On a Mathematical Model with Non-Pharmaceutical Interventions for Long-Term Dynamics of Viral Infections ()
1. Introduction and Background
Viral diseases remain a major global public health challenge, causing substantial mortality and persistent social and economic disruption [1]-[3]. Their rapid transmission, continuous evolution, and ability to spread through human, environmental, and behavioural pathways have contributed to some of the most devastating epidemics and pandemics in history, including influenza, Ebola, SARS, HIV/AIDS, and COVID-19 [4]-[8]. Increasing global mobility, urbanization, and pathogen evolution further increase the likelihood of large-scale outbreaks, while limited therapeutic options and viral mutation can complicate their control [9]. Consequently, effective disease control requires not only medical interventions but also surveillance, quarantine, isolation, public health education, and sustained behavioural compliance [10] [11].
Mathematical modelling provides a powerful framework for understanding disease transmission, identifying key epidemiological thresholds, and evaluating intervention strategies. Since the foundational compartmental models of Ross, Hamer, McKendrick, and Kermack [12] [13], numerous models have incorporated quarantine, behavioural responses, environmental transmission, and other epidemiological mechanisms [14]-[18]. However, these features are often considered separately. For example, models incorporating quarantine may neglect reinfection or environmental contamination, while environmentally mediated models may omit behavioural heterogeneity, treatment-centre capacity, or disease transmission from quarantined individuals [16]-[18]. This motivates the development of a more integrated framework capable of capturing the interacting mechanisms that shape long-term viral disease dynamics.
In this study, we develop a general deterministic compartmental framework that unifies key epidemiological, environmental, and behavioural mechanisms within a system of nonlinear ordinary differential equations. The model incorporates non-constant recruitment, limited treatment-centre capacity, reinfection, environmental viral particles, disease-induced mortality and cadaver-mediated transmission, contact tracing, quarantine and isolation, and behavioural heterogeneity among susceptible, suspected, and infectious freely roaming individuals. In particular, non-quarantined populations are stratified according to their adoption of barrier measures, allowing behavioural responses to influence transmission dynamically. To the best of our knowledge, this provides a unified framework for simultaneously capturing these interacting mechanisms while remaining sufficiently flexible for application to a broad range of viral infections through appropriate parameterization. The resulting model provides a mathematical platform for analysing disease thresholds, transmission pathways, intervention strategies, and behavioural feedback in long-term viral disease dynamics.
The rest of the paper is organised as follows. In Section 2, we outline the derivation of the model showing the state variables and parameters, their possible ranges and baseline values used and how they relate together in a conceptual framework; we present a mathematical analysis of the derived model to ascertain that the results are physically realizable and then re-parametrized the model. In Section 3, we present detail analysis of the general disease free model and on the epidemiological model with no barrier measures. Section 4 provides sensitivity analysis and numerical simulations. Finally, discussion of results and conclusion are provided in Section 5.
2. The Mathematical Model
In this section, we give a detailed description of the mathematical model studied. We start with the assumption that there exist
barrier/control measures
, put in place by a supervisory authority, and that the barrier measures have been combined into sets
,
, already ordered so that
. Each
, is a set that contains up to
barrier measures so that any individual
, indexed by the subscript
,
, is considered to adhere to all barrier measures
,
. We briefly write
to represent a vector of length
containing individuals with different adherent indices. Thus each individual can be adhering to any number of these barrier measures. Our proposed model shall therefore focus on dynamics involving non-pharmaceutical interventions such as quarantining and behavioural changes during a viral outbreak, captured in the form of barrier measures.
2.1. Model Formulation and Description
At any time
, we divide the total human population into compartments representing disease status as well as adherent state to barrier measure(s). The compartments include:
a vector of susceptible individuals,
, a vector of suspected asymptomatic freely-roaming individuals,
suspected asymptomatic quarantined individuals,
, a vector of symptomatic non-isolated infected/infectious freely-roaming individuals,
confirmed isolated symptomatic infectious at homes,
confirmed isolated symptomatic infectious at treatment centres,
recovered,
cadavers, and to these, we add a compartment for environmental transmission contamination by
. So, from a base set of
barrier measures, the vectors
, are each of length
as explained above, and we construct a system comprising
compartments linked by the viral disease pathogen in a dynamical system. The conceptual framework for the model is shown in Figure 1. The following model assumptions may be highlighted:
A1. Non-constant living human population.
A2. Infected individuals can shed viral particles onto the environment.
A3. Individuals can become infected when they come in contact with infected/infectious individuals, the cadavers of the viral disease victims or with a contaminated environment.
A4. Non-Pharmaceutical control is introduced in our model via barrier measures.
A5. Infected, suspected and infectious individuals in the population can be either quarantined or freely roaming.
A6. Quarantined/isolated individuals are assumed to adhere to all the barrier measures.
A7. All freely roaming humans can choose to adhere to none, one or more forms of barrier measures.
A8. On recovery, recovered individuals gradually lose their immunity to the viral disease and return into the susceptible compartment.
A9. The number of available hospital beds is limited by a fixed maximum capacity.
Figure 1. Conceptual framework of the compartmental viral outbreak model. Compartmental flows are described in the text, with notation defined in Tables 1-4.
The state variables, their descriptions, and their corresponding quasi-dimensions are summarised in Table 1.
Table 1. Description of state variables and their quasi-dimensions.
