40), then
$I_{1}(\cdot ,t)\equiv 0$
and
$ S(\cdot ,t)\to S^{*}(x)$
uniformly for
$x\in \bar {\Omega }.$
This shows
$\omega (\varphi ) =\{\bar {F}_{0}\}$
.
Define a continuous function

Apparently,
$\tau ^{-1}(0,\infty )\subseteq \mathbb{E}_{0}$
. The function
$\tau$
is a generalised distance function for the semiflow
$\tilde {J}_{1}(t)$
. In view of Claim 1 and Claim 2, we know that the sigleton
$ \{\bar {F}_{0}\}$
is an isolated invariant set for
$\tilde {J}_{1}(t)$
in
$ \mathbb{E}^{+}$
, then
$ W^{s}(\{\bar {F}_{0}\})\cap \mathbb{E}_{0}=\emptyset$
, where
$ W^{s}(\{\bar {F}_{0}\})$
represents the stable subset of
$ \{\bar {F}_{0}\}$
. Besides, no subset of
$ \{\bar {F}_{0}\}$
forms a cycle in
$ \partial \mathbb{E}_{0}$
. By [Reference Smith and Zhao40, Theorem 3], there exists a
$\vartheta _{1}\gt 0$
satisfying
$\lim _{t\to \infty }\inf \tau (\tilde {J}_{1}(t)\varphi )\ge \vartheta _{1},\ \forall \varphi \in \mathbb{E}_{0}$
. Moreover, from Corollary 4.8, there exists
$\tilde {t}_{1}\gt 0$
satisfying that
$ B_{1}(\cdot ,t)\leq \,\hat{\!M}_{\infty }$
,
$ B_{2}(\cdot ,t)\leq \,\hat{\!M}_{\infty }$
for
$ x\in \Omega$
and
$ t\ge \tilde {t}_{1}$
. Then, we get

Thus, we have
$\lim _{t\to \infty }\inf S(x,t\,;\,\varphi )\gt \vartheta _{2}:=\Lambda _{m}/((\alpha _{1}+\alpha _{2})\,\hat{\!M}_{\infty }+\mu ^{m})$
. Let
$ \bar {\vartheta }=\min \{\vartheta _{1},\vartheta _{2}\}$
. This establishes the uniform persistence. It follows from [Reference Magal and Zhao26, Theorem 4.7] that model (4.40) admits at least one steady state in
$\mathbb{E}_{0}$
, which is positive. This establishes Theorem4.9.
Based on above theorem and [Reference Zhao60, Theorem 1.3.6]. This establishes Theorem3.8.
4.5 Proof of Theorem3.10
We choose the Lyapunov function

where the constants
$ l_{1}\gt 0,l_{2}\gt 0,l_{3} \gt 0$
are to be determined, and
$ Y(x)=x-1-\ln x (x\gt 0)$
. By calculating the derivative of
$ \mathit{L}_{1}(t)$
, one gets

Since
$ \tilde {F}_{1}=(\tilde {S}^{a},\tilde {I}_{1}^{a},0,\tilde {B}_{1}^{a},\tilde {B}_{2}^{a},0)$
is the phage-free steady state of model (2.4), we derive

After a simple calculation, we have


By
$(\mathbf{H}_{\mathbf{3}})$
, one gets

Since
$ 1-x\leq -\ln x$
for
$ x\gt 0$
, we have

Similarly, we also have

Let
$ l_{1} = \left (\dfrac {\alpha _{1}\tilde {S}^{a}\tilde {B}_{1}^{a}}{\eta \tilde {I}_{1}^{a}(H_{1}+\tilde {B}_{1}^{a})}+\dfrac {\alpha _{2}\tilde {S}^{a}\tilde {B}_{2}^{a}}{\eta \tilde {I}_{1}^{a}(H_{2}+\tilde {B}_{2}^{a})}\right ),\ l_{2}=\dfrac {\alpha _{2}\tilde {S}^{a}\tilde {B}_{2}^{a}}{\delta _{1}\tilde {B}_{1}^{a}(H_{2}+\tilde {B}_{2}^{a})}, \ l_{3}=\dfrac {l_{1}}{\chi _{1}}$
, we derive

