Stability of a Delayed Stochastic Epidemic COVID-19 Model with Vaccination and with Differential Susceptibility ()
1. Introduction
Coronavirus disease 2019 (COVID-19) is a contagious disease caused by a virus, SARS-CoV-2. The first known case was identified in the city of Wuhan, China in December 2019. The disease has spread around the world, leading to the COVID-19 pandemic. The World Health Organization (WHO) declared the outbreak a public health emergency of international concern on January 30, 2020, and a pandemic on March 11, 2020. As of June 25, 2022, the pandemic has caused over 543 million cases and 6.32 million confirmed deaths, making it one of the deadliest in history.
In an attempt to control the COVID-19 pandemic and its consequences, many countries resorted to public health measures such as isolation, containment, and barrier measures that had disastrous long-term economic consequences [1] [2] [3] . Thus, vaccination has remained the most appropriate means of controlling a pandemic, particularly COVID-19 [4] [5] [6] . Since the first COVID-19 vaccines became available in 2021, several countries have implemented vaccination campaigns focusing on high-risk groups such as the elderly at high risk of exposure [7] [8] . Since, studies have shown that the severity of the disease increases with age and that the risk of developing symptoms increases by 4% per year in adults between 30 and 60 years of age (see [9] ). Studies on the efficacy of COVID-19 vaccination suggest primarily increased protection against severe cases rather than protection against infection. Thus, a vaccinated person may well be infected with COVID-19 but will only develop a severe form with a very low probability (see e.g. [7] ). What’s more, in difficult economic environments such as those in developing countries, vaccines may not be accessible to everyone. It is therefore highly appropriate to implement vaccination strategies targeting high-risk groups, such as the elderly.
Mathematical modeling has played an important role in controlling an epidemic in a population [10] [11] [12] . At the beginning of the COVID-19 pandemic, authors proposed mathematical models to study the spread of SARS-CoV-2 in some regions of the world [13] [14] [15] [16] . In [17] , it is reported that individuals infected with Sars-cov2 usually develop symptoms on average 5 - 6 days after infection. The median time to symptom onset for SARS-CoV-2 is estimated to be 3 days, the shortest 1 day and the longest 24 days [18] . In view of [19] , a person infected with Sars-cov2 has an average of 5.5 (95% CI: 5.1 - 5.9) days of latency period, which corresponds to the time between infection and when it becomes infectious. Thus, the average incubation period is a good approximation of the average latency period, with a difference of about one to two days. In the literature, many authors have used delay stochastic differential equations to model the dynamics of the spread of an infectious disease with a latency or incubation period (see e.g. [20] [21] [22] ). In [23] , the authors used a stochastic delayed model to study a deconfinement strategy in Morocco. In [24] , a stochastic epidemic SIRC (Susceptible-Infectious-Recovered-Cross immune) model with delay was proposed to analyze the effect of cross-immunity in the spread of COVID-19. In [25] , the authors studied the effectiveness of quarantine using a stochastic delayed SIAQR (Susceptible-Infectiouse-Asymptomatic-Quarantine-Recovered) model. In [26] [27] , the authors used stochastic SEIRV and SIRV models that account for vaccination in the transmission of COVID-19 to study its spread.
In deterministic framework, epidemics are commonly studied by using deterministic compartmental models where the population is divided into several classes, namely susceptible, infected, and recovered groups. For example in [28] , a delayed SIRS epidemic model is proposed, the authors use a nonlinear and functional incidence rate
where
is the number of susceptible at time t,
the number of infected individual at time
, g a probability density on
and
a function from
to
and satisfying certain assumptions. This class of incidence rate is used to model the spread of a disease in which the transmission of infection occurs through vectors that have an incubation time
to become infectious [29] [30] . This incidence rate stipulates that the susceptible at time t can only be infected by infectious people who have been infected at time
,
. Then, other authors have considered this type of incidence rate as a generalization of the standard bilinear incidence rate and which can be used to model diseases that are not vector-borne (see e.g. [31] [32] [33] ). In the stochastic framework, some authors have used this type of incidence rate with a random perturbation modeled by Brownian motion. In particular, in [26] [27] the authors use a delayed stochastic model with this class of incidence rate to study the spread of COVID-19.