Variable |
Description |
Quasi-dimension |
|
Density of living humans at time
|
|
|
Density of living humans together with cadavers at time
|
|
|
Vector of dimension
representing susceptible humans at time
. |
|
|
Vector of dimension
representing suspected humans at time
. |
|
|
Density of suspected asymptomatic quarantined humans at time
|
|
|
Vector of dimension
representing infected and infectious individuals at time
|
|
,
|
Densities of confirmed symptomatic infectious isolated humans at the treatment centres and at homes at any time
respectively |
|
|
Density of recovered humans at time
|
|
|
Density of viral disease related deaths at time
|
|
|
Density of humans due to natural deaths at time
|
|
|
Density of viral particles at time
|
|
2.2. The Model’s Equations
In this section, we describe the equations that govern the time rate of change of each of the entities in Table 1.
(i) The force of infection: The exposure rate of susceptible humans to infection. We denote by
,
, the exposure rate of susceptible humans of class
to the infection. We take into consideration susceptible individual’s contacts with infected/infectious humans, cadavers and the contaminated environments. We use a standard incidence model where we append the size of cadavers to
, the total living human population to get
. So that:
(1)
For all
, the equation for the force of infection takes the following form:
(2)
where
is defined in Equation (1). Each of the terms in Equation (2) are explained below by listing the numbers in the underbraces.
(1) Contacts between susceptible humans with adherence index
and suspected asymptomatic freely-roaming humans with adherence index
. Here, we have simply considered a contact pattern through the formula
according to standard mass action law with rate constant
,
. So the mixing pattern
will meet with contact rate
while
will meet with contact rate
. We shall demand for simplicity that the contact weight,
, shall be the same, and write,
(3)
Here,
is interpreted for each
as the effective contact rate. Two major requirements for the choice of
are: (i) monotonicity and (ii) positivity. That is,
and
. One form is shown in Equation (3) which we can identify with the entries of a finite Hilbert matrix [19]. Other forms for
, such as are possible.
(2) Infection from contacts between susceptible humans with adherence index
and freely-roaming infected individual with adherence index
. Using similar argument as in (1) above, we set,
(4)
Here,
,
is the effective contact rate. From our assumptions, one will expect that
.
(3) Infections from contacts between susceptible humans with adherence index
and suspected asymptomatic quarantined individuals.
(4) Infections from contacts between susceptible humans with adherence index
and confirmed isolated symptomatic individuals in the treatment centres.
(5) Infections arising from contacts between susceptible humans with adherence index
and confirmed self isolated symptomatic individuals at homes.
(6) Infections arising from contacts between susceptible humans with adherence index
and the cadavers of the viral infected victims.
(7) Infections from contacts between susceptible humans with adherence index
with the contaminated environments. While some authors, see for example [20], have considered an unbounded linear form for the function
, we shall assume that
is a bounded and monotone increasing function. In our
formulation,
is indexed with two parameters:
that measures the supremum of
and
to measure the concentration level where
.
We demand that,
as
and
as
. One such function is:
(5)
a Holling’s Type II functional response.
(ii) The susceptible individuals: This class of individuals represented by the variable
, comprises humans that have not in anyway been infected by the viral disease. The individuals in the
class are categorized into
groups;
determined by their adherence to barrier measures. For example,
,
are individuals that adhere up to
forms of barrier measures. The rate of change of the number of susceptible individuals with time decreases when members of this class become exposed and are either moved to the suspected asymptomatic quarantined compartment or to the suspected asymptomatic non-quarantined freely-roaming compartment. While the density increases when some confirmed quarantined individuals who returned negative tests, false suspected non-quarantined freely-roaming individuals who are not sick of the virus and those individuals who recovered from the disease and have lost their immunity all return to the susceptible pool. Figure 2(a) shows the various flows in and out of an arbitrary class
, of the susceptible compartment. So, the net rate of change of individuals in the
compartment, for
at any time
can be written in the form:
![]()
(a)
(b)
Figure 2. Conceptual diagram showing the flows for an arbitrary group.
(6)
where the parameters in
are as given in Equation (2). We suppose that the total out flow rate for individuals from the
class due to exposure to the viral infection is
, then we expect the conservation equation
, where
is as defined in Equation (2) to hold. Now, let
be the fraction of
individuals that were identified and placed in quarantine and the remaining
be the fraction that escaped detection and so enter the suspected freely roaming class. Our conservation equation will now take the form;
; for
, and
.
(iii) The suspected asymptomatic freely-roaming individuals: This class comprises individuals who came in contact with or where near a known viral infected patient. They are described by the variable
and are categorized into
freely-roaming suspected groups represented by the variables
. Outflow from this class is driven by the development of symptoms or that they were not infected of the viral disease at all. The rate of change of the density of members in this group decreases when some of these individuals return to the susceptible pool because they were not sick of the viral disease, some developed symptoms and progressed to the infected/infectious freely roaming compartment and others who developed symptoms, were identified and isolated either in the treatment centres or at homes. The density of these individuals increases when the susceptible individuals are exposed by having come in contact with or being associated with any of the possible infectious cases. For a particular class,
,
of the
compartment, the flows in and out of this subclass is as shown on Figure 2(b) and the equation that governs the rate of change of the
individuals at any time
, is given by:
(7)
where
and
,
.
