1 s2.0 S0307904X2100175X Main

Applied Mathematical Modelling 97 (2021) 281–307
Contents lists available at ScienceDirect
Applied Mathematical Modelling

journal homepage: www.elsevier.com/locate/apm
Review of fractional epidemic models

Yuli Chen a, Fawang Liu b,c,∗, Qiang Yu b, Tianzeng Li d
a
Fuzhou University Zhicheng College, Fujian 350001, China
b
School of Mathematical Sciences, Queensland University of Technology, GPO Box 2434, Brisbane, QLD 4001, Australia
c
College of Mathematics and Computer Science, Fuzhou University, Fujian 350116, China
d
School of Mathematics and Statistics, Sichuan University of Science and Engineering, Zigong 643000, China
a r t i c l e i n f o a b s t r a c t
Article history: The global impact of corona virus (COVID-19) has been profound, and the public health
Received 26 January 2021 threat it represents is the most serious seen in a respiratory virus since the 1918
Revised 4 March 2021
influenza A(H1N1) pandemic. In this paper, we have focused on reviewing the re-
Accepted 23 March 2021
sults of epidemiological modelling especially the fractional epidemic model and sum-
Available online 20 April 2021
marized different types of fractional epidemic models including fractional Susceptible-
Classification: Infective-Recovered (SIR), Susceptible-Exposed-Infective-Recovered (SEIR), Susceptible-
26A33 Exposed-Infective-Asymptomatic-Recovered (SEIAR) models and so on. Furthermore, we
97M60 propose a general fractional SEIAR model in the case of single-term and multi-term frac-
37M05 tional differential equations. A feasible and reliable parameter estimation method based
37N30 on modified hybrid Nelder-Mead simplex search and particle swarm optimisation is also
presented to fit the real data using fractional SEIAR model. The effective methods to solve
Keywords:
the fractional epidemic models we introduced construct a simple and effective analytical
Epidemic models
Fractional order differential equations technique that can be easily extended and applied to other fractional models, and can help
Multi-term epidemic models guide the concerned bodies in preventing or controlling, even predicting the infectious dis-
Parameter estimation ease outbreaks.
Implicit numerical method
© 2021 Elsevier Inc. All rights reserved.
Hybrid simplex search and particle swarm
optimisation
1. Introduction
Infectious diseases are generally considered as the enemy of human health in history and have continued to be the ma-
jor causes of suffering and mortality in developing countries. It is well known that the spread of a communicable disease
involves disease-related factors such as infectious agent, made of transmission, incubation period, infectious periods, suscep-
tibility and resistance. Moreover, infectious disease agents adapt and evolve, so that new infectious diseases have emerged
and some existing diseases have reemerged. Many identified diseases include Lyme disease (1975), Legionnaire’s disease
(1976), toxic-shock syndrome (1978), hepatitis C (1989), hepatitis E (1990), and hantavirus(1993). The human immunodefi-
ciency virus (HIV), which is the etiological agent for acquired immunodeficiency syndrome (AIDS), emerged in 1981 and has
become an important sexually transmitted disease throughout the world. Antibiotic-resistant strains of tuberculosis, pneu-
monia, and gonorrhea have evolved. Malaria, dengue, and yellow fever have reemerged and are spreading into new regions
as climate changes occur. Diseases such as plague, cholera, and hemorrhagic fevers (Bolivian, Ebola, Lassa, Marburg, etc.)
continue to erupt occasionally [1]. Since December 2019, an increasing number of cases of novel coronavirus (COVID-19) in-
fected pneumonia (NCIP) have been identified in Wuhan, a large city of 11 million people in central China on 31 December
∗
Corresponding author.
E-mail address: [email protected] (F. Liu).
https://doi.org/10.1016/j.apm.2021.03.044
0307-904X/© 2021 Elsevier Inc. All rights reserved.
Y. Chen, F. Liu, Q. Yu et al. Applied Mathematical Modelling 97 (2021) 281–307
2019. The COVID-19 pandemic is now a major global health threat [2]. It is clear that human or animal invasions of new
ecosystems, global warming, environmental degradation, increased international travel, and changes in economic patterns
will continue to provide opportunities for new and existing infectious diseases [3]. The emerging and reemerging diseases
have led to a revived interest in infectious diseases.
During the past 70 years, the study of infectious disease dynamics has matured into a rich interdisciplinary field at
the intersection of mathematics, epidemiology, computational physics, ecology, evolutionary biology, immunology, sociology,
and public health. Epidemiology is the branch of science which essentially deals with the mathematical modeling of spread
of diseases, and mathematical modeling in epidemiology is concerned with describing the spread of disease and its effect
on people [1]. This itself encompasses a range of disciplines, from biology, mathematics, and engineering to sociology and
philosophy, all of which are utilized to a better understanding and predicting of the spread of infection [4–7].
