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ARTICLE
EPITIME: A Computational Framework for Integral Epidemic Models with Structure-Preserving Discretizations
1 Department of Mathematics and Applications “Renato Caccioppoli”, University of Naples Federico II, Via Cintia, Naples, Italy
2 Institute for Applied Mathematics “Mauro Picone”, National Research Council of Italy, Via P. Castellino, Naples, Italy
3 Department of Mathematics and Computer Science, University of Ferrara, Via Saragat, Ferrara, Italy
* Corresponding Author: Bruno Buonomo. Email:
(This article belongs to the Special Issue: Advances in Mathematical Modeling: Numerical Approaches and Simulation for Computational Biology)
Computer Modeling in Engineering & Sciences 2026, 148(3), 27 https://doi.org/10.32604/cmes.2026.084828
Received 29 April 2026; Accepted 30 July 2026; Issue published 28 September 2026
Abstract
EPITIME, a computational framework for the simulation of two classes of integral epidemic models, namely an age of infection model and an information-dependent behavioural model, is presented. The main contributions of this work are the design and implementation of a modular MATLAB/Python software environment built upon previously developed structure-preserving non-standard finite difference discretizations. The solvers are complemented by input parsing and validation routines, performance indicators, reproducibility tools and user-oriented graphical interfaces. The preserved structures are specific to the underlying model and include positivity, monotonicity, final-size behaviour and extinction of infectivity for the age of infection model, and positivity, boundedness, positively invariant regions and equilibrium/threshold structure for the behavioural model. The numerical schemes for both model classes and their main analytical properties, including first-order convergence, are outlined. The software architecture is then described and its use is illustrated through numerical experiments on asymptotic behaviour, inverse reconstruction of an infectivity kernel from COVID-19 incidence data, and behavioural dynamics under different memory kernels. Performance, scalability and computational complexity analyses, together with comparisons against quadrature-based approaches, are also presented. Overall, EPITIME provides a reliable and accessible computational environment for the numerical study of renewal epidemic models.Keywords
Mathematical epidemiology has long relied on compartmental models to describe the spread of infectious diseases, with SIR- and SEIR-type systems providing a standard framework for the analysis of transmission dynamics, threshold quantities and control strategies [1,2]. However, several epidemiologically relevant mechanisms, including infection-age dependence, variable infectiousness and memory effects, are more naturally represented within integral formulations than through finite-dimensional compartmental systems alone [3]. Integral models replace constant transition rates with infectivity kernels, allowing for a more general representation of how infectiousness evolves over the course of the disease and naturally incorporating distributed delay effects, such as those induced by incubation and latency periods.
In this context, Brauer and coauthors [1] provided a comprehensive treatment of Age of Infection (AoI) epidemic models, clarifying their analytical properties and their connections to standard compartmental systems. Furthermore, Diekmann and collaborators developed a unified renewal-equation framework for epidemic models that systematically incorporates key biological features such as demography, non-permanent immunity and heterogeneous infectivity. Within this setting, the Force of Infection (FoI), that is the rate at which susceptibles become infected, is expressed through a scalar renewal equation driven by an infectivity function. Classical compartmental models are recovered as particular limiting cases [4,5].
In parallel, increasing attention has been devoted to epidemic models that account for behavioural adaptation, where transmission is affected not only by biological factors but also by changes in human behaviour driven by information, perceived risk, or epidemic awareness [6]. In this setting, integral formulations are particularly natural, since both infection-age effects and behavioural responses can be described through history-dependent terms and distributed kernels. This perspective is especially relevant for information-dependent epidemic models, in which transmission is modulated by an information index reflecting the effect of past epidemic trends on present contact behaviour [7–10].
The numerical approximation of integral epidemic models poses several challenges, especially when one aims to preserve crucial qualitative features of the continuous dynamics, such as positivity, boundedness, invariant regions, equilibrium structure and long-time behaviour. In epidemiological applications, the loss of these structural properties may lead to spurious numerical behaviour and unreliable long-time simulations. For this reason, Non-Standard Finite Difference (NSFD) methods and other structure-preserving discretization techniques have become increasingly relevant in the numerical analysis of epidemic models [11–13]. Appropriately constructed NSFD schemes can retain selected dynamical properties of the underlying continuous problem for arbitrary time steps, under the assumptions associated with each scheme.
Several numerical approaches have been developed for epidemic models with memory, including methods for delay differential equations, distributed-delay and integro-differential equations, fractional-order models and age-structured PDEs. Structure-preserving discretizations have also been proposed for delayed compartmental models, including NSFD schemes designed to retain positivity, boundedness, equilibria and stability or global-dynamics properties [14,15]. Distributed-delay and integro-differential problems can be addressed by direct quadrature and collocation methods [16], as well as by fast convolution techniques designed for evolution equations with memory [17,18]. Alternatively, reduction approaches may approximate the memory kernel by sums of exponentials or related expansions, thereby transforming the distributed-delay term into an enlarged ODE or DDE system [19]. A related but distinct line of research concerns fractional epidemic models, where memory effects are represented by nonlocal derivative operators. In this context, wavelet-based and related high-order methods have been proposed for delayed and piecewise-fractional epidemic dynamics [20,21]. These approaches are particularly relevant when the main objective is the accurate resolution of fractional or delayed fractional dynamics.
Beyond the choice of the numerical discretization, the availability of dedicated software represents a further practical issue. Compartmental epidemic models formulated as Ordinary Differential Equations (ODEs) can rely on widely available and well-established software environments, whereas software for epidemic models governed by integral equations is much less common. This gap is particularly relevant because the specific structure of integral epidemic models, with history-dependent terms, often requires dedicated implementations rather than the direct use of general-purpose solvers.
Several software environments have been developed to support epidemic modelling and simulation. For instance, EpiModel provides an R-based framework for deterministic compartmental, stochastic individual-contact and network epidemic models [22]. Agent- and individual-based epidemic simulation is supported by tools such as Covasim, originally developed for COVID-19 dynamics and intervention analysis [23], and EMOD, a modular individual-based platform for infectious-disease modelling [24]. Spatially explicit and metapopulation epidemic simulations are addressed by frameworks such as GLEAMviz, which combines stochastic epidemic models with global demographic and mobility data [25], and by the Spatiotemporal Epidemiological Modeler (STEM), an open-source environment for spatial and temporal infectious-disease modelling [26,27]. More recently, Epydemix has provided a Python-based framework for the specification, simulation and calibration of stochastic compartmental epidemic models, including demographic structure, contact matrices and Approximate Bayesian Computation tools [28]. Complementary statistical tools also include epidemia, an R package for semi-mechanistic Bayesian modelling of infectious diseases in which transmission dynamics are represented through renewal equations and used for inference, forecasting and scenario analysis [29].
Other computational tools address specific classes of dynamical systems with memory or delay. For example, DDE-BIFTOOL provides MATLAB routines for bifurcation and stability analysis of delay differential equations [30,31]. Similarly, the software collection developed within the CDLab (Computational Dynamics Laboratory), University of Udine, includes tools for the numerical analysis of delay equations and related dynamical systems, such as TRACE-DDE for the computation of characteristic roots and stability charts of delay differential equations [32,33].
Among recent epidemic simulation frameworks, MEmilio is especially relevant to the present work because it explicitly includes integro-differential, or age of infection, epidemic models within a broader multi-model software architecture [34,35]. MEmilio is a modular high-performance framework supporting ODE, integro-differential and agent-based models, together with mobility models and scalable computational implementations. Its IDE-based modelling component has also been developed in connection with NSFD numerical schemes for SECIR-type integro-differential epidemic models with non-exponentially distributed stay times [36].
Despite this broad range of available tools, dedicated computational frameworks for renewal-type integral epidemic models remain comparatively limited. In particular, the software environments discussed above mainly focus on compartmental, network-based, agent-based, individual-based, metapopulation or statistical inference formulations, while general-purpose delay-equation tools are mainly designed for stability, bifurcation or dynamical-systems analysis rather than for the direct simulation of integral epidemic models while preserving their epidemiologically relevant structure.
Motivated by these considerations, this work presents EPITIME (EPidemic Integral models TIMe-profile Explorer), a computational framework for the simulation of two classes of integral epidemic models: an age of infection model and an information-dependent behavioural model. The main focus of the present manuscript is the design and development of a dedicated modular software environment. The continuous epidemic models and the corresponding structure-preserving NSFD discretizations are based on earlier analytical and numerical results. These results are recalled here to provide the mathematical background for the software design and to identify the properties inherited by the implementation.
Compared with broad epidemic simulation environments such as MEmilio, EPITIME has a narrower and complementary scope. It is designed as a dedicated MATLAB/Python framework for selected renewal-type integral epidemic models. Both EPITIME and the IDE component of MEmilio employ structure-preserving non-standard discretizations for history-dependent epidemic dynamics. However, MEmilio implements a detailed SECIR integro-differential model based on transition flows, whereas EPITIME focuses on compact renewal formulations in which the FoI is expressed directly through infectivity kernels.
The MATLAB and Python implementations include input parsing and validation, parameter handling, consistency checks, warning mechanisms and performance indicators to support reproducible numerical experimentation. Furthermore, the interdisciplinary nature of epidemic modelling motivates the development of graphical interfaces that make computational tools accessible to researchers and professionals with diverse scientific backgrounds, including epidemiologists, public-health specialists and policy planners, whose expertise may not extend to the technical aspects of code implementation and numerical analysis. The capabilities of EPITIME are illustrated through representative case studies, including long-time simulations, final-size computations, behavioural dynamics under different memory kernels, and inverse reconstruction of an infectivity kernel from COVID-19 incidence data. Computational performance and scalability are also analysed, with particular attention to history-dependent convolution terms and the implemented truncation strategy. Fast convolution techniques are discussed as a possible future extension.
The paper is organized as follows. Section 2 presents the two epidemic models considered in this work. Section 3 introduces a unifying formulation and reviews the corresponding NSFD discretizations and their main qualitative properties. Section 4 is devoted to the description of the EPITIME software environment, including its MATLAB and Python implementations and the graphical user interface. Section 5 reports a selection of numerical experiments, including tests on asymptotic behaviour, inverse-problem reconstruction and simulations illustrating the qualitative dynamics of the behavioural model. Final remarks are given in Section 6. Two appendices precede the References section, collecting a unified notation guide (Appendix A) and indications on software validation and reproducibility (Appendix B).
In the following sections, two classes of integral epidemic models are considered, distinguishing between formulations in which the FoI depends solely on biological factors and those that explicitly incorporate human behavioural feedback through information-dependent transmission mechanisms.
2.1 The Age of Infection Epidemic Model
The model defined in [1, Chapter 4.5] traces the evolution of an epidemic within a closed population taking into account the cumulative contribution of past infections to the current FoI. The model reads
and we refer to Table 1 for a complete description of the variables, parameters and functions.