(iv) The suspected asymptomatic quarantined individuals: This class comprises the other group of suspected individuals who were in contact with or in the vicinity of a known infected patient but are traced, via contact tracing or some other means and quarantined. Members in this class, described by the variable
, are either self-quarantined or isolated in approved facilities. Individuals in this class move to the susceptible class (following a negative test result) or they move to the confirmed infected/infectious symptomatic isolated classes (following a positive test result) and depending on the availability of space at the treatment centres. The rate of change of the density of individuals increases when a fraction of the susceptible individuals who got exposed get traced and quarantined. The density is reduced when some of these individuals returned to the susceptible pool after returning negative viral test results, while those who are confirmed positive, either move to the treatment centres depending on whether there is space or are forced to isolate at homes. Thus:
(8)
(v) The symptomatic non-isolated infected/infectious freely-roaming population: This class is made up of those asymptomatic non-quarantined freely-roaming individuals who are infectious but do not exhibit symptoms or may exhibit symptoms but for some reason, cannot get a test. These are the super spreaders. They are described by the variable
and are categorized into
subgroups represented by the indexed variables
. We believe these are key disease drivers in the community and their level of contribution to disease spread via human-to-human contacts and rate of viral shedding into the environment would be determined by the respective level of compliance to the barrier measures. We assume that the rate of viral shedding in to the environment, in terms of the subgroups is in the order
whereby individuals in the subgroup
could be termed super disease spreaders. The rate of change of the density of symptomatic infected/infectious freely roaming individuals in the population increases when a fraction of the suspected asymptomatic freely-roaming individuals developed symptoms, progressed to this class. Outflow from this class occurs when some of these individuals are removed by recovery from the disease at rate
, by death caused by the virus at rate
or to isolated units at homes or in treatment centres at rates
and
respectively while others die due to natural death. For an arbitrary class,
, of the
compartment, the equation that governs the rate of change of the
individuals at any time
, is given by:
(9)
where
and
.
(vi) The confirmed isolated symptomatic infectious individuals at homes: This class of individuals comprises all those individuals who are now presenting with symptoms. They are described by the variable
. Recruitment into this class depends on whether the treatment centre has attained it carrying capacity,
or not. The rate of change of the number of
increases as a result of flow from the
and were unable to be admitted at the treatment centres because there is no space in the treatment centres or they chose to isolate themselves at homes, from
class who developed symptoms, and then forced to isolate themselves at homes. Further more, increment in this class is also caused by cases from the
class. The rate of change of the density of
class is reduced when some of the individuals are removed, or moved to the treatment centres. Removal could be as a result of recovery at rate
or as a result of disease induced death at rate
, or of natural cause at rate
. At time
, we have:
(10)
where the function
measures the flow rate into the
compartment as a function of the size of the treatment centre and it is given by:
(11)
for
,
, and
is the total out flow rate from this compartment with:
(12)
where
is is the floor of
, which is also the greatest integer smaller or equal to
. Mathematically,
,
. Thus
is the effective number of individuals at the treatment centres, capped by the maximum treatment centre carrying capacity
.
(vii) The confirmed isolated symptomatic infectious individuals in treatment centres: This is the class of individuals who at some point had tested positive and were asymptomatic, not exhibiting any viral disease-like symptoms but are now presenting with symptoms. They are described by the variable
, flow into this compartment is greatly conditioned on the size of the treatment centre. The rate of change of the
individuals increases as a result of flow from the
class by individuals who returned positive viral tests, from
class who developed symptoms, were traced and then taken to the treatment centres. Increment is also caused by cases from the
class, when it is noticed that there is space at the treatment centre and, from the
class. The rate of change of the density of
individuals is reduced when some of the individuals are removed as a result of recovery at rate
or as a result of disease related death at rate
and lastly, as a result of natural death at rate
. At time
, we have:
(13)
where the function
measures the flow rate into the
compartment as a function of the size of the treatment centre and it is modelled by:
(14)
(viii) The recovered individuals: The class of recovered individuals denoted by
, contains all individuals who once got infected by the virus and did not die of the disease. Since recovery from the disease may not confer permanent immunity against further infections, these recovered individuals eventually return into the susceptible pool and can be reinfected if proper precautions are not taken. The equation governing the rate of change of recovered individuals at time
, takes the form:
(15)
where
.
(ix) The cadavers: Here, we have two kinds of deaths; (i) disease induced deaths, collected into the compartment
at rates
,
and
form the
,
and
compartments respectively. (ii) natural deaths collected into the compartment
at a constant rate
from all living population classes. It is known that the dead bodies of some viral disease victims are still very infectious and can still infect susceptible individuals upon effective contact. Thus, in this work, we consider
to be the rate at which cadavers are properly disposed of through burial or cremation. The rate of change of the population of disease induced deceased individuals at time
is:
(16)
In Equation (16),
are disease related disposed cadavers. It is a collection class modelled by;
. Next, we define
, another collection class
that tracks all natural deaths, occurring at rate
, from all the living population classes. It is modelled by:
(17)
We use the classes
and
, only as place holders.
(x) The environmental transmission contributors: This compartment comprises all viral particles shed by infected humans into the environment and it is described by the variable
. The shedding of these viral particles by infected/infectious humans occur at different rates depending on the adherence index of the infected human. Thus, the rate of change of the density of viral particles shedded into the environment at time
, is modelled by the equation:
(18)
In the absence of viral disease,
decays steadily to zero at rate
.
(xi) Dynamics of the total human populations: The total living human population is not constant since the model accounts for births and deaths. We assume that all new births, enter the class of susceptible individuals who adhere to all
control measures. Let
, where
and
are positive
constants. So that the net rate of new births that enters the susceptible compartment,
, at any time
is given by:
(19)
At any given time
, the rate of change of the total living population is:
(20)
Equation (20) shows the dependence of the size of the living population on disease related deaths. If
for
, then all deaths in the system are only due to natural causes and the total living human population
satisfies the equation:
; which can be solved directly to have
, where
,
,
and
. Clearly, if (i)
,
as
and if (ii)
,
as
. In either case,
remains bounded as
. We shall assume that
. Also, applying similar arguments, the equation for the rate of change of the total living human population and the cadavers is given as:
(21)
Putting all the equations together, we get:
(22)
The equations for the total living human populations are given by:
(23)
where
is as given in Equation (2);
, Equation (6);
and
, Equation (7);
, Equation (8);
and
, Equation (9);
, Equation (11) and
Equation (14).