One of the early triumphs of mathematical epidemiology was a formulation of a model in [8] to predict the behavior of
a disease. In order to control the spread of infectious diseases, researchers have built a great deal of mathematical models
to study the dynamical behavior of infectious diseases. Communicable disease models describing a directly transmitted vital
or bacterial agent in a closed population. The formulation of a model is a process which includes statement of the relevant
assumptions, relationship among variables, and parameters and relations governing their behaviors. Of course, the choice of
these factors is critical to the model and depends largely on the particular disease to be modeled and the intended purpose
of that model [6]. Mathematical models and computer simulations are useful experimental tools for building and testing
theories, assessing quantitative conjectures, answering specific questions, determining sensitivities to changes in parameter
values, and estimating key parameters from data [9–11]. The practical challenges range from establishing appropriate data
collection to managing increasingly large volumes of information. The theoretical challenges require fundamental study of
many-layered, non linear systems in which infections evolve and spread, and where key events can be governed by un-
predictable pathogen biology or human behavior. Understanding the transmission characteristics of infectious diseases in
communities, regions, and countries can lead to better approaches to decreasing the transmission of these diseases. Coupled
to continuous dialogue between decision makers and the multidisciplinary infectious disease community, and by draw-
ing on new data streams, mathematical models can lay bare mechanisms of transmission and indicate new approaches to
prevention and control that help to shape national and international public health policy. By fitting these models with epi-
demiological data proper interpretation can be made through the estimated parameters. The numerical solutions for these
models will be visualized via a graphical user interface which will allow users to tune the parameters to reveal important
characteristics about the models and infectious diseases. As such, epidemiology modeling can contribute to the design and
analysis of epidemiological surveys, suggest crucial data that should be collected, identify trends, make general forecasts,
and estimate the uncertainty in forecasts [5].
Although a model for smallpox was formulated and solved by Daniel Bernoulli in 1760 in order to evaluate the effective-
ness of variolation of healthy people with the smallpox virus, deterministic epidemiology modeling seems to have started in
the 20th century [1]. In 1906 Hamer formulated and analyzed a discrete time model in his attempt to understand the recur-
rence of measles epidemics. His model may have been the first to assume that the incidence (number of new cases per unit
time) depends on the product of the densities of the susceptibles and infectives. Ross was interested in the incidence and
control of malaria, so he developed differential equation models for malaria as a host-vector disease in 1911. Other deter-
ministic epidemiology models were then developed in papers by Ross, Ross and Hudson, Martini, and Lotka. Starting in 1926
Kermack and McKendrick published papers on epidemic models and obtained the epidemic threshold result that the density
of susceptibles must exceed a critical value in order for an epidemic outbreak to occur. Mathematical epidemiology seems to
have grown exponentially starting in the middle of the 20th century (the first edition in 1957 of Bailey’s book is an impor-
tant landmark), so that a tremendous variety of models have now been formulated, mathematically analyzed, and applied to
infectious diseases. Reviews of the literature show the rapid growth of epidemiology modeling. The recent models have in-
volved aspects such as passive immunity, gradual loss of vaccine and disease-acquired immunity, stages of infection, vertical
transmission, disease vectors, macroparasitic loads, age structure, social and sexual mixing groups, spatial spread, vaccina-
tion, quarantine, and chemotherapy. Special models have been formulated for diseases such as measles, rubella, chickenpox,
whooping cough, diphtheria, smallpox, malaria, onchocerciasis, filariasis, rabies, gonorrhea, herpes, syphilis, and HIV/AIDS.
The breadth of the subject is shown in the books on epidemiology modeling [12,13].
The important mathematical model describing the evolution infectious diseases is called compartmental model which
was originally established by Kermack and Mckendrick (1927) to study the spread of the infectious diseases [8]. In the
compartmental system, the population is divided into three separate compartments, these compartments are defined with
respect to disease status. Namely, the susceptible compartment S, the infected compartment I, and the removed compart-
ment R. In the system, the susceptible person get infected and becomes an infected person making contact with an infected
person, and the infected person can be recovered taking treatments, the individuals who reach this class have permanent
immunity for the relevant disease. This type of model is called the SIR (susceptible-infected-removed) model whose variants
are widely being studied and applied in studying specific disease such as dengue and leptospirosis epidemics.