Here,
A numerical approximation method for (1), specifically designed to unconditionally preserve selected qualitative properties of the continuous solution, is recalled in Section 3.1. Furthermore, some insights on the asymptotic behaviour of the continuous and numerical solutions to (1) are provided in Section 5.2.
2.2 The Integral Behavioural Epidemic Model
Here, an integral epidemic model is considered that accounts for changes in individual behaviour during an epidemic outbreak by incorporating a time-varying information index
Table 2 provides the unknowns, parameters and known functions of model (2), together with their interpretations and the associated assumptions. Some of the key functions involved are described in more detail in what follows.

In particular, the function
Model (2) can be regarded as a natural extension of the work by Breda et al. [4], starting from their formulation and incorporating a dependence of the FoI on the information index. A variant of (2) including incidence–dependent contact patterns is outlined in [9]. There,
Section 3.2 reviews a numerical approximation technique for model (2) that is specifically constructed to unconditionally preserve selected qualitative properties of its solution.
To improve readability, Appendix A summarizes the main symbols that are used across the two model classes, their discrete counterparts, and the software implementation. Model-specific notation, assumptions and qualitative properties are reported separately in Tables 1 and 2.
3 Solution Methods and Algorithms
To discuss efficient simulation methods for the models introduced in the previous sections, a unifying
is addressed, where the constants
and, for
respectively.
The numerical discretizations presented in the subsequent sections are based on previously developed structure-preserving NSFD methods, which are briefly recalled here to highlight the qualitative properties preserved within the EPITIME software environment. The schemes used in this work exploit the following first-order non-standard approximations of the derivative and integral operators
which hold for each fixed
3.1 The NSFD Discretization for the Age of Infection Model
Throughout this section, problem (1) is considered and it is assumed that the non-negative function
is prescribed. As discussed in [43],
with equality attained when all such individuals have infection age zero at
Let
for

The method (7) belongs to the class of NSFD methods, originally developed for differential equations (see [11] and references therein) and recently extended to integral formulations [13,42]. The following result establishes first-order convergence on finite time intervals. For a detailed error analysis, the reader is referred to Lemma 3.1, Theorems 3.2 and 4.1 in [12].
Theorem 1: Consider problem (1) and assume that
A key advantage of the NSFD discretization (7) is that it unconditionally preserves the positivity, the monotonicity and the asymptotic behaviour of the continuous solution to (1). These properties, established in Theorem 3.4 in [12] are summarized in the following result.
Theorem 2: Let
3.2 The NSFD Discretization for the Integral Behavioural Epidemic Model
Following the approach and the model formulations presented in [44], to solve the integro-differential system (2), the forcing terms
are assumed to be given non-negative functions. More precisely, these functions are chosen as suggested in [44]:
Discretizing the system (2) as detailed in Eqs. (4a) and (4b), with
where
A comprehensive analysis of the discrete system (9a)–(9c) is carried out in [44], where the existence and stability of the discrete equilibria are also investigated. In what follows, only a brief overview of these findings is presented, starting from the linear convergence of the method (9a)–(9c).
Theorem 3: Consider the problem (2) and assume that
Assume, in addition to the properties listed in Table 2, that
Under the above assumptions, the rectangular quadrature rule gives,