One form of initial conditions could be those that start off the process with some initial density of the form:
(24)
(25)
where the variables with superscript
are typical variables at time
whose values will be provided as initial conditions.
Definition 2.1 (Realistic solution). A solution of system (22) is called realistic if it is non-negative and bounded.
For all intents and purposes, since the rates are polynomials and rational functions, we can easily establish using standard techniques as shown in [21] that system (22) is mathematically and physically well-posed. Also, the solutions lie in the bounded region,
(26)
2.3. Non-Dimensionalisation and Re-Parametrisation
To scale the system, we make the following change of variables:
where
,
,
,
,
,
,
,
,
,
,
,
and
, are reference quantities associated with the different human and viral compartments, and
is a characteristic time frame for the system. We set;
(27)
and then define the following dimensionless parameter groupings:
(28)
With
. This leads to the scaled system:
(29)
and the total populations satisfy the scaled equations:
(30)
where:
(31)
(32)
and
(33)
For,
.
Table 2. Model’s parameter values and their Quasi-dimensions.
Parameter |
Description |
Units |
Range of possible values |
Baseline values |
References |
|
Recruitment rate of humans |
|
|
|
[22] |
|
Natural mortality rate of humans. |
|
|
|
[22] |
|
Human environmental carrying capacity |
|
Varies |
106 |
Assumed |
|
Proportions of susceptible individuals with adherence index
who become suspected asymptomatic freely-roaming individuals with adherence index
, (respectively, suspected asymptomatic quarantined individuals). |
1 |
|
0.75(0.25) |
Assumed |
(
) |
Total outflow rate for suspected asymptomatic freely-roaming (and suspected quarantined) individuals with adherence index
. |
|
|
|
[23] |
|
Flow rate from the
class in the suspected freely-roaming compartment
to the
class in the susceptible compartment. |
|
|
0.04375 |
Assumed, weighted with
. |
|
Rate at which individuals from the
class in the suspected
freely-roaming compartment
progressed to the
class in the symptomatic infectious freely-roaming compartment. |
|
|
0.025 |
Assumed, weighted with
. |
|
Rate at which suspected freely roaming individuals are removed and isolated at homes. |
|
|
0.04375 |
Assumed, weighted with
. |
|
Rate at which suspected freely roaming individuals are removed and isolated into the treatment centres. |
|
|
0.0125 |
Assumed, weighted with
. |
|
Rate at which suspected quarantined individuals moved to the susceptible
class
. |
|
|
0.04375 |
Assumed, weighted with
. |
|
Rate at which suspected quarantined individuals who are confirmed to be infected with the virus progressed to the isolated infectious individuals at the treatment centre. |
|
|
0.05 |
Assumed, weighted with
. |
|
Rate at which suspected quarantined individuals who are confirmed to be infected with the virus progressed
to the isolated infectious individuals
at homes. |
|
|
0.03125 |
Assumed, weighted with
. |
|
Rate at which recovered individuals lose immunity. |
|
|
1/120 |
[24]. |
,
,
|
Rates at which susceptible, suspected freely-roaming and infectious
freely-roaming individuals change
their adherence status, from adherence status index
to adherence status index
within the respective compartments. |
|
Varies |
Varies |
Estimated |
,
,
|
Total outflow rates for individuals
who are infected/infectious symptomatic freely-roaming, symptomatic isolated at homes and
at treatment centres with adherence index
,
|
|
|
|
[25] [26] |
|
Rate at which infectious freely
roaming individuals are removed
and isolated into the treatment
centres. |
|
|
0.0375 |
Assumed, weighted with
. |
Table 3. Model’s parameter values and their Quasi-dimensions.
Parameter |
Description |
Units |
Range of possible values |
Baseline values |
References |
|
Rate at which infectious freely roaming individuals are removed and isolated at homes. |
|
|
0.0375 |
Assumed, weighted with
. |
|
Recovery rate of confirmed infected/infectious symptomatic freely roaming individuals with adherence index
. |
|
|
0.0375 |
Assumed, weighted with
. |
|
Disease related death rate for infected/infectious symptomatic freely roaming individuals with adherence index
. |
|
|
0.0375 |
Assumed, weighted with
. |
|
Rate at which confirmed isolated symptomatic infectious individuals at homes recover from the infection. |
|
|
0.075 |
Assumed, weighted with
. |
|
Rate at which confirmed isolated symptomatic infectious individuals at homes become confirmed isolated symptomatic infectious individuals in treatment centres. |
|
|
0.03 |
Assumed, weighted with
. |
|
Disease related death rates for confirmed symptomatic self-isolated individuals at homes. |
|
|
0.045 |
Assumed, weighted with
. |
|
Recovery rate of confirmed isolated symptomatic infectious individuals in treatment centres. |
|
|
0.09 |
Assumed, weighted with
. |
|
Disease related death rate for confirmed symptomatic isolated individuals in treatment centres. |
|
|
0.06 |
Assumed, weighted with
. |
|
Entries of Hilbert-Like matrix for contacts between susceptible humans with adherence index
and suspected freely-roaming humans or infected/infectious freely roaming humans with adherence index
,
. |
1 |
[0, 1] |
Varies |
Assumed |
|
Effective contact rate between susceptible humans with adherence index
and infected/infectious freely-roaming individuals with adherence index
. |
|
|
0.18 |
[20] [25] [27] [28] |
|
Proportions of
,
,
,
,
and
humans who come in contact with
humans. Here,
|
1 |
[0, 1] |
Varies |
Assumed |
|
Contact rate between susceptible humans with adherence index
and suspected asymptomatic freely-roaming humans with adherence index
. |
|
|
0.15 |
Weighted with
. |
|
Contact rate between susceptible humans with adherence index
and confirmed infected/infectious symptomatic freely-roaming humans with adherence index
. |
|
|
0.18 |
Weighted with
. |
|
Effective contact rate between susceptible humans with adherence index
and suspected quarantined asymptomatic humans. |
|
|
0.06 |
Weighted with
. |
|
Effective contact rate between susceptible humans with adherence index
and confirmed isolated symptomatic infected/infectious humans in the treatment centre. |
|
|
0.09 |
Weighted with
. |
Table 4. Model’s parameter values and their Quasi-dimensions.