Based on the Kermack-McKendrick model, various epidemic models have been developed in recent decades. The choice
of which compartments to include in a model depends on the characteristics of the particular disease being modeled and
the purpose of the model [1]. The passively immune class M and the latent period class E are often omitted, because they
are not crucial for the susceptible-infective interaction. Acronyms for epidemiology models are often based on the flow pat-
terns between the compartments such as MSEIR, MSEIRS, SEIR, SEIRS, SEIAR, SIR, SIRC, SIRS, SEI, SEIS, SI, SIS, SVIR, and
282
SVEIR (where S, V, I and R denote the populations of susceptible, vaccinated, infectious and recovered individuals). Such
as SIS models in which system there exists a high possibility of recovered individuals to be re-injected. Depending on the
actual disease, more or less of these classes may be used. For example, some disease models only include the S and I
classes, while others may have a forth class which represents a state in which a disease is latent(SEIR models) or has a
cross-immune state(SIRC models) such as Salmonella Bacterial infection. Diseases like Gonorrhea, Chagas and Rocky Moun-
tain Spotted fevers are modeled using SIS models because people become susceptible as soon as the recover from infection.
For disease like AIDS, influenza A(H1N1), measles, SEIR model is more appropriate as there is a latent period, when the
virus is present in the host but has still not infected the host. And it is not suitable for modeling endemic diseases as it
cannot display endemic behavior. It is more appropriate to propose multigroup epidemic models to describe the transmis-
sion dynamics of many infectious diseases in heterogeneous host populations, such as dengue fever, leptospirosis; some
disease process includes the quarantined state such as measle, mumps, gonorrhea, HIV/AIDS, West-N:le virus; some disease
state has vaccinated process using SVIR or SVEIR models, investigation of shigellosis and norovirus can use SEIAR model
while smoking epidemic model using POSQL (the potential smoker, occasional smoker, smoker, temporarily quit smoker
and permanently quit smoker) model. Over the years, more complex models have been derived. On the human population,
the memory relates to the individual awareness [14]. In epidemic and endemic area’s awareness about infection will lessen
the contact rate between the different compartments such as human and the mosquitoes in dengue SIR-SI model [15,16],
while the vaccinated people tend to have strong awareness of past epidemics, more than susceptible people in SVEIR model.
There should be a scientific means to combine the models and observations such that experts will be able to extract as
much information from available data as possible before making drastic decisions. Out of this overview, we refer to some
obstacles in these models and takes a look at some intriguing approaches focusing on development of general structures
for such models and proposes an alternative approach, namely fractional calculus, whose main features can be briefly sum-
marized as follows: reflecting memory effects, capturing fractality, multiscale nature and better data fitting. The fractional
derivative epidemic models provide a powerful instrument for incorporation of memory and hereditary properties of the
systems as opposed to the integer order models, where such effects are neglected or difficult to incorporate. In addition,
when fitting data, the fractional models has one more degree of freedom than the integer order model. We therefore, re-
view several articles on fractional epidemic models and count models based on dynamics with derivative of fractional order
and metapopulation models and propose that developing numerical techniques by which mathematical models are fitted to
actual data can help guide the concerned bodies in preventing or controlling the infectious disease outbreaks.
In this paper, we mainly consider the fractional-order epidemic system with the fractional derivatives defined in
Section 2 and introduce epidemiology modeling by formulating review in Section 3. Based on the numerical solution for
the model review, we study the corresponding inverse problem of parameter estimation for the fractional differential equa-
tion by the novel techniques and optimization algorithm in Section 4 and 5. Then, we take the Norovirus infectious as an
example about application to parameters estimation of fractional SEIAR model in Section 6 and propose a general multi-term
fractional-order epidemic system with the new fractional orders and parameters in Section 7, for verifying the efficiency and
accuracy of the proposed methods in dealing with the fractional inverse problem, a numerical example with experimental
data is studied. Our general epidemic system is capable of providing numerical results that agree very well with the real
data.
2. Preliminary knowledge
Fractional calculus is an old yet novel mathematical tool that unifies and generalises the derivative and integral of integer
order into any arbitrary order. The theory of derivatives of non-integer order originated
√ from the L’Hospital letter to Leibniz
discussing the meaning of the derivative or what does the derivative of order 1/3 or 2 of a function mean in 1695. Leading
from that, it has caught the interest of mathematicians during 18th to 19th centuries to study this area. A well-known scien-
tist, Abel in 1823 has become the first scientist to implicitly apply fractional calculus for investigating tautochrone problems.