In the transmission process of some infectious diseases, the susceptibility to infection differs between groups of people, for example, age groups, immunological status, or fragile subgroups such as pregnant women for malaria. In the deterministic framework, many researchers have considered an epidemic model in which the susceptibility varies from individual to individual [34] [35] [36] [37] . In the reality of the spread of the COVID-19 disease, the susceptibility to infection of individuals and the burden depends on the age group. In [38] , the authors compiled several serological studies from around the world and deduced the following observations: young adults under the age of 35 had the highest seroprevalence of almost any age group; infection rates in people over the age of 55 were significantly lower than in people aged 18 - 54; the highest infection rates in New York State were in people aged 45 - 54. They also note that the age group for which the seroprevalence estimate is highest varies according to location. An analysis of the number of COVID-19 cases in Mali as of June 5, 2022 [39] confirms the same trend. In Mali, the age group under 34 years represented up to 44.7% of confirmed cases, the age group 35 - 54 years represented 36.1% of confirmed cases while the age group Age 55 and over represented 19.2% of confirmed cases. Likewise in Mali, the risk of hospitalization or death following infection by SARS-CoV-2 increases significantly with age. Recently, many studies on COVID-19 transmission have emphasized the heterogeneity in the number of cases and the severity across age groups [9] [40] [41] .
In the current literature, to our knowledge, there is no stochastic delayed SIRS model with vaccination that takes into account this differential susceptibility aspect for COVID-19. This work therefore allows the development of a new stochastic delayed SIRS with vaccination subgroup epidemic model taking into account not only the differential susceptibility but also a general transmission rate for the spread of COVID-19 and which can be used by public health authorities to adopt control strategies for COVID-19 and any other similar epidemic. In this work, we first propose a deterministic model describing the spread of COVID-19 under the hypothesis of differential susceptibility according to age groups and recourse to vaccination of the oldest subgroup. More precisely, we assume that the population is subdivided into age classes (1 - 35, 36 - 54 and >54). In order to take into account the effect of random variations in the environment on the contact process, we add a random disturbance in the contact rate of the deterministic model. We thus obtain a stochastic epidemic model described by a stochastic differential equation with delay. To ensure that the model is well-posed, we first prove the existence and uniqueness of a positive global solution. Based on the Lyapunov technique combined with stochastic analysis, we establish disease extinction below the threshold
, where
is the basic reproduction number of the deterministic model. Finally, numerical simulations are carried out to illustrate the theoretical results in a practical context.
The remainder of this work is structured as follows. In Section 2 we describe the model and Section 3 presents some definitions and notation. In Section 4 we study the consistency of the model, i.e. the well-posedness. In Section 5 we analyze the almost stability of the disease-free-equilibrium state of the model and in Section 6 we illustrate our theoretical results with numerical simulations. Finally, in section 7 we conclude and present some perspectives.
2. Model Formulation
In this work, we propose a stochastic SVIRS (susceptible-vaccinated-infectious-retired-susceptible) epidemic model with delay and different types of susceptible individuals in which the incidence rate is
.
2.1. Deterministic Model
4As mentioned above, the severity and the transmission of COVID-19 to a susceptible individual by an infectious individual depends on several factors, for instance, the behaviour of susceptible individuals and the age groups. In the previous section, we explained that vaccination does not protect against SARS-CoV-2 infection but does protect against severe forms of the disease [7] [8] . It is therefore entirely appropriate to implement vaccination strategies targeting high-risk groups such as the elderly. On the other hand, studies carried out in [9] [38] show us that the severity and probability of catching COVID-19 depends on the age group. In some cases, such as Mali, the variability in susceptibility according to age group (1 - 35, 36 - 54 and >54) was relevant. To take into account some of these specificities, we then assume that the entire population
at time t is divided into six compartments, namely susceptible individuals
,
,
, vaccinated individuals
, infected individuals
and recovered individuals
.
2.1.1. Model Assumption
1) The population is subdivided into three age groups represented by the compartments S1, S2, S3 and defined as follows:
S1: the sub-population of susceptibles who are 35 years old or younger;
S2: the sub-population of susceptibles over 35 and under 55 years old;
S3: the sub-population of susceptibles 55 years or older.
2) Only the susceptible sub-population aged 55 or older are vaccinated and denoted by V. Moreover, the vaccinated individuals develop immunity related to the vaccination and move into the R compartment of recovered individuals.
3) Births occur only in the susceptible class S1 at the rate Λ, since the newborns are less than one year old.
4) The functions
and g satisfy the following assumptions A1-A3:
(A1)
is Lipschitz continuous on
and satisfies
,
.
(A2)
is monotone increasing on
, with
(A3) g is a probability density function with support
.
2.2.2. Parameter Description and the Model Chart Flow
In this model, the births occur only in the susceptible class S1 at the rate Λ. The parameters
,
,
,
,
and
are respectively the mortality rates in the sub-populations S1, S2 and S3 of susceptible individuals and those in the compartments V, I and R.