Parameter |
Description |
Units |
Range of possible values |
Baseline values |
References |
|
Effective contact rate between susceptible humans with adherence index
and confirmed isolated symptomatic infected/infectious humans at home. |
|
|
0.12 |
Weighted with
. |
|
Effective contact rate between cadavers of confirmed isolated/non-isolated symptomatic individuals and susceptible individuals with adherence index
. |
|
|
0.03 |
Weighted with
. |
|
The environmental contamination factor, standing for the per capita rate of people who interact with the environment daily |
|
|
0.000007 |
[20] |
|
Effective contact rate between susceptible humans with adherence index
and viral contaminated environment. |
|
|
|
Weighted with
. |
|
Decay rate of viral particles from the environment. |
|
|
0.85 |
[20] |
|
Rate at which cadavers are removed and buried. |
|
|
|
[29]-[31] |
|
Measures the maximum possible concentration of viral particles in the environment. |
|
|
30,000 |
Assumed |
|
Measures the concentration level when the maximum concentration of viral particles in the environment is exactly half
|
|
|
15,000 |
Assumed |
|
Rate of shedding viral particles into the environment by the infected/infectious symptomatic freely-roaming individuals with adherence index
. |
|
|
|
[20] [32] |
|
Proportions with
|
1 |
[0, 1] |
Varies |
Assumed |
|
Rate of shedding viral particles into the environment by the suspected quarantined individuals with adherence index
. |
|
|
|
Weighted with
. |
|
Rate of shedding viral particles into the environment by confirmed symptomatic infected/infectious self isolated individuals at homes. |
|
|
|
Weighted with
. |
|
Rate of shedding viral particles into the environment by confirmed isolated symptomatic infected/infectious individuals in the treatment centres. |
|
|
|
Weighted with
. |
|
Rate of shedding viral particles into the environment by the suspected quarantined individuals. |
|
|
|
Weighted with
. |
,
|
Per capita birth rate of humans per unit time |
|
Varies |
Varies |
|
|
A real-valued function representing the force of infection. The index
indicates the flow rate from the
class in the
compartment to the
compartment, where
. |
|
Varies |
Varies |
Estimated |
|
A real-valued function representing the force of infection. The index
indicates the flow rate from the
class in the
compartment to the
compartment, where
. |
|
Varies |
Varies |
Estimated |
3. Mathematical Analyses of the Scaled Model
In this section, we perform mathematical analyses on the scaled system (29).
3.1. The Scaled Disease Free Model
In the absence of the disease, system (29)-(30) reduces to:
(34)
(35)
Here, the dimensionless parameters;
and
are as defined in Equation (28). When there is no barrier measure, that is when
,
and Equation (34) reduces to
(36)
a single equation which can be rearranged to give Equation (35). Equation (35) can be solved directly to have, ,
with
.
Now, as
,
. Thus, based on the scaling adopted, the equation for the scaled total living human population is always bounded, i.e.,
. Let , and
(37)
Then system (34)-(35) can be written in the form:
(38)
Let us further define, and .
Theorem 1 (On the existence of steady states). The disease free system (34)-(35), has two steady states: 1) the trivial steady state; given by
, with
a
zero vector and 2) the non-trivial steady state given by
.
Proof. At equilibrium, . From Equation (35), or 1. For
, Equation (34) gives for all
, yielding the trivial steady state. For , Equation (34) gives , where
has negative diagonal and non-negative off-diagonal entries. By the Gershgorin Circle Theorem [33],
is nonsingular; hence exists, establishing the non-trivial disease-free steady state.
Theorem 2 (Stability of the steady states).
The steady states defined by Theorem 1 have the following stability properties: (i) The trivial steady state is locally unstable for all parameters, and (ii) The non-trivial steady state is globally asymptotically stable.
Proof. Stability is determined by the eigenvalues of the Jacobian at the steady states. From the block structure of the Jacobian, the characteristic equation can be written as
(39)
where
is defined in Equation (37). At the trivial steady state
,
, implying instability. At the non-trivial steady state
,
, while
has negative diagonal and non-negative off-diagonal entries. Hence, by the Gershgorin Circle Theorem [33] [34], all eigenvalues of
have negative real parts, establishing local asymptotic stability of
. Moreover, the corresponding solution remains bounded as
[21], completing the proof. □
3.2. The Epidemiological Model with No Barrier Measures
In this subsection, our goal is to analyse the scaled epidemiological system when there are no barrier measures (that is
) but other non-pharmaceutical interventions such as quarantine are still in place. From our scaling and when
, we observe that
,
. System (29) now reduces to:
(40)
The total populations satisfy the scaled equations:
(41)
and
(42)
where
. The dimensionless parameters in the case when
can be deduced from the parameter groupings in Equation (28).