Later several fundamental works on various aspects of fractional calculus have appeared [17,18]. As one would expect, since
fractional order differential equation systems allow greater degrees of freedom and incorporate memory effect in the model,
they have become an excellent tool in modelling epidemiology properties and provide an interesting modeling technique
in the context of epidemiology. Although the fractional derivative is more complicated than the classical model, there exist
several numerical methods for solving such systems. Fractional calculus has been the subject of worldwide attention in the
last decades [19], due to its broad range of applications in chemistry [20], biology [21–24], physics [25], engineering [26],
viscoelastic materials [25], and image processing[27]. Recently, fractional calculus is experiencing an intensive progress in
both theory and applications [28]. Fractional differential equations have been shown to be more adequate and can give a
more realistic interpretation of natural phenomena than integer-order derivatives for describing phenomena associated with
nonlocality, since the fractional-order derivative provides an excellent tool for the description of the memory and heredi-
tary properties of various materials and processes [29]. Hence, fractional derivatives based on epidemic systems have also
been used to deal with some epidemic behaviors [30–32]. The classical first-order differential equations was unable to re-
produce the statistical data collected in a real outbreak of the disease with a sufficient degree of accuracy, in general, this
basic/classical model does not provide enough good results. In order to have better results, that fit the reality, more specific
and complicated set of differential equations have been investigated in the literature [33–35], we propose a slightly modified
system of equations where we now use differential equations of fractional order.
283
Fractional SIR epidemic model equations are obtained from the classical SIR epidemic equations in mathematical mod-
elling by replacing the first-order derivatives with fractional derivative of order α (0 < α ≤ 1 ). Several universal phenomena
can be modeled to a great degree of accuracy by using the property of these evolution equations. In contrast to integer-
order differential operators, which are local operators, a fractional-order differential operator is non-local in the sense that
it takes into account the fact that the future state not only depends upon the present state but also on the history of its
previous states. For this realistic property, the usage of fractional-order systems is becoming popular to model the behaviour
of real systems in various fields of science and engineering. It is to be noted that the present states of any real-life dynamic
system are dependent upon the history of its past states. Such circumstances have motivated the researchers to study the
SIR epidemic model which has a great physical relevance from the perspective of public health policies and its consideration
as fractional-order system in allied problems is valid [36].
In the recent years, the dynamic behaviors of fractional-order differential systems have received increasing attention. The
existence of solutions of initial value problems for fractional order differential equations have been studied in the literature
and the references there in [27,37–39]. Many definitions for fractional derivatives have been wildly studied. In this paper,
we give three commonly used definitions: the Riemann-Liouville (RL), Caputo and the Grünwald-Letnikov (GL) definitions
[29].
Definition 1. The fractional integral a Dt−α of function f (t ) is defined as follows:

t
−α 1
a Dt f (t ) = (t − τ )α−1 f (τ )dτ , (1)
(α ) a
∞
where the fractional order α > 0 and (z ) = 0 t z−1 e−t dt is the gamma function.
Definition 2. The Caputo derivative with order α of function f (t ) is given as

t
dn 1
C α
a Dt f (t ) = 0Dt−(n−α ) f (t ) = (t − τ )n−α−1 f (n) (τ )dτ , (2)
dt n (n − α ) a
where n − 1 < α < n, n ∈ Z + .
Definition 3. The Riemann-Liouville derivative with order α of function f (t ) is defined as

t
RL α dn − ( n −α ) 1 dn
a Dt f (t ) = a Dt f (t ) = (t − τ )n−α−1 f (τ )dτ , (3)
dt n (n − α ) dt n a
where n − 1 < α < n, n ∈ Z + .
It follows from the definitions of fractional derivatives that the Riemann-Liouville and Caputo definition are not equiva-
lent, and their relation is expressed by the following:
n−1

C α RL α (t − a )k−α f (k) (a )
a Dt f (t ) = a Dt f (t ) − . (4)
(k − α + 1 )
k=0
The Caputo derivative is equivalent to the Riemann-Liouville derivative if the initial conditions f (k ) (a ) = 0, k = 0, 1, · · · , n −
1.
Definition 4. The Grünwald-Letnikov derivative with order α of function f (t ) is defined as follows:

m
α
GL α −α
a Dt f (t ) = lim h (−1 ) r
f (t − rh )
h→0 r
mh=t r=0
n−1
t
f (k ) (a )t k−α 1
= + (t − τ )n−α−1 f (n) (τ )dτ , (5)
(k + 1 − α ) (n − α ) a
k=0
where n − 1 < α < n.
It follows from the definitions of fractional derivatives that the Grünwald-Letnikov fractional derivatives and Riemann-
Liouville derivatives are equivalent. The Riemann-Liouville and Caputo definition are not equivalent, and their relation can
be expressed by

n−1
n−1

C α RL α (t − a )k−α f (k) (a ) RL α (t − a )k f (k) (a )
a Dt f (t ) = a Dt f (t ) − = a Dt f (t ) − , (6)
(k − α + 1 ) k!
k=0 k=0
Due to the relation (6), the Caputo derivative is equivalent to the Riemann-Liouville derivative if the initial conditions satisfy
f ( k ) ( a ) = 0, k = 0, 1, · · · , n − 1.