Hence, based on
$l_{1}\leq \mu \chi _{1}/\alpha \eta$
and
$ \tilde {B}_{1}^{a}\leq m/\chi _{1}b_{1} = \tilde {B}_{1}^{b}$
, we have
$ d\mathit{L}_{1}(t)/dt\leq 0$
. Moreover,
$ d\mathit{L}_{1}(t)/dt=0$
if and only if
$ S=\tilde {S}^{a},I_{1}=\tilde {I}_{1}^{a},I_{2}=0, B_{1}=\tilde {B}_{1}^{a}, B_{2}=\tilde {B}_{2}^{a}, P=0$
. The largest invariant set of
$ \left \{(S,I_{1},I_{2},B_{1},B_{2},P)|\frac {d\mathit{L}_{1}(t)}{dt}=0\right \}$
is the singleton
$\{\tilde {F}_{1}\}$
. Then, from LaSalle invariant principle [Reference Hale and Lunel12, Reference Henry15],
$\tilde {F}_{1}$
is globally asymptotically stable.
4.6 Proof of Theorem3.11
Before proving Theorem3.11, we first give some preliminaries.
We define

and

Define
$\widetilde{F}_{\partial}\,:=\{\varphi \in \partial \mathbb{H}_{0}\,:\,\bar {J}_{1}(t)\varphi \in \partial \mathbb{H}_{0}\},$
for
$t\ge 0$
, and
$\widetilde{\omega }(\varphi )$
be the omega limit set of the orbit
$\widetilde{\mathit{G}}^{+}\,:=\{\bar {J}_{1}(t)\varphi\,:\,t\geq 0\}$
. Similar to the proof of Theorem4.9,
$ \mathbb{H}_{0}$
is the positive invariant set for solution semiflow
$\bar {J}_{1}(t)$
of model (2.4), and we have the following claim.
Claim 1. If
$\ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
, there exists
$\tilde {\delta }\gt 0$
such that the semiflow
$\bar {J}_{1}(t)$
of model (2.4) satisfies
$\lim _{t\to \infty }\sup \|\bar {J}_{1}(t)\varphi -\tilde {F}_{0}\|\ge \tilde {\delta }$
for all
$ \varphi \in \mathbb{H}_{0}$
.
Claim 2. If
$\ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
, and
$\tilde {B}_{1}^{a}\gt \tilde {B}_{1}^{b}$
holds, there exists
$\,\hat{\!\delta }\gt 0$
such that the semiflow
$\bar {J}_{1}(t)$
of model (2.4) satisfies
$\lim _{t\to \infty }\sup \|\bar {J}_{1}(t)\varphi -\tilde {F}_{1}\|\ge \,\hat{\!\delta }$
for all
$ \varphi \in \mathbb{H}_{0}$
.
Based on
$\tilde {B}_{1}^{a}\gt \tilde {B}_{1}^{b}$
, we can choose a sufficiently small
$\,\hat{\!\delta }\gt 0$
such that

By way of contradiction, assuming that there exists a
$\varphi _{0}\in \mathbb{H}_{0}$
satisfying
$\lim \limits _{t\to \infty }\sup \|\bar {J}_{1}(t)\varphi _{0}-\tilde {F}_{1}\|\lt \,\hat{\!\delta }.$
This implies that there exists a
$ \tilde {t}_{2} \gt 0$
satisfying
$\tilde {B}_{1}^{a}-\,\hat{\!\delta }\lt B_{1}(x,t\,;\,\varphi _{0})$
. Hence, we have

Since
$\varphi _{0}\in \mathbb{H}_{0}$
, and the results mentioned above, it follows that
$ P(x,t)\gt 0$
for
$x\in \bar {\Omega }$
and
$ t\gt 0$
. This implies that there is a constant
$p_{1}\gt 0$
such that
$ P(x,t\,;\,\varphi _{0}) \ge p_{1}P^{0}(x)$
. By applying the standard comparison principle, one gets