3.2.1. Basic Reproduction Number of the Epidemiological Model
The basic reproduction number,
, measures the average number of secondary infections generated in an absolutely susceptible population by a single infectious individual throughout the period within which the individual is infectious [35]. To compute
using the next generation matrix approach [36], we identify the vector of new infection,
, and the vector of transitions,
, and identify
as the dominant eigenvalue of the next generation matrix
where
,
,
. Here,
is the non-trivial disease free steady state of system (40)-(41). To proceed, we identify all state variables for the infection from system (40) as,
,
,
,
,
,
,
, and their corresponding equations to be:
(43)
It is known that the value of
obtained from the next generation approach is sensitive to the manner in which we interpret transitions and new infections [37]. Here, we can interrogate possibilities concerning the viral particles and the environment: (i) Environmental contamination seen as a transition, (ii) Environmental contamination seen as new infections.
CASE I: The contaminated environment as a transition. This pathway is common with viral infections whereby the viral particles’ population cannot maintain itself through growth in the environment. So, the shedding of viral particle terms by infectious individuals are placed in the transition state rather than the new infection state, giving:
(44)
For;
;
, and
;
. Where:
(45)
The quantities
and
,
, defined in Equation (44), correspond, respectively, to the average number of secondary infections through human-to-human and environment-to-human transmissions caused by one infectious individual in its infectious lifetime. From the expression of
defined in Equation (44), the contribution of each transmission pathway in a viral disease outbreak is separable. Hence, the control efforts can be focused on infectious individuals or the contaminated environment depending on the amount of effort required to reduce the sum of
and
,
, to less than unity.
CASE II: Contaminated environment as a reservoir of infection. By this we mean the environment is assumed to act as a reservoir, where secondary viral particles are added into the environment solely through viral particle shedding by infectious host. By this, we mean, infectious individuals shed viral particles into the environment, these viral particles exists independently, they accumulate and decay over time. Also, these viral particles go on to infect new individuals. Intuitively, infection can happen even after infectious individuals leave, through the environment. Hence, all the shedding rates are placed in the
matrix. Then, after some calculations, we have:
(46)
Here,
and
,
, retain their definitions above. Thus,
separates human-to-human and environmental transmission. Hence,
allows the contributions of quarantined individuals, non-quarantined individuals, human transmission, environmental transmission, or all pathways to be examined separately. We therefore obtain the following result for
in Equation (46).
Lemma 3. Let
and
be given. Define:
(47)
(i) If
, then
.
(ii) If
, then
and if
, then
. Thus,
, and
.
(iii)
and
.
Proof. The proofs of (i) and (ii) are straightforward and are therefore omitted. We prove only the first part of (iii); the second part follows by a similar argument. Suppose
,
and rationalizing
defined in Equation (47) we get
□
Theorem 4. Let
and
be given as in Equations (44) and (46) respectively. Then:
(i)
.
(ii)
whenever
and
whenever
.
(iii)
whenever
, and
whenever
and
.
Proof. We will prove only the first point here as the second point has been proven already in Lemma 3 and the third point is straightforward.
□
Remark. Throughout this article, we shall continue with
defined by Equation (46) and simply refer to it as
.
3.2.2. Existence and Stability of Steady States
We consider only realistic solutions in the sense of Definition 2.1.
Theorem 5 (Existence of steady state solutions). System (40) possesses:
(i) A trivial disease free steady state:
, which exists whenever ;
(ii) a non-trivial disease free steady state:
, which exists whenever ; and
(iii) an endemic steady state: , which exists whenever where satisfies:
or(48)
(49)
The coefficients
are as defined in Equation (64) and
are as defined in Equation (65).
Proof. The steady states of system (40) are solutions of the algebraic system of equations obtained by setting the right hand sides to zero. Let
be a steady state solution of system (40), we get;
(50)
(51)
(52)
(53)
(54)
(55)
(56)
with
(57)
(58)
and
(59)
From (51),
(60)
We now express , , , , , and as a function of and consider the following cases.
Case 1
Let us now consider the case where . Here, ; ; ; ; ;
and . Expressing in Equation (56),
in Equation (50), in Equation (55) each in terms of and substituting appropriate expressions into Equation (57), we get;
(61)
for
(62)
where
and
are as defined in Equation (45). Now, using Equations (60) and (61), we have that, either
(63)
Therefore, implies that, . Which gives
or . Hence, we obtain the trivial and non-trivial disease free equilibria given by
and
respectively. Replacing , and
in Equation (63) and simplifying, we obtain the third order degree polynomial, as defined in Equation (48) where:
(64)
Case 2
This is the case when . Following similar steps as in the first case, we obtain the cubic polynomial in Equation (49), where:
(65)
For
(66)
□
Theorem 6 (On the existence of an endemic steady state). Let
. If,
(67)
(68)
then there exists at least one real positive solution of in Equation (48) and Equation (49) in the interval
.
Proof. We examine two cases: (i) Case One: When . In this case, , a third degree polynomial in
as defined in Equation (48) is a continuous function on the interval
.
and
whenever inequality (67) holds. Also, after some calculations,
and
whenever
. Thus, by the Intermediate Value Theorem, there exists at least one positive real solution of the equation
, for whenever
.
(ii) Case Two: When . In this case, is as defined in (49), and proceeding in a similar manner, Equation (68) holds. Thus, by the Intermediate Value Theorem, there exists at least one positive real solution of .
□
Lemma 7. The disease free steady states defined by Theorem 5 have the following stability properties:
1) The trivial steady state,
, is locally unstable for all parameters, and
2) The non-trivial steady state,
, is locally asymptotically stable if
and unstable if
.
Proof. The local stability of
is determined by the eigenvalues of the Jacobian matrix evaluated at this equilibrium. By exploiting the block structure of the Jacobian and applying the Gershgorin Circle Theorem [33], sufficient conditions ensuring that all eigenvalues have negative real parts are obtained. For , these conditions simplify to:
(69)
where
and
. Similarly, for , we obtain
(70)
Hence,
is locally asymptotically stable whenever the corresponding threshold condition is satisfied. □
Theorem 8 (Global Stability of the non-trivial disease free steady state). The non-trivial disease free steady state of system (40) defined in Theorem 5 is globally asymptotically stable whenever
and unstable whenever
.