284
3. Model formulation review
3.1. Mathematical modeling of dengue epidemics (SIR-SI MODEL)
This global pandemic is attributed to the unprecedented population growth, the rising level of urbanization without
adequate domestic water supplies, increasing movement of the virus between humans (due to tourism, migration, or in-
ternational trade), and lack of effective mosquito control [40]. Dengue virus is transmitted to humans through the bite of
infected Aedes mosquitoes, specially Aedes Aegypti. Once infected, a mosquito remains infected for life, transmitting the
virus to susceptible individuals during feed. Dengue fever is a disease that has been found to cause problems whose mag-
nitude has increased dramatically over the last two decades. In fact, the World Health Organization recently stated that it is
the most important arthropod-borne viral disease of humans [41]. Therefore, it is very important to have a detailed under-
standing of the rules that the spread of the infection follows, so that the control of the vectors is the only possible strategy
to combat the disease at the moment. More recent models indicate that in the coming decades the vectors transmitting the
disease are likely to spread to even larger parts of the world, including most of central and even northern Europe. Some
mathematical models have been proposed to study the outbreak of dengue fever. Nishiura [42] studied the mathematical
and statistical analyses of the spread of dengue. Hales et al. [43] studied the global distribution of dengue fever on the
basis of vapor pressure, which is a measure of humidity. Rodrigues et al. [44] studied the stability of the classic dengue
disease model. Sardar [45] proposed a mathematical model of dengue transmission with memory. Pooseh et al. [46] stud-
ied the fractional-order dengue system with Riemann-Liouville-type derivatives of the same order. Diethelm [47] proposed
a fractional-order model based on the Caputo-type derivative for the simulation of an outbreak of dengue fever, in which
some orders are the same. However, in these papers, the parameters of the dengue model are given directly. In some papers,
the numerical solution of these systems only provides a poor match with the real number of the infected humans.
In [46], the researchers assumed that the host population is divided into three classes: susceptible, Sh (t ), individuals
who can contract the disease; infected, Ih (t ), individuals capable of transmitting the disease to others; and resistant, Rh (t ),
individuals who have acquired immunity at time t. The total number of hosts is constant, i.e., Nh = Sh (t ) + Ih (t ) + Rh (t ). Sim-
ilarly, they also have two compartments for the mosquito: Sm (t ) and Im (t ) with Nm = Sm (t ) + Im (t ). The model is described
by the system of differential equations
dSh (t ) Im
= μh Nh − (Bβm h + μh ) S h ,
dt Nh
dIh (t ) Im
= Bβm h S − (ηh + μh )Ih ,
dt Nh h
dRh (t )
= ηh Ih − μh Rh , (7)
dt
dSm (t ) Ih
= μm Nm − (Bβh m + μm ) S m ,
dt Nh
dIm (t ) Ih
= Bβh m Sm − μm Im .
dt Nh
A particular feature of this system can be observed that
dNh dS dI dRh
= h + h + = μh (Nh − Sh − Ih − Rh ) = 0, (8)
dt dt dt dt
i.e., the total number of humans is constant. This fact reflects the observation that indeed the number of people dying from
dengue fever is extremely small. For example, in the outbreak considered below, less than 0.035% of the infected people
eventually died from the disease. Similarly,
dNm dSm dIm
= + = A − μm (Sm + Im ) = A − μm Nm , (9)
dt dt dt
where A is a constant recruitment rate for the mosquitoes. Subject to given initial conditions Sh (0 ), Ih (0 ), Rh (0 ), Sm (0 ) and
Im (0 ). The recruitment rate of human and vector populations are denoted as μh Nh and μm Nm , respectively. The natural
death rate for humans and mosquitoes is described by the parameters μh and μm , respectively. They assumed that B is the
average daily biting (per day) of the mosquito whereas βm h and βh m are related to the transmission probability (per bite)
from infected mosquitoes to humans and vice versa. The recovery rate of the human population is denoted by ηh . Therefore,
substitute the first-order derivatives by Riemann-Liouville derivatives of order α we have:
RL α Im
0 Dt Sh (t ) = μh Nh − (Bβm h + μh ) S h ,
Nh
RL α Im
0 Dt Ih (t ) = Bβm h S − (ηh + μh )Ih ,
Nh h
RL α
0 Dt Rh (t ) = ηh Ih − μh Rh , (10)
285
RL α
0 Dt Sm (t ) = μm Nm − Bβh m h + μm Sm ,
Nh
RL α Ih
0 Dt Im (t ) = Bβh m Sm − μm Im .
Nh
Note that the fractional system reduces to classical system if α → 1. Researchers used classical methods to obtain an
approximate solution to the original fractional system and solved numerically using data that outbreak occurred in 2009 in
Cape Verde and concluded the best order is 0.987, as the percentage error is thirteen as compared to classical model is sixty
two [46].