With this choice the normalization condition
is defined, where the upper bounds are given by
With
Theorem 4: Suppose that
The discrete model (9a)–(9c) always admits the disease-free equilibrium
and independently of the choice of the kernel
3.2.1 Approximation of the Infinite Discrete Normalization Sum
The exact normalization factor in (11) involves an infinite series. In the current implementation, two alternatives are available for the treatment of the memory normalization, with the choice left to the user. Both options retain first-order consistency. The qualitative properties of the continuous solution are preserved, as detailed in what follows.
Unnormalized option. A straightforward choice is to set
Truncated-renormalized option. The infinite series in (11) is replaced by a truncated sum. Specifically, given
assuring the exact discrete normalization. Here, the cutoff index
for a prescribed constant
The computational cost of this strategy depends on the shape of the memory kernel and, in particular, on its decay rate, since non-monotone or slowly decaying kernels generally require larger values of
Condition (16) is the theoretical requirement ensuring that the neglected discrete tail is of the same order as the time-discretization error. In the implementation, this condition is approximated by the practical block criterion described below, which is used as a heuristic stopping rule. In practice, the cutoff index
are grouped into consecutive blocks of fixed length
the contributions of the last
where
In the present implementation, the values
are set, which are adequate for all the kernels considered in this work.
4 Tool Description and Core Kernels
This section presents the software packages developed for the numerical methods introduced in Section 3. The codes are freely available at github.com/ghitan/EPITIME. The implementations are designed to prioritize vectorized operations and adopt a modular organization. They are structured into clearly identified code blocks (CB), which are consistently referenced throughout this section. Each block corresponds to a specific component of the package and is labelled MCB:A – MCB:G in MATLAB and PCB:A – PCB:G in Python.
The NSFD scheme (7) is implemented in MATLAB and Python within the function NSFD_AoI. Each solver accepts either a structured input (struct/dict) or individual arguments and automatically assigns default values to any missing fields. The main inputs of our routines are:
• the initial susceptible population
• the final time
• the contact rate
• a verbosity binary flag that controls warning messages (0 to suppress them, 1 to enable them).
The primary outputs are the discrete time vector t and the solution matrix Y, whose


The total CPU time (elapsed_time) is measured with the built-in tic/toc functions in MATLAB and with time.time() in Python. The memory usage (memory_bytes) is estimated through the whos routine in MATLAB and through the .nbytes attribute in Python. The total number of floating-point operations (flops_number) is computed by counting the arithmetic operations at each time step. This yields, at the
The core time-stepping blocks implementing the NSFD update are shown in Listings 3 and 4. Both versions rely on vectorized operations and compute the discrete convolution through optimized matrix-vector products, thus avoiding explicit summation loops. A minor implementation detail concerns the case in which the final time


In addition to the core solver, the implementation relies on two auxiliary functions that handle input parsing and validation. Their purpose is to define default parameter values, complete missing entries and ensure the consistency of the problem definition before the time-stepping begins. The first auxiliary function, denoted parse_input in MATLAB (MCB:F) and_parse_input in Python (PCB:F), collects the user-provided arguments and fills any missing values with predefined defaults. In MATLAB, the defaults are
defaults = struct(’S0’, 990, ’N’, 1000, ’T’, 10, ’h’, 0.1, ’beta’, …
2.5e-3, ’A’, @(t) exp(-3*t), ’phi0’, [], ’verbosity’, 1);
and in Python the corresponding dictionary is
defaults = { ’S0’: 990, ’N’: 1000, ’T’: 10, ’h’: 0.1, ’beta’: 2.5e-3,
’A’: lambdat: np.exp(-3.0*t), ’phi0’: None, ’verbosity’: 1}
If the field phi0 is not provided, it is automatically defined as
The second auxiliary function, check_input in MATLAB (MCB:G) and _check_input in Python (PCB:G), verifies all input fields in accordance with the properties summarized in Table 1. Scalar parameters such as
validateattributes(S0, {’numeric’}, {’scalar’, ’positive’, ’finite’}, ...
mfilename, ’S0’);
while in Python an analogous test is
if S0 <= 0 or not np.isfinite(S0):
raise ValueError(’S0 must be positive and finite.’)
Furthermore, vector inputs corresponding to the kernel
if any(P0(:) > (N - S0) * A_val(:) + eps)
warning(’Some phi0 values exceed theoretical upper bound’);
end
and in Python using NumPy operations
Eps = np.finfo(np.float64).eps
if np.any(P0.flatten() > (N - S0) * A_val.flatten() + Eps):
print(’Warning: Some phi0 values exceed theoretical upper bound’)
Any violation of essential constraints triggers an error that immediately stops execution, whereas minor inconsistencies generate warnings if the verbosity flag is active. This layered validation ensures that the solver operates on a fully defined and consistent problem before entering the time-stepping phase.
4.2 The NSFD_behavioural Software
The NSFD scheme (9a)–(9c) for the behavioural model is developed in both MATLAB and Python within the function NSFD_behavioural. Specifically, our codes implement the non-standard discretization of (2), expressed in terms of the standardized quantities
with normalization factor
The NSFD_behavioural solver supports both structured inputs and explicit argument passing, with default values automatically assigned whenever optional parameters are omitted. The primary inputs are described below:
• the final time
• the initial susceptible population
• the total population size
• the infectivity function
• a boolean parameter compGamh for the automatic computation of the cutoff index (0 to disable it, 1 to enable it),
• a verbosity binary flag that controls warning messages (0 to suppress them, 1 to enable them).
As main outputs, the epidemiologically most relevant quantities only are retained,
The corresponding approximations for the functions in the original model (2) may be retrieved by multiplying these normalized values by the constant


The execution time (elapsed_time) is recorded using native timing utilities in the two environments, namely the tic/toc pair in MATLAB and the time.time() function in Python. The amount of memory required by the algorithm (memory_bytes) is evaluated by relying on built-in inspection tools, specifically the whos command in MATLAB and the .nbytes property in Python. The total number of floating-point operations (flops_number) is estimated by explicitly counting the arithmetic operations performed at each time step. The update of
The core time-stepping routines for the present method (see Listings 7 and 8) adhere to the same implementation principles outlined in the previous section. A minor yet relevant difference is the preliminary computation of the non-standard weight