From (4.45), we obtain
$\lim _{t\to \infty }P(x,t)=\infty$
, which contradicts the boundedness of
$ P(x,t)$
. This establishes Claim 2.
Proof of Theorem
3.11
First, we prove that
$\widetilde{\omega }(\varphi )=\{ \tilde {F}_{0}\}\cup \{ \tilde {F}_{1}\}, \varphi \in \widetilde{F}_{\partial }$
. For any
$\varphi \in \widetilde{F}_{\partial }$
, we have
$\bar {J}_{1}(t)\varphi \in \widetilde{F}_{\partial }, t\ge 0$
. Thus,
$ I_{1}(\cdot ,t)\equiv 0$
or
$ I_{2}(\cdot ,t)\equiv 0$
or
$ B_{1}(\cdot ,t)\equiv 0$
or
$ B_{2}(\cdot ,t)\equiv 0$
or
$ P(\cdot ,t)\equiv 0$
for
$ t\ge 0$
. In the case that
$ I_{1}(\cdot ,t)\equiv 0$
, we can derive that
$ B_{1}(\cdot ,t)\equiv 0$
,
$ B_{2}(\cdot ,t)\equiv 0$
from the second equation of model (2.4). Then we have
$ I_{2}(\cdot ,t)\equiv 0$
from the fourth equation of model (2.4). Besides, we obtain
$ S(\cdot ,t)\to S^{*}(x)$
uniformly for
$ x\in \bar {\Omega }$
, then from the sixth equation of model (2.4), one gets
$\lim _{t\to \infty }P(\cdot ,t)=0$
. This shows
$\widetilde{\omega }(\varphi )=\{\tilde {F}_{0}\}$
. In the case that
$ B_{1}(\cdot ,t)\equiv 0$
, we can derive that
$ I_{1}(\cdot ,t)\equiv 0$
,
$ I_{2}(\cdot ,t)\equiv 0$
. Similarly, we also have
$ B_{2}(\cdot ,t)\equiv 0$
,
$ S(\cdot ,t)\to S^{*}(x)$
uniformly for
$ x\in \bar {\Omega }$
and
$\lim _{t\to \infty }P(\cdot ,t)=0$
. This shows
$\widetilde{\omega }(\varphi )=\{\tilde {F}_{0}\}$
. In the case that
$ B_{2}(\cdot ,t)\equiv 0$
, we can derive that
$ B_{1}(\cdot ,t)\equiv 0$
from the fifth equation of model (2.4). Then we have
$ I_{1}(\cdot ,t)\equiv 0$
,
$ I_{2}(\cdot ,t)\equiv 0$
and
$ S(\cdot ,t)\to S^{*}(x)$
uniformly for
$ x\in \bar {\Omega }$
and
$\lim _{t\to \infty }P(\cdot ,t)=0$
. This also shows
$\widetilde{\omega }(\varphi )=\{\tilde {F}_{0}\}$
. In the case that
$ P(\cdot ,t)\equiv 0$
, it implies that
$ I_{2}(\cdot ,t)\equiv 0$
. Conversely, if
$ I_{2}(\cdot ,t)\equiv 0$
, then we also have
$ P(\cdot ,t)\equiv 0$
. Thus, model (2.4) becomes

If
$ \, \ \;\widetilde{\!\!\!\mathscr{R}}_{0}\gt 1$
, model (4.46) has a positive steady state
$\bar {F}_{1}=(\tilde {S}^{a},\tilde {I}_{1}^{a},\tilde {B}_{1}^{a},\tilde {B}_{2}^{a})$
. We choose the Lyapunov function

By applying the similar proof in Theorem3.10, we have

Apparently, we can obtain
$d\mathit{L}_{2}(t)/dt\leq 0$
. Moreover,
$ d\mathit{L}_{2}(t)/dt=0$
if and only if
$ S=\tilde {S}^{a}, I_{1}=\tilde {I}_{1}^{a}, B_{1}=\tilde {B}_{1}^{a}, B_{2}=\tilde {B}_{2}^{a}$
. The largest invariant set of
$ \left \{(S,I_{1},B_{1},B_{2})|\frac {d\mathit{L}_{2}(t)}{dt}=0\right \}$
is the singleton
$\{\bar {F}_{1}\}$
. Then, from LaSalle invariant principle [Reference Hale and Lunel12],
$\bar {F}_{1}$
is globally asymptotically stable. Hence, we have
$ \lim _{t\to \infty }(S(x,t),I_{1}(x,t),B_{1}(x,t),B_{2}(x,t))=(\tilde {S}^{a},\tilde {I}_{1}^{a},\tilde {B}_{1}^{a},\tilde {B}_{2}^{a})$
. This also shows
$\widetilde{\omega }(\varphi )=\{\tilde {F}_{1}\}$
. We conclude that
$\widetilde{\omega }(\varphi )=\{ \tilde {F}_{0}\}\cup \{ \tilde {F}_{1}\}$
for any
$ \varphi \in \widetilde{F}_{\partial }$
. Define a continuous function