In 2013, the researchers assumed that mosquitoes and humans behave in a different way and used two different or-
ders of the differential operators, αh and αm [47]. They first replaced the fractional calculus system using fractional Caputo
derivatives as following [47]:
C αh βh b
0 Da Sh = μh (Nh − Sh ) − Sh Im ,
Nh
C αh βh b
0 Da Ih = Sh Im − (μh + γ )Ih ,
Nh
C αh
0 Da Rh γ Ih − μh Rh ,
= (11)
C αm βm b
0 Da Sm = μm Nm − Sm Ih − μm Sm ,
Nh
C αm βm b
0 Da Im = Sm Ih − μm Im .
Nh
To make sure that the right-hand sides of these equations have same dimensions, they modified the right-hand sides to
make the dimensions match as following [47]:
C αh βh bαh
0 Da Sh = μαh h (Nh − Sh ) − Sh Im ,
Nh
C αh βh bαh α
0 Da Ih = Sh Im − (μh h + γ αh )Ih ,
Nh
C αh
0 Da Rh γ αh Ih − μαh h Rh ,
= (12)
C αm αm βm bαm
0 Da Sm = μm Nm − Sm Ih − μαmm Sm ,
Nh
C αm βm bαm
0 Da Im = Sm Ih − μαmm Im .
Nh
The authors numerically simulated using Adams method and used the data based on the 2009 dengue fever outbreak
in Cape Verde islands. It can be clearly seen that both fractional models provide almost identical results up to the peak of
the number of infected humans whereas the later phase of the epidemic is more accurately modeled by the system using
the modified parameters. The authors have demonstrated that a nonlinear fractional order differential equation model can
simulate the dynamics of the epidemic much more accurately than the classical model based on first derivatives. In partic-
ular, it has turned out that the behavior of the human population follows a model of a different order than the mosquito
population.
In 2019, the researchers proposed a new and general fractional-order dengue fever system using Caputo derivatives with
different orders [48]:
βh b
λα1 C0Dtα1 Sh = μh (Nh − Sh ) − S Im ,
Nh + m h
βh b
λα2 C0Dtα2 Ih = S Im − (μh + γ )Ih ,
Nh + m h
λα3 C0Dtα3 Rh = γ Ih − μh Rh , (13)
βm b
λα4 C0Dtα4 Sm = μm (Nm − Sm ) − Sm Ih ,
Nh
βm b
λα5 C0Dtα5 Im = Sm Ih − μm Im ,
Nh + m
α
where C0 Dt i denotes the Caputo fractional derivative with order αi . For searching a better dengue fever system which is
capable of providing numerical results that agree much better with the real data, they present the multi-term fractional
order dengue model as follows [48]:
C α1 ,··· ,αr ,α0 βh b
0 Dt Sh = μh (Nh − Sh ) − S Im ,
Nh + m h
286
C α1 ,··· ,αr ,α0 βh b

0 Dt Ih = S Im − (μh + γ )Ih ,
Nh + m h
C α1 ,··· ,αr ,α0
0 Dt Rh = γ Ih − μh Rh , (14)
C β1 ,··· ,βr ,β0 βm b
0 Dt Sm = μm (Nm − Sm ) − Sm Ih ,
Nh
C β1 ,··· ,βr ,β0 βm b
0 Dt Im = Sm Ih − μm Im ,
Nh + m
α ,··· ,αr ,α0 β ,··· ,βr ,β0
where the 0 Dt 1 and 0 Dt 1 are defined as

r
C α1 ,··· ,αr ,α0
0 Dt x (t ) = λi · 0Dtαi x(t ) + λ0 · 0Dtα0 x(t ), (15)
i=1
and

r
C β1 ,··· ,βr ,β0
0 Dt x (t ) = λi · 0Dtβi x(t ) + λ0 · 0Dtβ0 x(t ), (16)
i=1
with 0 < α1 < · · · < αr < α0 = 1, 0 < β1 < · · · < βr < β0 = 1, and the weighted coefficient λi , λi (i = 1, 2, · · · , r ) ∈ R+ which
are used to retain the same units on both sides of the equations.