Similarly to the NSFD_AoI function, the solver NSFD_behavioural is complemented by auxiliary routines devoted to input parsing and validation. These auxiliary modules assign default values, complete missing parameters and verify the consistency of the problem setup before the time-stepping phase. Since their functionality mirrors that already described in Section 4.1, only the differences in the prescribed default values are reported here. The input-handling function is denoted by parse_input in MATLAB (MCB:F) and the default parameters are set as follows:
defaults = struct(’T’,1000,‘h’,1,’N’,5e7,’mu’,1/(75*365), ...
’S0’,0.2*5e7,’A’,[],’K’,[],’betaM’,[], ...
’g’,[],’CompGamh’,1,’verbosity’,1);
The corresponding function in Python is denoted as _parse_input (PCB:F), and the default parameters are
defaults = {’T’: 1000, ’h’: 1, ’N’: 5e7, ’mu’: 1 / (75 * 365),
’S0’: 0.2 * 5e7, ’A’: None, ’K’: None,
’betaM’: None, ’g’: None, ’CompGamh’: 1, ’verbosity’: 1}
If any of the core functions are not provided, they are automatically initialized with the following default definitions
with
The interdisciplinary nature of epidemic modelling often requires numerical tools to be used by researchers and professionals whose expertise lies in epidemiology, public health or policy planning rather than in numerical analysis and scientific programming. To address this need, EPITIME includes a MATLAB Graphical User Interface (GUI) that provides direct access to the AoI simulation tool without requiring users to modify or run the underlying code. Practical instructions for launching and operating the interface are reported in Appendix B.3.
Through the GUI, users can specify the epidemiological parameters and the model functions
Fig. 1 shows the interface after a simulation with the default functions
and parameters

Figure 1: The AoI simulation GUI after a successful run with the default model functions
Two representative examples illustrate how the GUI can support numerical exploration. In the first test, the functions
are considered together with

Figure 2: The AoI simulation GUI for
The second test reproduces the experiment defined in (20) and discussed in Section 5.2. In this case, the GUI connects the analytical results with their numerical counterpart by allowing the predicted asymptotic behaviour to be examined directly from the computed profiles. Fig. 3 shows the resulting simulation. More generally, this type of experiment enables users to vary the model data and assess how infection-age profiles and epidemiological parameters affect transient and long-time dynamics.

Figure 3: The AoI simulation GUI for the test case defined in (20) and discussed in Section 5.2.
A Python interface with equivalent functionality is also provided in the EPITIME repository as an interactive Jupyter notebook (AoI_Simulation_Tool.ipynb).
4.4 Theoretical Assumptions and Software Validation
The analytical properties stated in Sections 2 and 3 rely on the assumptions listed in Tables 1 and 2. In particular, the infectivity and memory kernels are assumed to be non-negative and integrable on
In the software implementation, only those assumptions that can be checked numerically are enforced. Specifically, the sampled values of the user-defined kernels on the computational grid are required to be finite and non-negative. For the behavioural model, the discrete memory kernel is normalized through the factor
If a user provides kernels that violate the numerical checks, the solver returns an error or a warning, depending on the severity of the violation. When the analytical assumptions are not satisfied, the code may still produce a numerical trajectory, but the structure-preserving and convergence results proved in the paper are no longer guaranteed.
5 Numerical Experiments and Case Studies
This section presents numerical experiments designed to illustrate the accuracy, structure-preserving properties, and practical applicability of the proposed schemes.
The evaluation of the history-dependent convolution terms in (1) and (2) requires the accumulation of contributions from all previously computed time levels. Consequently, as discussed in Section 4, the computational cost of the proposed software framework is expected to scale quadratically with respect to the number
The analysis is carried out on the fixed time interval
Specifically, two performance indicators are considered. The first is the execution time. In MATLAB, this quantity is measured through the built-in timeitroutine, which automatically performs multiple evaluations of the target function and returns a statistically robust estimate of the execution cost. In Python, the execution time is measured through the standard timeit module by performing several batches of repeated solver evaluations and retaining the minimum average runtime. This procedure closely mirrors the philosophy of MATLAB’s timeit routine and reduces the influence of transient system disturbances. The second indicator is the memory requirement. For both implementations, this quantity is extracted from the optional performance structure P returned by the solver (cf. Listings 5 and 6).
Fig. 4 reports the NSFD_AoI runtime and memory requirements in semi-log scale together with the reference growth laws

Figure 4: Experimental scalability analysis of the NSFD_AoI solver implemented in MATLAB (a) and Python (b). For both implementations, memory consumption (left panel within each subfigure) and execution time (right panel within each subfigure) are reported as functions of the number
Similar outcomes, reported in Fig. 5, are obtained for both the implementations of the NSFD_behavioural solver.

Figure 5: Experimental scalability analysis of the NSFD_behavioural solver implemented in MATLAB (a) and Python (b). For both implementations, memory consumption (left panel within each subfigure) and execution time (right panel within each subfigure) are reported as functions of the number
5.2 The Final Size and the Basic Reproduction Number
The first test case examines the asymptotic behaviour of the NSFD solution to (1), with particular emphasis on the convergence of the numerical final size towards its continuous counterpart. To begin with, recall that the final size of the epidemic, defined as
where
is the basic reproduction number, that is the expected number of secondary cases generated by a single primary case in a fully susceptible population in the absence of interventions [1]. Furthermore, under suitable regularity assumptions (see, for instance, Section 3 in [46]) it follows that
At the discrete level, the numerical final size
Note that, in addition to the assumptions listed in Table 1, if
then
Specifically, the scenario in which

Figure 6: Time evolution of the susceptible population

To further illustrate the importance of structure-preserving discretizations, we repeat the previous experiment with
Although more accurate for sufficiently small step-sizes, the TrapDQ method produces physically inadmissible solutions for

Figure 7: Comparison between the NSFD and TrapDQ solutions for the AoI test case (20), with
5.3 An Inverse Problem Framework for Inferring COVID-19 Infectivity Kernel
Despite the modeling potential of the integro-differential system (1), the identification of a contact rate
Focusing on the first equation of model (1), the normalized incidence and its NSFD approximation are defined as
where

Figure 8: Normalized daily COVID-19 incidence in Italy (24 February 2020–8 January 2025), including raw data from [52] and the corresponding smoothed profile obtained via quadratic regression. Here, the normalization is performed with respect to the maximum value, yielding
To select a functional form for the kernel
where the coefficients
which yields the data-informed contact rate
• a mean squared error over the entire dataset, measuring the global discrepancy between observed and simulated incidences;
• a peak error term, enforcing accuracy at the time of maximum observed incidence;
• an initial-time penalty, ensuring consistency at the onset of the epidemic;
• a yearly error term, enforcing accurate reconstruction of early-stage dynamics over the first 365 days.
The weights
to lie within a prescribed plausible range. These bounds, set to
The model calibration problem formulated in (21) is addressed in the MATLAB live script NSFD_AoI_LIVE. This implementation allows the user to select both the dimension of the Bernstein polynomial space (we take

Figure 9: Comparison of the empirical COVID-19 normalized incidence in Italy with the simulated incidence (left panel), the corresponding estimated infectivity kernel (middle panel) and the pointwise quadratic error relative to the data (right panel). Here, the optimized contact rate is
Remark 1: The present case study serves as a data-driven benchmark to assess the reliability of the EPITIME framework, rather than a standalone identifiability analysis. The underlying inverse problem is inherently ill-posed and presents several coupled methodological challenges. Specifically, the inverse map may lack full identifiability from incidence data, as distinct infectivity kernels can produce identical incidence trajectories. Regarding approximation, while the implicit smoothing of the Bernstein representation promotes stability, the procedure could benefit from explicit Tikhonov-type regularization (see, for instance, [55]). Furthermore, the characteristically slow convergence of Bernstein expansions requires high polynomial degrees to ensure sufficient representational capacity, leading to the heuristic selection of
5.4 Qualitative Properties of Solutions to the Integral Behavioural Epidemic Model
Before presenting the numerical experiments, the main qualitative properties of the behavioural integral epidemic model (2) and of its discrete counterpart (9a)–(9c) are briefly recalled. Under the assumptions stated in Section 3.2, the continuous model admits a positively invariant region, always possesses the disease-free equilibrium DFE, and admits a unique endemic equilibrium EE whenever
In this section, we illustrate two numerical examples based on the non-standard discretization (9a)–(9c) of model (2). In both experiments, the NSFD scheme is applied with
The infectivity function
For the first numerical experiment, the following values are considered:
where
with
Fig. 10 shows the time evolution of the driving factor of the FoI,
with