,
,
,
are the contact coefficients (disease transmission rate).
is the rate of recovery of infectious and the incubation period
of the disease is assumed to be distributed in
. The transfer rate from compartment S1 to compartment S2 and from compartment S2 to compartment S3 are
and
, respectively.
is the vaccination rate of those in compartment S3, i.e., those who are older than 55 years. The parameter
is the rate at which the vaccinated individuals develop immunity related to the vaccination.
is the rate of loss of immunity of the recovered individuals while
are the transfer rates from the compartment of recovered individuals to the compartments of susceptible individuals S1, S2, and S3 respectively. The model is described by the following flowchart.
2.2. Stochastic Model
Throughout this work, we let
be a complete probability space with a filtration
satisfying the usual conditions (i.e.,
contains all P-null sets of
and
) and we let
be a scalar Brownian motion defined on the probability space. To obtain the stochasticity of the model, we integrate random fluctuations in the form of white noise to reveal the effect of random environmental perturbations on the parameters. Previously, we assume that
each contact rate
is given as a random variable with average value
plus some random fluctuation term
with a mean zero. So, in the small time interval
, each infected individual makes
potentially infectious contact with susceptible individuals. Based on the same argument as in [42] , we fund that
or
, where
is the increment of a standard scalar Brownian motion
that follows
. It follows that,
where
is the noise intensity with
.
Naturally, the increase in the number of infectious individuals occurs with certain spatial dispersion of these infectious individuals that increase the level of the variability (variance) of the contact process due to the change of environment. To include this in the model, we assume that the noise intensity
at time t, depends on infectious population size
. Therefore, by replacing
in the deterministic model described by the flow chart (see Figure 1) with
and by setting
, we obtain the following delayed stochastic differential equation describing the model,
(1)
with initial condition
Figure 1. The chart flow of model describing the transfer rule between the model compartments.
where the set
will be defined in the next section and the functional
is given by
3. Definition and Notation
Let
and a real
, we define
,
and
respectively as the spaces of continuous functions from
to
, from
to
and from
to
, endowed with the supremum norm. For any
,
denotes the segment process of
given by
,
,
. For any vector
, we denote by
the Euclidean norm and for any
, we denote by
the supremum norm.
Consider the general n-dimensional stochastic functional differential equation
(2)
where
,
and
is an m-dimensional Brownian motion
. Moreover,
denote the set of
-valued random variables that are
-measurable.
Let
denote the family of all continuous non-negative functions
defined on
such that they are continuously twice differentiable in x and once in t. For any
, we define the function
by
(3)
where
,
,
.
In what follows, we consider the stochastic system (1) which is of the form (2) with dimension
. We always assume that the initial value
which is the set of
-valued random variables and is
-measurable.
4. Existence of Unique Global Positive Solution
In general, we are interested in positive solutions since our study concerns processes describing the size of population compartments. The drift and diffusion coefficients of the system (1) are locally Lipschitz continuous under the assumptions A1-A3, for any given initial value. Then system (1) has a unique local solution
, where the explosion time
(see Mao [43] ) is defined by
In order to guarantee that the unique local solution is global, it is necessary to establish its non-explosion in a finite time. The following result assures us of the existence and uniqueness of the global positive solution.
Theorem 1. Let’s assume that A1-A3 is valid. Then, for any initial value
, the model (1) has a unique positive solution on
,
Proof. As mentioned above, under assumptions A1-A3, model (1) has a unique local solution
on
, for any initial value
. Let us define the following stopping time as in [44]
In a similar way, we define
groups S2, S3, V, I and R respectively.
We can see from (1) that
satisfies the linear stochastic differential equation. Thus, by (Mao [43] , Chap.3.) one has
where
is considered as
-adapted and almost surely locally bounded process.
We have
where
Therefore, we deduce that
almost surely.
For the second group of susceptible, we have
where
It follows that
a.s.
For the third group of susceptible, we have
where
So, we get
a.s. In the same way as before, we have
a.s.
The recovered population
satisfies the linear stochastic differential equation
where
is an
-adapted and almost surely locally bounded process.
where
Since
, thus
become negative after only
is negative. That is
almost surely.
For the infected group, we have
and
with
.
We propose to show in the following step that
almost surely by establishing that
almost surely. To do this, we proceed by contradiction.
Suppose that there exists a Borel set B of Ω with
and for all
we have
. By definition of
In view of assumption (A2) and the fact that
a.s., for all
and for all
, it follows that
Therefore
which leads to a contradiction. Necessary, we must have
almost surely.
□
Let us put
The following result gives us the boundness of any local solution of the model (1) and achieves the proof of existence and uniqueness of global positive solution.