To verify the effectiveness and correctness of the proposed methods, they used the data of 2009 dengue fever outbreak
on the Cape Verde island given by Diethelm as the known data to perform the inverse problem by parameter estimation
method [48]. They studied the effect of every parameter on the number of infected humans with the other parameters fixed.
The results showed a better fitting between the numerical solutions of the multi-term fractional-order dengue fever model
with the estimated parameter values and the real data than other models. Hence, this paper provides effective parameter
estimation methods for a fractional application in the dengue fever model.
In [49], a study on a basic fractional order epidemic model of dengue transmission is conducted using the SIR-SI model,
including the aquatic phase of the vector. In the formulation of the model, the total number of human and mosquito pop-
ulation is assumed to be constant. Assumed that the infection is produced by only one serotype of dengue viruses. The
dynamics of female Aedes mosquito includes aquatic phase, Am , and adult mosquito stage. The adult stage is divided into
two compartments which are susceptible Ms and infectious Mi . The total human population is partitioned into three com-
partments that are susceptible Hs , infectious Hi , and recovered Hr individuals. The fractionalization is done following the
work of Diethelm [47]. The governing equation is as follows:
C α Am
0 Dt Am = qφ (1 − ) M − ( σ A + μA ) A m ,
C
α
b βm
C α
0 Dt Ms = σA A m − Ms Hi − μm Ms ,
H
C α bα βm
0 Dt Mi = Ms Hi μm Mi , (17)
H
C α bα βh
0 Dt Hs = μh (H − Hs ) − Hs Mi ,
H
α
b βh
C α
0 Dt Hi = Hs Mi − (γh + μh )Hi ,
H
C α
0 Dt Hr = γh Hi − μh Hr ,
with the condition of Nh = H = Hs + Hi + Hr , we have Hr = H − Hs + Hi . Thus, the authors wrote down the corresponding
system for human population exclusive of the Hr differential equation as follows [49]:
C α bα βh
0 Dt Hs = μh (H − Hs ) − Hs Mi ,
H
C α bα βh
0 Dt Hi = Hs Mi − (γh + μh )Hi ,
H
C α Am
0 Dt Am = qφ (1 − ) M − ( σ A + μA ) A m , (18)
C
C α bα βm
0 Dt Ms = σA Am − Ms Hi − μm Ms ,
H
α
b βm
C α
0 Dt Mi = Ms Hi μm Mi .
H
In this study [49], the values related to the human describe the reality of an infected period in Malaysia. The data used
is based on the dengue fever cases recorded in Malaysia for 2016, taken from The Ministry of Health Malaysia. Table 1
summarised the fractional-order dengue epidemics models and the contribution to the research works in recent years.
287
Table 1
Summary of dengue epidemics models.
Year Author Model Contribution
2011 Pooseh et al. [46] fractional-order SIR-SI model with The best order α is 0.987. The percentage error is 13 as
Riemann-Liouville derivatives of the same compared to classical model is 62.
order
2013 Diethelm et al. [47] fractional-order SIR-SI model with Caputo A particularly good approximation was obtained with
derivatives of two different orders αh = 1 and αm ∈ [0.75, 0.8]. The improved simulation
results by setting αm = 0.95 and μm = 0.196.
2014 Al-Sulami et al. [50] fractional-order SIR-SI model with Caputo It very sensitive to the order of differentiation α : a small
derivatives of the same order change in α may result in a big change.
2015 T. Sardar et al. [14] fractional-order SIR-SI model with Caputo Increase in human memory (α → 0) will reduce the
derivatives of two different orders considering dengue transmission; Increase in memory of vectors
the dimension match of the system (β → 0) will increase the dengue transmission.
2018 Hamdan et al. [51] fractional-order SI-SIR model with Caputo DFE is locally asymptotically stable when R0 < 1 and is
derivatives by including the aquatic stages unstable when R0 > 1.
2019 Hamdan et al. [49] fractional-order SIR-SI model using Caputo The disease-free equilibrium of system is locally
derivatives including aquatic phase asymptotically stable if the corresponding R0 < 1
2019 T. Li et al. [48] fractional-order SIR-SI model using Caputo A better fitting between the numerical solutions of the
derivatives with different orders multi-term fractional-order dengue model with the
estimated parameter values and the real data than other
models.
2020 Ozlem Defterli[52] Fractional-order vector-host dengue model Stability analysis is performed and the local asymptotic
using Caputo derivatives by including stability of the disease-free equilibria is obtained. The
temperature dependent features in highest danger of dengue transmission exists at
entomological parameters. temperature 28◦C.