Figure 10: Normalized driving factor of the force of infection,
As a second numerical experiment, the trapezoidal infectivity function given by
is considered instead, where
with
The corresponding results are displayed in Fig. 11. As discussed in more detail in [8], in this case no convergence to the endemic equilibrium is observed. Instead, self-sustained oscillations arise, suggesting that the endemic equilibrium is numerically unstable.

Figure 11: Normalized driving factor of the force of infection,
5.5 Estimation of the Epidemic Peak
A further computational task supported by EPITIME is the estimation of epidemic peaks and peak times. For classical compartmental models, and in particular for the autonomous SIR model, peak-time formulae and approximations have been investigated in several works [57–60]. Related peak-date estimates have also been obtained for generalized SEIR and infection-age structured models [61]. Recent renewal-equation analyses have also investigated final-size and peak-size relations for infection-age models incorporating latency and behaviour-dependent transmission. Analytical information on peak quantities can be obtained for some reduced model structures [62]. For general renewal and age of infection models with arbitrary infectivity kernels, closed-form peak-time formulae are generally unavailable, and peak quantities must be estimated from the numerical solution. For the AoI model (1), we define the epidemic peak and the corresponding peak time in terms of the force of infection as
The minimum selects the first global peak when the maximum is attained at more than one time. At the discrete level, EPITIME computes
To validate this peak-detection procedure in a benchmark case where a SIR reference is available, the exponential infectivity kernel
is considered. With this choice, the AoI formulation recovers the classical autonomous SIR dynamics. The reference peak times


Figure 12: Convergence of the epidemic peak time approximation. The relative error exhibits a linear decay with respect to
Regarding the behavioural model, in the context of epidemic peak estimation, we investigated both the driving factor of the FoI,
The corresponding numerical peak time is obtained as the time point associated with the maximum value of the selected observable. As illustrated in Fig. 13 and Table 5, when several local maxima occur, as may happen in the presence of behavioural feedback and memory, both local and global peak times can be reported.

Figure 13: Epidemic peaks for the driving factor of the FoI

6 Conclusions and Future Directions
A computational framework, EPITIME, has been developed for the simulation of two classes of renewal-type epidemic models: an age of infection model and an information-dependent behavioural model. The framework combines structure-preserving NSFD discretizations with modular implementations in MATLAB and Python. The solvers are complemented by input-validation routines, performance indicators, reproducibility tools and graphical interfaces. The numerical experiments have illustrated the use of the framework for the study of final-size behaviour, the reconstruction of an infectivity kernel from incidence data, the analysis of behavioural dynamics under different memory kernels, and the detection of epidemic peaks.
A main strength of EPITIME is the close connection between the analytical properties of the models and their numerical implementation. The schemes preserve model-specific properties such as positivity, monotonicity, boundedness, invariant regions, extinction of infectivity and equilibrium or threshold structure. This makes the framework particularly suitable for long-time simulations, for which standard discretizations may produce non-physical solutions. At the same time, the modular organization of the software allows the kernels and behavioural response functions to be changed without modifying the main solver structure.
The present release is intentionally focused on the two deterministic models considered in this work. This choice makes it possible to provide clear mathematical guarantees, but it also defines a natural path for future development. The framework is planned to be extended to a more general renewal formulation, which includes the age of infection model as a special case. Further extensions will address heterogeneous populations, the distinction between symptomatic and asymptomatic infections, and viral shedding effects. Vaccination dynamics also represent an important direction. In the AoI setting, vaccination could be introduced through additional vaccinated classes, allowing vaccine-induced changes in susceptibility, breakthrough infections and waning immunity to be represented within the renewal formulation. Vaccination-induced changes in infectivity could also be accounted for by suitable infectivity kernels. In the behavioural model, vaccine uptake could additionally be coupled with information-dependent responses and memory effects, extending ODE-based formulations with vaccination choices driven by information and perceived risk.
Further work will also concern the numerical methods. The schemes implemented in the current release are first-order accurate and favour robustness and structure preservation. Fine temporal grids may nevertheless be required when high accuracy is needed for rapidly varying solutions, peak times or peak sizes. Higher-order structure-preserving discretizations and more accurate procedures for the estimation of epidemic peaks will therefore be investigated. Their construction will have to retain the unconditional qualitative properties that characterize the present methods.
The direct vectorized evaluation of the history terms provides a transparent implementation that closely follows the discrete equations, but its computational cost is quadratic in the number of time steps. This may become restrictive for very long simulations or inverse problems involving repeated solver evaluations. Future versions are intended to include suitable acceleration strategies. For exponential and Erlang kernels, auxiliary recursions or linear-chain representations may reduce the computational cost to linear complexity. For more general kernels, possible approaches include FFT-based and other fast convolution techniques, and sum of exponentials approximations. A central part of this development will be the control of the additional approximation error and the verification that positivity, kernel normalization and equilibrium properties are not lost.
Finally, the theoretical guarantees of the solvers depend on assumptions on the user-defined kernels and behavioural functions, such as non-negativity, integrability and sufficient regularity. These conditions cannot all be verified automatically, and future releases will include more extensive diagnostic checks and clearer guidance on admissible inputs. The inverse reconstruction presented in this work should also be viewed as a computational benchmark rather than as a complete epidemiological inference procedure. Further investigations will address identifiability, regularization, data preprocessing, measurement noise and uncertainty propagation, together with validation on additional datasets. The graphical interfaces will be developed in parallel by adding context-sensitive help and concise instructions, with the aim of making the framework easier to use while preserving a clear connection with its mathematical background.
6.1Acknowledgement: This work has been performed under the auspices of the Italian National Group for Scientific Computing (GNCS) and the Italian National Group for Mathematical Physics (GNFM) of the National Institute for Advanced Mathematics (INdAM).
Funding Statement: The authors received no specific funding for this study.
Author Contributions: The authors confirm contribution to the paper as follows: Conceptualization, Bruno Buonomo and Eleonora Messina; methodology, Eleonora Messina, Mario Pezzella and Gaetano Zanghirati; software, Claudia Panico, Mario Pezzella and Gaetano Zanghirati; validation, Bruno Buonomo, Eleonora Messina, Claudia Panico, Mario Pezzella and Gaetano Zanghirati; formal analysis, Claudia Panico, Mario Pezzella and Gaetano Zanghirati; investigation, Eleonora Messina, Claudia Panico, Mario Pezzella and Gaetano Zanghirati; data curation, Mario Pezzella; writing—original draft preparation, Claudia Panico, Mario Pezzella and Gaetano Zanghirati; writing—review and editing, Bruno Buonomo, Eleonora Messina, Mario Pezzella and Gaetano Zanghirati; visualization, Claudia Panico, Mario Pezzella and Gaetano Zanghirati; supervision, Bruno Buonomo, Eleonora Messina, and Gaetano Zanghirati. All authors reviewed and approved the final version of the manuscript.
Availability of Data and Materials: The EPITIME software described in this work is publicly available at https://github.com/ghitan/EPITIME (accessible since May 6, 2026). The numerical results presented in this paper were obtained with version 1.0. The software is distributed under the GNU General Public License v3.0 (GPL-3.0). The data that support the findings of this study are openly available at [52] and [53].
Ethics Approval: Not applicable.
Conflicts of Interest: The authors declare no conflicts of interest.
Abbreviations
The following abbreviations are used in this manuscript:
| AoI | Age of Infection |
| CDLab | Computational Dynamics Laboratory |
| COVID-19 | COrona VIrus Disease-(20)19 |
| EPITIME | EPidemic Integral models TIMe-profile Explorer |
| FoI | Force of Infection |
| GUI | Graphical User Interface |
| MCB | MATLAB Code Block |
| NSFD | Non-Standard Finite Difference |
| PCB | Python Code Block |
| SEIR | Susceptible, Exposed, Infected, Recovered model |
| SIR | Susceptible, Infected, Recovered model |
Appendix A Unified Notation Guide
Table A1 provides a unified notation guide for the continuous variables, discrete quantities, and implementation-level variables used throughout the manuscript. The assumptions associated with each model are reported separately in Tables 1 and 2.