Corollary 1. Assume that A1-A3 hold. Then, the system (1) has a unique global positive solution
for any initial value
. Moreover, there exists a
for any sufficiently small
such that for all
this solution remains in
with probability 1. In particular, if
this solution lies in Γ almost surly.
Proof. By Theorem 1, for any initial value
, the model (1) has a unique positive solution
. To prove that this solution is global, it suffices to prove that it is bounded. We have
a.s. on
, where
. Therefore
because naturally
.
We denote by
the solution of the following differential equation
, with the same initial value
.
Therefore, by the comparison theorem [45] , we have
For any
, there exists
such that for all
□
5. Stability Analysis and Asymptotic Behavior
This section deals with the stability analysis of the stochastic epidemic model (1). A simple analysis established that this model has a unique disease free-equilibrium
where
, which is given by:
where
By using a change of variable, we first reduce the analysis of the stability of the equilibrium point
to the study of the stability of the trivial equilibrium point zero of another system. We first establish that the solution of the system obtained by change of variable remains in suitable subset
. Then, by using a Lyapunov functional technique and a local martingale convergence result, we deduce the almost sure stability of the disease-free equilibrium
of the model (1) under the condition
. In the following, we consider the class of initial conditions
such that
.
Let’s put
(4)
Then, by virtue of Itô’s formula, we get the following system
(5)
with initial condition
where
It is easy to see that the stability analysis of the disease-free equilibrium
of the model (1) can be obtained from the stability analysis of the trivial solution
of the model (5). Before studying the stability analysis of the trivial solution of the model (5), we need some information about the sign of the components of its solution.
Theorem 2. Either
the solution of the system (1) with initial condition
. Suppose that
(6)
and
(7)
Then, we have
Proof. To arrive at the result, reformulate the equilibrium states
,
,
,
. A simple analysis gives us
Based on the proof of the Theorem 1 and the Corollary 1, we get
where
Let
, the quadratic variation
of
is locally bounded by Corollary 1. So, by the strong law of large numbers for local martingales (see e.g. [43] ) we have
when
. Therefore, there exists
large enough, such that for all
such that
It follows for all
that
On the other hand, it is easy to see that
(8)
In view of Corollary (1) and assumptions A1-A2, we have
(9)
Therefore
(10)
By combining (8), (9) and (10), we deduce that
Consequently, under the condition (7), for all
, we get
(11)
And
(12)
Now, let put
. So, there exists two positive reals
and
such
. Therefore, for all
, we have
Let us put
, it is straightforward to see that
. Based on (11) and (12), we get for all
As
Letting
, given the fact that the population may be without infectious (
), we deduce that
(13)
Taking this result into account and repeating the same reasoning on the following expressions
where
where
and
where
respectively, we deduce almost surly, that
(14)
Let us put
,
,
,
,
et
, therefore
. In view of (5), we get
Under the condition (6), it follows that
Therefore
so we get
Consequently, for all
,
(15)
On the other hand,
,
,
,
,
where
,
,
and
,
with
,
,
,
,
,
.
Therefore, based on (15), we have almost surly
for all
.
Let us assume
, that is
. It follows that
, for all
.
In particular
that leads to a contradiction, necessarily we must have
. By (13) and (14), finally obtain almost surly
□
The following corollary which is necessary to establish our stability result is a consequence of the previous result of Theorem (2).
Corollary 2. Assume that the assumptions A1-A2 and the condition (6) in Theorem (2) are satisfied. Then, the system (5) has a unique global solution
for any initial value
such that
. Moreover, for any
such that for
,
we have
for all
,
a.s.
.
Proof. Let us put
,
,
,
,
,
. It’s easy to see that the system (1) with initial condition
is equivalent to the system (5) with the initial condition
such that
. Therefore, in view of the Corollary 1, the system (5) has a unique solution global solution. Moreover, the condition,
, for
,
imply that
,
and
a.s. That is
In view of the Theorem 2, the solution
of the system (1) is such that
Therefore for all
,
a.s.
. □
Now, we establish a stability result for the trivial solution
of the model (5) by combining a stochastic Lyapunov technique and martingale convergence theory (see [42] [46] ).
Theorem 3. Let’s assume that
, then the disease-free equilibrium
of model (5) is globally asymptotically stable almost surely for any initial condition
such that
.
The proof of this Theorem requires the useful non-negative semimartingale convergence result ( [43] Theorem 1.3.9, p.14).