Proof. Using the result of Kamgang and Sallet [38], system (40) can be written in the form:
(71)
where is the vector of states. We then decompose this vector of states into which represents densities of susceptible individuals, recovered individuals and the total human population with cadavers, and which represents densities of suspected freely roaming/quarantined individuals, infected/ infectious freely roaming individuals, infected/infectious individuals at homes and treatment centres, disease induced death, and the environmental contributing
compartment respectively, so that
. Thus, and
, where
represents derivative with respect to time. When , the matrices
,
and
are given as;
(72)
(73)
and
(74)
where the
’s and the
’s are matrix entries expressed in terms of the corresponding scaled parameters. Let us now consider the bounded set
defined by
(75)
We write the disease free steady state
as
with
and
.
Using these notations and following the approach in [38], one can easily verify that conditions H1 - H5 are fully satisfied by our system in the bounded set,
as defined in Equation (75). This therefore establishes the fact that the non-trivial steady state
is GAS for system (40). □
4. Sensitivity Analysis and Numerical Simulations
In this section, we carry out simulations in the original parameters of the system when the treatment centres are not full, that is
. Thus system (22) with no barrier measures is given by:
(76)
The equations for the total living human populations
(77)
(78)
and
(79)
4.1. Sensitivity Analysis
Sensitivity analysis identifies parameters that most influence
and hence disease transmission. It may be local or global; here, the Forward Sensitivity Analysis is employed to quantify parameter effects through derivatives of
at a fixed point [39]. The corresponding parameter set is therefore considered in the original parameterization as follows:
According to Chitnis et al. [40], the normalized forward sensitivity index of
with respect to a factor, say
is the ratio of the relative change in
to the relative change in
and represented as:
. For example,
using the baseline parameter values defined on Tables 2-4, we obtained specific values of the normalized local sensitivity coefficients, summarized in Table 5 and illustrated in Figure 3. With this set of values, we got
.
Figure 3. Graph of sensitivity indices of
with respect to the model parameters.
A positive sensitivity index indicates that increasing (decreasing) a parameter leads to an increase (decrease) in
, while a negative index implies the opposite effect. For example,
(Figure 3, Table 5) implies that a 10% increase (decrease) in
results in a 3.36277% increase (decrease) in
, thereby enhancing (reducing) disease transmission. Biologically,
represents the fraction of susceptible individuals who become suspected and freely roaming in the community, suggesting that reducing this rate can help control disease spread.
Table 5. Local sensitivity indices of the threshold parameter
using the parameters’ baseline values on Tables 2-4.
Parameter |
Sen. Index |
Parameter |
Sen. Index |
|
+0.336277 |
|
−0.183905 |
|
+0.201837 |
|
0.000000 |
|
−0.201837 |
|
+0.201837 |
|
−0.009693 |
|
−0.091473 |
|
−0.238855 |
|
+0.034792 |
|
+0.002696 |
|
+0.009601 |
|
+0.091413 |
|
+0.115214 |
|
−0.072646 |
|
+0.072646 |
|
+0.037839 |
|
−0.062352 |
|
+0.283790 |
|
+0.023996 |
|
−0.030942 |
|
+0.018234 |
|
+0.056741 |
|
+0.053897 |
|
−0.012682 |
|
−0.012016 |
|
−0.010151 |
|
−0.017267 |
|
−0.020474 |
|
−0.024526 |
|
−0.009748 |
|
−0.106333 |
|
−0.040885 |
|
0.000000 |
|
−0.040400 |
|
−0.009693 |
It is important to note that model parameters influence
differently. To illustrate the effects of parameter variations, Figure 4 represents 2-D, and 3-D plots of
as a function of: (i)
and
sub-plots 4(a)-(c); (ii)
and
sub-plot 4(b)-(d) respectively with all other parameters as given on Tables 2-4 fixed.
(a) (b)
(c) (d)
Figure 4. 2-D, and 3-D plots of
.
4.2. Numerical Simulation
In this subsection, we perform some numerical simulations on the system (76), using the parameter values on Tables 2-4. In all choices, we used the initial conditions:
(80)
Scenario I: The impact of effective contact rate. Using the baseline parameter values in Tables 2-4, we obtain
,
, and
, with the corresponding numerical trajectories shown in Figure 5(a), Figure 5(c), Figure 5(e) and Figure 5(g). Reducing the effective contact rate to 10% (
), while keeping all other parameters unchanged, yields
,
, and
, as illustrated in Figure 5(b), Figure 5(d), Figure 5(f) and Figure 5(h). These results demonstrate the substantial impact of reducing effective contact on disease transmission.
(a) (b)
(c) (d)
(e) (f)
(g) (h)
Figure 5. Time series curves for system (76).
Scenario II: Estimation of cumulative infection burden and peak sensitivity.
To quantify the cumulative disease burden over the 300-day simulation period, we compute the time-integrated infectious prevalence
(81)
where
denotes a parameter of interest. The quantity
represents the cumulative infectious person-time (person-days), thereby accounting for both the magnitude and duration of infection. Since
is obtained numerically, the integral is evaluated using the composite Simpson’s rule implemented in scipy.integrate.simpson, with 2001 uniformly spaced points over
days, corresponding to a step size of
as illustrated in Figure 6(a) and Figure 6(c).
(a) (b)
(c) (d)
Figure 6. Cumulative burden and peak infectious to parameter variations over 300 days for system (76).