Appendix B Software Validation and Reproducibility
All numerical experiments presented in this paper can be reproduced using the publicly available implementations provided in the EPITIME repository. Relevant information concerning the software environment, hardware platform, code version and dependencies of the solvers codes is reported in Table A2. We point out that the MATLAB Optimization Toolbox is used exclusively for the kernel calibration in Section 5.3. It is not part of the EPITIME framework and is required only for this specific application.

Appendix B.1 Organization of the Github Repository
This appendix lists the source files in the EPITIME GitHub repository associated with the numerical experiments and examples presented throughout the manuscript.
• Section 4.1—Codes: NSFD_AoI.m and NSFD_AoI.py
• Section 4.2—Codes: NSFD_behavioural.m and NSFD_behavioural.py
• Section 5.1—Codes: AoI_Performance_Benchmark.m, AoI_Performance_Benchmark.py, behavioural_Performance_Benchmark.m and behavioural_Performance_Benchmark.py
• Section 5.2—Codes: AoI_Final_Size.m and AoI_Final_Size.py
• Section 5.3—Code: NSFD_AoI_LIVE.mlx (Part 3.4)
• Section 5.4—Codes: Behavioural_unimodal_IF.m, Behavioural_trapezoidal_IF.m, Behavioural_unimodal_IF.py and Behavioural_trapezoidal_IF.py
• Section 5.5—Codes: AoI_Peak_Estimation.m, AoI_Peak_Estimation.py, Behavioural_Peaks_Estimation.m and Behavioural_Peaks_Estimation.py
Appendix B.2 Cross-implementation Verification
In what follows, we perform a cross-implementation verification of the EPITIME computational framework. To this end, the benchmark problems presented in Section 5 are independently reproduced using both the MATLAB and Python implementations, and the quantities of interest generated by the two software versions are systematically compared.
Concerning the AoI model, the test problem defined by (1)–(20) is chosen. For every simulation and for both implementations, the discrete solution sequences
and the asymptotic behaviour mismatches are addressed with the following pointwise final-time differences
The results of the comparison, reported in Table A3, show errors at the level of machine precision and confirm the consistency of the two independent implementations. Analogous outcomes are obtained by comparing the two implementations of the NSFD_behavioural solver.