Apparently,
$\tilde {\tau }^{-1}(0,\infty )\subseteq \mathbb{H}_{0}$
. The function
$\tilde {\tau }$
is a generalised distance function for the semiflow
$\bar {J}_{1}(t)$
. By the above discussions, we know that the sigleton
$\widetilde{\omega }(\varphi )=\{ \tilde {F}_{0}\}\cup \{ \tilde {F}_{1}\}$
is an isolated invariant set for
$\bar {J}_{1}(t)$
in
$ H^{+}$
, then
$ W^{s}(\{\tilde {F}_{0}\})\cap \mathbb{H}_{0}=\emptyset$
,
$ W^{s}(\{\tilde {F}_{1}\})\cap \mathbb{H}_{0}=\emptyset$
, where
$ W^{s}(\{\tilde {F}_{0}\})$
and
$ W^{s}(\{\tilde {F}_{1}\})$
represent the stable subset of
$ \{\tilde {F}_{0}\}$
and
$ \{\tilde {F}_{1}\}$
, respectively. Besides, no subset of
$ \{ \tilde {F}_{0}\}\cup \{ \tilde {F}_{1}\}$
forms a cycle in
$ \partial \mathbb{H}_{0}$
. By [Reference Smith and Zhao40, Theorem 3], there exists a
$\tilde {\vartheta }_{1}\gt 0$
satisfying
$\lim _{t\to +\infty }\inf \tilde {\tau }(\bar {J}_{1}(t)\varphi )\ge \tilde {\vartheta }_{1},\ \forall \varphi \in \mathbb{H}_{0}$
. Recall that
$\vartheta _{2}$
in proof of Theorem4.9. Let
$\tilde {\vartheta }=\min \{\tilde {\vartheta }_{1},\vartheta _{2}\}$
. The proof is complete.
5 Concluding remarks
Cholera is a waterborne infectious disease that can easily lead to large-scale outbreaks in areas with poor sanitation, causing persistent distress and threats. Consequently, researchers actively seek methods and measures to control cholera outbreaks. Jensen et al. discovered that under biologically plausible conditions, bacteriophages can mitigate cholera epidemics [Reference Jensen, Faruque, Mekalanos and Levin19]. This is attributed to the cholera-specific lytic bacteriophages potentially reducing cholera prevalence by eliminating bacteria present in reservoirs and infected human hosts. Additionally, recent research findings in [Reference Hartley, Morris and Smith14] indicated that V. cholerae exhibits a hyperinfectious state upon entering the gastrointestinal tract, diminishing to a lower-infectious state within hours. The different infectivity states of cholera vibrio influence the transmission dynamics of cholera outbreaks differently.
This paper incorporated the interaction between bacteriophages and HI vibrios and LI vibrios, as well as the intrinsic growth rate of V. cholerae, and proposed a degenerate reaction-diffusion cholera model. We divided the infected human hosts into two parts for study: one part consists of human hosts infected only with V. cholerae, denoted as
$I_{1}$
, while the other part consists of human hosts that are simultaneously infected with V. cholerae and bacteriophages, indicating the parasitism of bacteriophages within the host cells (bacteria), denoted as
$I_{2}$
. We also introduce the interaction between HI vibrios and LI vibrios and bacteriophages in this process.
In this work, we originally established the existence and uniform boundedness of the solution, and then derived the well-posedness of the solutions. In a spatially heterogeneous case, the basic reproduction number
$\mathscr{R}_{0}$
is defined as the spectral radius of the sum of two linear operators associated with HI vibrios infection and LI vibrios infection. Generally speaking, it is very challenging to discuss the threshold-type results in the case of multi-class steady states. Fortunately, in this paper, we derived the existence and stability analysis of multi-class steady states for some special cases. We showed the existence of phage-free steady state in a heterogeneous environment. An appropriate Lyapunov function was constructed to discuss the global stability of the phage-free steady state in a homogeneous environment.
In considering the constraints established by our mathematical model, which mandates that disease transmission occurs through the consumption of bacteria rather than through human-to-human contact, there is potential for future research to explore the incorporation of direct interpersonal transmission pathways to enhance this approach. Furthermore, the examination of global stability of the phage-free steady state in a homogeneous environment requires two additional conditions. Future studies could seek to investigate the global stability of the phage-free steady state independently of additional conditions. The global stability of the phage-present steady state of model (2.4) also poses some challenges [Reference Wang, Wang and Fan54]. Moreover, the existence and uniform persistence of the phage-present steady state of model (2.1) are difficult to obtain due to the spatial heterogeneity and other mathematical difficulties. The situation in a heterogeneous environment presents several interesting open problems. We consider these challenges for further investigation.
Acknowledgements
We thank the anonymous referees and the handling editor for their valuable comments, which have led to a substantial improvement in the revision.
Financial support
Wei Wang gratefully acknowledges support from Shandong Provincial Natural Science Foundation of China (ZR2024QA006) and the National Natural Science Foundation of China (No. 12271308, 11901360). Hao Wang gratefully acknowledges support from the Natural Sciences and Engineering Research Council of Canada (Discovery Grant RGPIN-2020-03911 and NSERC Accelerator Grant RGPAS-2020-00090) and the Canada Research Chairs program (Tier 1 Canada Research Chair Award).
Competing interests
The authors declare no competing interests.