To further assess the influence of key epidemiological parameters, a numerical sensitivity analysis was performed over the same 300-day period. Each parameter range was discretized into 1000 equally spaced values, and the corresponding peak values of
and
were computed. These peaks represent, respectively, the maximum number of confirmed infectious freely roaming individuals and the maximum density of viral particles shed into the environment during the simulation period as illustrated in Figure 6(b) and Figure 6(d).
5. Discussion and Conclusions
We developed a comprehensive mathematical framework for the long-term transmission dynamics of viral diseases that incorporates human behavioural dynamics, non-pharmaceutical interventions, quarantine, re-infection, and environmental viral contamination. The model distinguishes individuals according to their adoption of barrier measures and allows behavioural responses to evolve across disease stages. Treatment-centre capacity is incorporated through two occupancy-dependent regimes. When the treatment-centre occupancy reaches the prescribed capacity
, newly arising cases that cannot be accommodated are redirected to home isolation. The full-capacity and non-full-capacity regimes are therefore formulated and analysed separately, providing the appropriate framework for describing the resulting regime switching at the capacity boundary. Fundamental properties of the model, including existence, uniqueness, non-negativity, and boundedness of solutions, were established. The model was subsequently reparametrized and non-dimensionalized to facilitate its mathematical analysis and numerical investigation.
The analysis of the scaled system considered both the general disease-free model with
barrier measures and the epidemiologically relevant case without barrier measures. The disease-free model admits a non-trivial globally stable equilibrium, with the scaled total human population remaining bounded. For the epidemiological model, the existence of disease-free and endemic equilibria was established, and the basic reproduction number
was derived using two transmission scenarios corresponding to treatment centres being non-full or full. In both cases,
naturally decomposes into human-to-human and environmental contributions, allowing the relative roles of quarantined and non-quarantined individuals and the different transmission pathways to be assessed.
Numerical simulations using SARS-CoV-2-related parameter values demonstrate the strong influence of effective contact rates on disease transmission. In particular, reducing the effective contact rate between susceptible and freely roaming infectious individuals substantially decreases
and can drive the system towards disease control when
. This highlights the importance of effective contact tracing, rapid identification of infectious individuals, and appropriate quarantine enforcement. However, when contact rates remain sufficiently high, quarantine alone may be inadequate to eliminate transmission and may instead support persistent endemic infection. The model further demonstrates that environmental contamination can make a non-negligible contribution to viral transmission, particularly during the early stages of an outbreak. Incorporating environmental viral particles therefore provides a more comprehensive representation of transmission pathways and enhances the potential applicability of the framework to broader One Health settings. The results also emphasize that accurate estimation of
is essential for effective policy design, since both overestimation and underestimation may result in inappropriate levels of intervention and associated epidemiological or socio-economic consequences.
Overall, the findings demonstrate that human behavioural dynamics, contact tracing, isolation, quarantine, and environmental exposure play important roles in shaping viral disease transmission. Although the basic epidemiological model incorporates intervention-related mechanisms such as contact tracing, isolation, and quarantine, the present epidemiological threshold and numerical analyses primarily consider the no-barrier case. Consequently, the implications regarding adherence to multiple barrier measures should be interpreted prospectively. The adherence-transition rates are treated as fixed parameters within each simulation and represent behavioural changes that may reflect prevailing disease risk, public awareness, beliefs, and policy sensitization. Thus, the framework captures behavioural responses through adherence stratification without imposing an explicit prevalence-dependent feedback mechanism, while providing a flexible basis for investigating how adherence, reductions in effective contact rates, and reduced environmental exposure may influence disease transmission.
A limitation of the present study is that the numerical simulations are scenario-based rather than calibrated predictions, as several transition, contact, and viral-shedding parameters are assumed or weighted using available information rather than estimated from a specific population-level dataset. Explicit analysis of interactions among multiple barrier measures, vaccination and other pharmaceutical interventions, as well as stochastic effects, remains an important direction for future work. In addition, incorporating well-defined epidemiological datasets and appropriate statistical parameter-estimation methods will improve model calibration and predictive capacity, thereby providing a more comprehensive representation of viral disease dynamics.
Acknowledgements
JAN, GAN and MIT-E acknowledge the component of Canada’s International Development Research Center Grant No. 109559-001, to the University of Buea in 2020, when aspects of this work were conceived. GAN and JAN also acknowledge support from the Cameroonian Ministry of Higher Education through the initiative for the modernisation of research in Cameroon’s Higher Education for the 2023, 2024 and 2025 granting seasons. JAN acknowledges support from the Erasmus+ student mobility grants enabling him to make significant progress on this work at Cotbus university in Germany. He additionally acknowledges support from the CDC-IMU programme for Graduate Assistantship in Developing Countries (GRAID) for the 2021, 2022 and 2023 granting seasons. All Authors acknowledge the sponsorship of the Commission for Developing Countries (CDC) in conjunction with the International Mathematics Union (IMU) through the CDC-ADMP (African Diaspora Mathematicians Program) grant that made it possible for interactive collaborative work during the 2018 and 2019 grant sponsored visits to the University of Buea by MIT-E during which period the international collaboration was forged.
Author Contributions
Conceptualization, the model was jointly developed by all three authors; methodology, all three authors agreed on the methodology and the analyses presented; formal analysis, was conducted by James A. Njongwe under the surpervisor of G.A. Ngwa and M.I. Teboh-Ewungkem; writing, review and editing, was done by all three authors in a concensus framework; visualization, James A. Njongwe did the simulations; supervision, was done by G.A. Ngwa and M.I. Teboh-Ewungkem; project administration, G.A. Ngwa; funding acquisition, G.A. Ngwa and M.I. Teboh-Ewungkem. All authors have read and agreed to the published version of the manuscript.