Appendix B.3 Practical Use of the Graphical Interface
The MATLAB GUI currently supports the AoI model only. It is distributed as the file EPITIME_SimulationTool.mlapp, together with the associated software resources. It can be launched from the Apps panel in the MATLAB main window or opened directly from the folder containing the application file.
The interface is organized into two main panels. The left panel contains the model inputs and simulation controls, while the right panel displays the input functions and numerical results. The upper part of the left panel contains the parameters required by the NSFD_AoI function, as described in Section 4.1. Each field is initialized with its default value and accepts only inputs satisfying the prescribed type and range constraints.
The functions
The Run simulation button starts the computation, whereas Reset restores all fields to their default values. A message area reports validation errors, warnings and information returned by the NSFD_AoI routine.
The upper part of the output panel displays the profiles of
The complete numerical output is also exported automatically to the MATLAB workspace. The variables t_AoI, Y_AoI and P_AoI contain, respectively, the time grid, the numerical solution and the performance data. They can therefore be used for additional processing, plotting or comparison outside the GUI.
References
1. Brauer F, Castillo-Chavez C, Feng Z. Mathematical models in epidemiology. New York, NY, USA: Springer; 2019. doi:10.1007/978-1-4939-9828-9. [Google Scholar] [CrossRef]
2. Martcheva M. An introduction to mathematical epidemiology. In: Texts in applied mathematics. New York, NY, USA: Springer; vol. 61, 2015. doi:10.1007/978-1-4899-7612-3. [Google Scholar] [CrossRef]
3. Kermack WO, McKendrick AG. A contribution to the mathematical theory of epidemics. Proc R Soc Lond Ser A Contain Pap A Math Phys Character. 1927;115(772):700–21. doi:10.1098/rspa.1927.0118. [Google Scholar] [CrossRef]
4. Breda D, Diekmann O, de Graaf WF, Pugliese A, Vermiglio R. On the formulation of epidemic models (an appraisal of Kermack and McKendrick). J Biol Dyn. 2012;6(sup2):103–17. doi:10.1080/17513758.2012.716454. [Google Scholar] [CrossRef]
5. Diekmann O, Inaba H, Thieme HR. Mathematical epidemiology of infectious diseases: an ongoing challenge. Jpn J Ind Appl Math. 2025;42(4):1563–90. doi:10.1007/s13160-025-00742-1. [Google Scholar] [CrossRef]
6. Manfredi P, d’Onofrio A, editors. Modeling the interplay between human behavior and the spread of infectious diseases. New York, NY, USA: Springer; 2013. doi:10.1007/978-1-4614-5474-8. [Google Scholar] [CrossRef]
7. Bai Z. Global dynamics of a SEIR model with information dependent vaccination and periodically varying transmission rate. Math Methods Appl Sci. 2014;38(11):2403–10. doi:10.1002/mma.3231. [Google Scholar] [CrossRef]
8. Buonomo B, Messina E, Panico C, Vecchio A. An integral renewal equation approach to behavioural epidemic models with information index. J Math Biol. 2024;90(1):8. doi:10.1007/s00285-024-02172-y. [Google Scholar] [CrossRef]
9. Buonomo B, Messina E, Panico C. Minimal epidemic models with information index: from compartmental to integral formulation. Boll Unione Mat Ital. 2025;18(4):1181–202. doi:10.1007/s40574-025-00473-8. [Google Scholar] [CrossRef]
10. d’Onofrio A, Manfredi P. Information–related changes in contact patterns may trigger oscillations in the endemic prevalence of infectious diseases. J Theor Biol. 2009;256(3):473–8. doi:10.1016/j.jtbi.2008.10.005. [Google Scholar] [CrossRef]
11. Mickens RE. Nonstandard finite difference schemes: Methodology and applications. Singapore: World Scientific; 2020. [Google Scholar]
12. Messina E, Pezzella M, Vecchio A. A non-standard numerical scheme for an age-of-infection epidemic model. J Comput Dyn. 2022;9(2):239–52. doi:10.3934/jcd.2021029. [Google Scholar] [CrossRef]
13. Lubuma JMS, Terefe YA. A nonstandard Volterra difference equation for the SIS epidemiological model. Rev Real Acad Cienc Exactas Fis Nat A Mat. 2014;109(2):597–602. doi:10.1007/s13398-014-0203-5. [Google Scholar] [CrossRef]
14. Sekiguchi M, Ishiwata E. Global dynamics of a discretized SIRS epidemic model with time delay. J Math Anal Appl. 2010;371(1):195–202. doi:10.1016/j.jmaa.2010.05.007. [Google Scholar] [CrossRef]
15. Xu J, Geng Y. A nonstandard finite difference scheme for a multi-group epidemic model with time delay. Adv Differ Equ. 2017;2017(1):358. doi:10.1186/s13662-017-1415-8. [Google Scholar] [CrossRef]
16. Brunner H. Collocation methods for Volterra integral and related functional differential equations. In: Cambridge monographs on applied and computational mathematics. Cambridge, UK: Cambridge University Press; vol. 15, 2004. doi:10.1017/CBO9780511543234. [Google Scholar] [CrossRef]
17. Schädle A, López-Fernández M, Lubich C. Fast and oblivious convolution quadrature. SIAM J Sci Comput. 2006;28(2):421–38. doi:10.1137/050623139. [Google Scholar] [CrossRef]
18. López-Fernández M, Lubich C, Schädle A. Adaptive, fast, and oblivious convolution in evolution equations with memory. SIAM J Sci Comput. 2008;30(2):1015–37. doi:10.1137/060674168. [Google Scholar] [CrossRef]
19. Guglielmi N, Hairer E. Applying stiff integrators for ordinary differential equations and delay differential equations to problems with distributed delays. SIAM J Sci Comput. 2025;47(1):A102–23. doi:10.1137/24M1632413. [Google Scholar] [CrossRef]
20. Mohammad M, Trounev A, Rihan FA. A wavelet framework for fractional epidemic models with delay. J Math Epidemiol. 2025;1(2):167–80. doi:10.64891/jome.15. [Google Scholar] [CrossRef]
21. Mohammad M, Sweidan M, Trounev A. Piecewise fractional derivatives and wavelets in epidemic modeling. Alex Eng J. 2024;101(772):245–53. doi:10.1016/j.aej.2024.05.053. [Google Scholar] [CrossRef]
22. Jenness SM, Goodreau SM, Morris M. EpiModel: an R package for mathematical modeling of infectious disease over networks. J Stat Softw. 2018;84(8):1–47. doi:10.18637/jss.v084.i08. [Google Scholar] [CrossRef]
23. Kerr CC, Stuart RM, Mistry D, Abeysuriya RG, Rosenfeld K, Hart GR, et al. Covasim: an agent-based model of COVID-19 dynamics and interventions. PLoS Comput Biol. 2021;17(7):e1009149. doi:10.1371/journal.pcbi.1009149. [Google Scholar] [CrossRef]
24. Bershteyn A, Gerardin J, Bridenbecker D, Lorton CW, Bloedow J, Baker RS, et al. Implementation and applications of EMOD, an individual-based multi-disease modeling platform. Pathog Dis. 2018;76(5):277. doi:10.1093/femspd/fty059. [Google Scholar] [CrossRef]
25. Van den Broeck W, Gioannini C, Gonçalves B, Quaggiotto M, Colizza V, Vespignani A. The GLEaMviz computational tool, a publicly available software to explore realistic epidemic spreading scenarios at the global scale. BMC Infect Dis. 2011;11(1):37. doi:10.1186/1471-2334-11-37. [Google Scholar] [CrossRef]
26. Edlund SB, Davis MA, Kaufman JH. The spatiotemporal epidemiological modeler. In: Proceedings of the 1st ACM International Health Informatics Symposium; 2010 Nov 11–12; Arlington, VA, USA. p. 817–20. doi:10.1145/1882992.1883115. [Google Scholar] [CrossRef]
27. Douglas JV, Bianco S, Edlund S, Engelhardt T, Filter M, Günther T, et al. STEM: An open source tool for disease modeling. Health Secur. 2019;17(4):291–306. doi:10.1089/hs.2019.0018. [Google Scholar] [CrossRef]