Lemma 4. Let A1 and A2 be two continuous adapted increasing processes on
with
a.s. Let M be a real-valued continuous local martingale with
a.s. Let Z be a non-negative measurable random variable such that
. Define
If X is non-negative, then
where
a.s., means
.
In particular, if
a.s., then
That is, all of the processes X, A2, and M converge to finite random variables.
Proof of Theorem 3. We will first establish separately the almost sure asymptotic stability of the trivial solution of the component
of the system (5), then we deduce that the trivial solution
of the system (5) is asymptotically stable almost surly.
For any
, let us define
. So the component
of the system (5) is described by the following equation
(16)
with initial condition
for any
such that
.
Let us consider the Lyapunov functional
where
,
.
In view of (3) and Corollary (2), we get that
In view of Theorems 3 in [47] , if
, we obtain that
, where p is a positive constant. That is, if
there exists two positive constants p1 and p2 such that
(17)
In this step we will prove that
, where
. From Corollary 2, it is clear that
almost surly.
Let put
. According to Corollary 1, the quantity
is bounded for all
, consequently
is a local martingale.
From the four first equations of the model (5) and the fact that
, we obtain
In view of Corollary 1, Hölder inequality and (17), we obtain
Therefore, by virtue of Lemma 4, we get
In accordance with Theorems 2,
is positive for all
. Therefore, we get
(18)
Assume that
does not converge almost surely to 0. Then there is a set
with
such that for all
,
Then, there exists a
such that
for all
. It follows that
Therefore,
, where
. Hence
, which contradicts (18). So, we have
Finally, we have proved that, when
,
a.s. □
Following the result of Theorem 3 and the change of variable (4), we deduce the following corollary which gives us the almost sure stability of the disease-free equilibrium
of the model (1) under the condition
.
Corollary 3. If
, then the disease-free equilibrium
of model (1) is stable almost surly for any initial condition
.
6. Numerical Simulation and Commentary
In this section, we give an illustration of the stability result and the effect of noise intensity in the model by numerical simulation. We use the Euler-Maruyama method (see e.g [48] ) to simulate the sample paths of the model (1) with
(i.e.
) for all
and
for all
, null otherwise. Ten sample paths of the stochastic model (1) under the condition
given in Figure 2, we effectively observe the stability of the disease-free equilibrium
. In Figure 3, we represent a sample path of model (1) with
, in this case, the disease persists in the population (
,
). We therefore see that these numerical simulations (Figure 2 and Figure 3) agree well with the analytical results of theorem 3. Finally, in Figure 4, we illustrate model (1) under the condition
and with higher noise intensity compared to the case of Figure 2. Thus, we observe that the increase in noise intensity increases the intensity of fluctuations in the model with larger extreme values.
Figure 2. Ten (3) sample paths of the stochastic SVIRS epidemic models (1) with
. The initial values are:
,
,
,
,
,
for
. The values of the parameters are given by:
,
,
,
,
,
,
,
,
,
,
,
,
,
. The conditions
of the theorem 3 is checked. We observe then that the disease-free equilibrium E0 is asymptotically stable almost surly.
Figure 3. Sample paths of the stochastic SVIRS epidemic models (1) with
. The initial values are:
,
,
,
,
,
for
. The values of the parameters are given by:
,
,
,
,
,
,
,
,
,
,
,
,
,
. In this case
.
Figure 4. Sample paths of the stochastic SVIRS epidemic models (1) with
. The initial values are:
,
,
,
,
,
for
. The values of the parameters are given by:
,
,
,
,
,
,
,
,
,
,
,
,
,
. In this case
.
7. Conclusion and Perspective
We considered a stochastic epidemic SIRS model represented by a delayed stochastic differential equation to describe the spread of COVID-19 in a population where susceptibility to the disease varies across age groups and where a fraction of people over 55 years of age are vaccinated. First, we established the consistency of the model, i.e. the existence and uniqueness of the global and positive solution (see Corollary 1). Then, we have established the almost sure asymptotic stability of the
disease-free equilibrium of the model when
(see Theorem 3). The work performed in this paper could be improved by taking into account time-related parameters, which would allow taking into account seasonal effects or times of the year favoring large gatherings, where contact rates can increase. We can also imagine the possibility of using delay-dependent contact rates. This is relevant in certain situations where supporting measures are required, such as Contact tracing of an infected person can reduce the number of infectious contacts over time, so an increase in the length of the latency period can reduce the contact rate. Finally, given the large amount of data on COVID-19 globally, we can improve this work by adding parameter estimation methods to adapt the model to reality.
Acknowledgement
Sincere thanks to the members of JAMP for their professional performance, and special thanks to managing editor Hellen XU for a rare attitude of high quality.