28. Gozzi N, Chinazzi M, Davis JT, Gioannini C, Rossi L, Ajelli M, et al. Epydemix: an open-source Python package for epidemic modeling with integrated approximate bayesian calibration. PLoS Comput Biol. 2025;21(11):e1013735. doi:10.1371/journal.pcbi.1013735. [Google Scholar] [CrossRef]
29. Scott JA, Gandy A, Mishra S, Bhatt S, Flaxman S, Unwin HJT, et al. Epidemia: an R package for semi-mechanistic bayesian modelling of infectious diseases using point processes. arXiv:2110.12461. 2021. doi:10.48550/arXiv.2110.12461. [Google Scholar] [CrossRef]
30. Engelborghs K, Luzyanina T, Roose D. Numerical bifurcation analysis of delay differential equations using DDE-BIFTOOL. ACM Trans Math Softw. 2002;28(1):1–21. doi:10.1145/513001.513002. [Google Scholar] [CrossRef]
31. Sieber J, Engelborghs K, Luzyanina T, Samaey G, Roose D. DDE-BIFTOOL manual—Bifurcation analysis of delay differential equations. arXiv:1406.7144. 2016. doi:10.48550/arXiv.1406.7144. [Google Scholar] [CrossRef]
32. Breda D, Maset S, in V R. TRACE-DDE: a tool for robust analysis and characteristic equations for delay differential equations. In: Topics in time delay systems. Berlin/Heidelberg, Germany: Springer; 2009. p. 145–55. doi:10.1007/978-3-642-02897-7_13. [Google Scholar] [CrossRef]
33. CDLab–Computational Dynamics Laboratory. Software. Department of Mathematics, Computer Science and Physics, University of Udine. [cited 2026 Mar 23]. Available from: https://cdlab.uniud.it/software. [Google Scholar]
34. Bicker J, Gerstein C, Kerkmann D, Korf S, Schmieding R, Wendler A, et al. MEmilio: A high performance modular EpideMIcs simuLatIOn software for multi-scale and comparative simulations of infectious disease dynamics. arXiv:2602.11381. 2026. doi:10.48550/arXiv.2602.11381. [Google Scholar] [CrossRef]
35. Kühn MJ, Abele D, Kerkmann D, Korf S, Zunker H, Wendler A, et al. MEmilio v2.0.0—A high performance modular EpideMIcs simuLatIOn software. Zenodo. 2025. doi:10.5281/zenodo.15168968. [Google Scholar] [CrossRef]
36. Wendler A, Plötzke L, Tritzschak H, Kühn MJ. A nonstandard numerical scheme for a novel SECIR integro-differential equation-based model allowing nonexponentially distributed stay times. Appl Math Comput. 2026;509(6):129636. doi:10.1016/j.amc.2025.129636. [Google Scholar] [CrossRef]
37. Diekmann O, Gyllenberg M, Metz JAJ. Finite dimensional state representation of linear and nonlinear delay systems. J Dyn Differ Equ. 2018;30(4):1439–67. doi:10.1007/s10884-017-9611-5. [Google Scholar] [CrossRef]
38. Diekmann O, Inaba H. A systematic procedure for incorporating separable static heterogeneity into compartmental epidemic models. J Math Biol. 2023;86(2):29. doi:10.1007/s00285-023-01865-0. [Google Scholar] [CrossRef]
39. Bai F. An age-of-infection model with both symptomatic and asymptomatic infections. J Math Biol. 2023;86(5):82. doi:10.1007/s00285-023-01920-w. [Google Scholar] [CrossRef]
40. Brauer F, Watmough J. Age of infection epidemic models with heterogeneous mixing. J Biol Dyn. 2009;3(2):324–30. doi:10.1080/17513750802415822. [Google Scholar] [CrossRef]
41. Messina E, Pezzella M, Vecchio A. A long-time behavior preserving numerical scheme for age-of-infection epidemic models with heterogeneous mixing. Appl Numer Math. 2024;200:344–57. doi:10.1016/j.apnum.2023.04.009. [Google Scholar] [CrossRef]
42. Messina E, Pezzella M, Vecchio A. Nonlocal finite difference discretization of a class of renewal equation models for epidemics. Math Biosci Eng. 2023;20(7):11656–75. doi:10.3934/mbe.2023518. [Google Scholar] [CrossRef]
43. Brauer F. Age-of-infection and the final size relation. Math Biosci Eng. 2008;5(4):681. doi:10.3934/mbe.2008.5.681. [Google Scholar] [CrossRef]
44. Buonomo B, Messina E, Panico C, Vecchio A. A stable numerical method for integral epidemic models with behavioral changes in contact patterns. Electron Trans Numer Anal. 2024;61:137–56. doi:10.1553/etna_vol61s137. [Google Scholar] [CrossRef]
45. Song Y, Baker CTH. Perturbation theory for discrete Volterra equations. J Differ Equ Appl. 2003;9(10):969–87. doi:10.1080/1023619031000080844. [Google Scholar] [CrossRef]
46. Brauer F. The Kermack–McKendrick epidemic model revisited. Math Biosci. 2005;198(2):119–31. doi:10.1016/j.mbs.2005.07.006. [Google Scholar] [CrossRef]
47. Davis PJ, Rabinowitz P. Methods of numerical integration. 2nd ed. In: Computer science and applied mathematics. New York, NY, USA: Academic Press (Elsevier); 1984. doi:10.1016/C2013-0-10566-1. [Google Scholar] [CrossRef]
48. Messina E, Pezzella M, Vecchio A. Asymptotic solutions of non-linear implicit Volterra discrete equations. J Comput Appl Math. 2023;425(1):115068. doi:10.1016/j.cam.2023.115068. [Google Scholar] [CrossRef]
49. Pijpers FP. A non-parametric method for determining epidemiological reproduction numbers. J Math Biol. 2021;82(5):37. doi:10.1007/s00285-021-01590-6. [Google Scholar] [CrossRef]
50. Hritonenko N, Satsky C, Yatsenko Y. Integral model Of COVID-19 spread and mitigation in UK: identification of transmission rate. Math Model Anal. 2022;27(4):573–89. doi:10.3846/mma.2022.15708. [Google Scholar] [CrossRef]
51. Breda D, Tanveer M, Wu J. Sparse identification of delay equations with distributed memory. Appl Math Comput. 2026;531:130234. doi:10.48550/arXiv.2512.2107. [Google Scholar] [CrossRef]
52. Il Sole 24 Ore. Coronavirus Italia–Dati di incidenza; 2025 [cited 2025 Aug 30]. Available from: https://lab24.ilsole24ore.com/coronavirus. [Google Scholar]
53. Eurostat. Population on 1 January; 2025. Dataset code TPS00001. [cited 2025 Dec 23]. Available from: https://ec.europa.eu/eurostat/databrowser/view/tps00001/. [Google Scholar]
54. Lorentz GG. Bernstein polynomials. New York, NY, USA: Chelsea Publishing Company; 1986. [Google Scholar]
55. Engl HW, Hanke M, Neubauer A. Regularization of inverse problems. Dordrecht, The Netherlands: Springer; 1996. doi:10.1007/978-94-009-1740-8. [Google Scholar] [CrossRef]
56. Aldis GK, Roberts MG. An integral equation model for the control of a smallpox outbreak. Math Biosci. 2005;195(1):1–22. doi:10.1016/j.mbs.2005.01.006. [Google Scholar] [CrossRef]
57. Hynd R, Ikpe D, Pendleton T. Two critical times for the SIR model. J Math Anal Appl. 2022;505(2):125507. doi:10.1016/j.jmaa.2021.125507. [Google Scholar] [CrossRef]
58. Carvalho AM, Gonçalves S. An analytical solution for the Kermack–McKendrick model. Physica A Stat Mech Appl. 2021;566:125659. doi:10.1016/j.physa.2020.125659. [Google Scholar] [CrossRef]
59. Schlickeiser R, Kröger M. Analytical solution of the SIR-model for the temporal evolution of epidemics: part B. Semi-time case. J Phys A Math Theor. 2021;54(17):175601. doi:10.1088/1751-8121/abed66. [Google Scholar] [CrossRef]
60. Turkyilmazoglu M. A highly accurate peak time formula of epidemic outbreak from the SIR model. Chin J Phys. 2023;84(4):39–50. doi:10.1016/j.cjph.2023.05.009. [Google Scholar] [CrossRef]
61. Moussaoui A, Meziane M. On the date of the epidemic peak. Math Biosci Eng. 2024;21(2):2835–55. doi:10.3934/mbe.2024126. [Google Scholar] [CrossRef]
62. Cheng T, Zou X. On final and peak sizes of an epidemic with latency and effect of behaviour change. J Math Biol. 2025;91(2):19. doi:10.1007/s00285-025-02249-2. [Google Scholar] [CrossRef]
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Copyright © 2026 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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