3.2. Mathematical modeling of leptospirosis epidemics (SIR-SI MODEL)
Leptospirosis disease is an important infectious disease. This kind of infection occurs in urban areas of industrialized and
developed countries and also in the rural areas. The people of the city who walk in dirty water are mostly infected. Workers
planting rice, sewer cleaners, cleaning canals workers, and agriculture labor get the disease easily. The disease flourishes
due to delay in diagnosis and unavailability of clinical infrastructure. The cause of the disease is bacteria. It is potentially
fatal infection of brain, kidney, liver, heart, and lung. The people who can get infection are those who have contact with
infected animals, soil, or water in which the bacteria is present. The outdoor people, who work with animals, face the risk
of leptospirosis infection, similarly workers in farms, sewer, mine, slaughter houses, dairy farmers, and animal caretakers and
those who work with fishes and military personnel. Those people who work outdoors like swimming, rafting, and kayaking
also face the risk of infection.
The researchers had made many efforts for modeling of leptospirosis epidemic disease since 2011 [53–58]. They proposed
a mathematical model that describes the epidemic leptospirosis disease given by:
dSh (t )
= b1 − μh Sh − β2 Sh Iv − β1 Sh Ih + λh Rh ,
dt
dIh (t )
= β2 Sh Iv + β1 Sh Ih − (μh + δh + γh )Ih ,
dt
dRh (t )
= γh Ih − μh Rh − λh Rh , (19)
dt
dSv (t )
= b2 − γv Sv − β3 Sv Ih ,
dt
dIv (t )
= β3 Sv Ih − (γv + δv )Iv ,
dt
where Sh (t ), Ih (t ), Rh (t ), Sv (t ) and Iv (t ) represent the population of susceptible human, infected human, recovered human,
susceptible vector, and infected vector at time t, respectively. The rate at which the population of human increases is shown
by b1 . The natural mortality rate for the human population is μh ; β1 , β2 , and β3 represent the transmission coefficients.
The parameter λh shows the individuals who become susceptible again. The death from the disease that occurs to humans is
shown by δh . The rate of recovery from infection for the human is denoted by γh . The growth rate of the vector population
is represented by b2 ; γv is the natural death rate for vector and disease related death rate for the vector is δv . The fractional
model presented by [54] is given by system above which represents a system of nonlinear ODE and is given as follows:
C α h
0 Dt S (t ) = b1 − μh Sh − β2 Sh Iv − β1 Sh Ih + λh Rh ,
C α h
0 Dt I (t ) = β2 Sh Iv + β1 Sh Ih − (μh + δh + γh )Ih ,
C α h
0 Dt R (t ) = γh Ih − μh Rh − λh Rh , (20)
288
C α v
0 Dt S (t ) = b2 − γv Sv − β3 Sv Ih ,
C α v
0 Dt I (t ) = β3 Sv Ih − (γv + δv )Iv .
The parameter which describes the general response expression in representing the order of fractional derivative gives
different results for different values. Obviously, the integer-order system can be viewed as a special case of the fractional-
order system by putting the time-fractional order of the derivative equal to one. To put it simple, for the higher in order,
the behavior of the fractional order system is the same in the case of integer order. This is the first work, which is available
on the epidemic model of leptospirosis in fractional order. They solved the fractional systems and compared with classical
Runge Kutta and concluded that the results obtained by multi-step generalized differential transform have a good agreement
with the Runge Kutta of order 4 [59].
3.3. Mathematical modeling of salmonella bacterial infection epidemics(SIRC MODEL)
The Salmonella infection is a major zoonotic disease which is transmitted between humans and other animals. Most
persons infected with Salmonella develop diarrhea, fever, and abdominal cramps 12 to 72 hours after infection. The illness
usually lasts 4 to 7 days, and most persons recover without treatment. However, in some persons, the diarrhea may be so
severe that the patient needs to be hospitalized. Salmonella live in The intestinal tracts of humans and other animals, in-
cluding birds. Salmonella are usually transmitted to humans by eating foods contaminated with animal feces. Contaminated
foods usually look and smell normal. Contaminated foods are often of animal origin, such as beef, poultry, milk, or eggs, but
any food, including vegetables, may become contaminated. Therefore, Salmonella is considered as a serious problem for the
public health throughout the world. There are no doubts that mathematical modeling of Salmonella bacterial infection plays
an important role in gaining understanding of the transmission of the disease in specific environment and in predicting the
behavior of any outbreak.
The researchers introduced a new compartment into SIR model, which is called cross-immune compartment to be called
SIRC model [60]. The new compartment cross-immune describes an intermediate state between the fully susceptible and the
fully protected one. Recently, the fractional order SIRC model of influenza, a disease in human population, was investigated
[61]. The researchers considered the fractional order SIRC model associated with evolution of Salmonella bacterial infection
in animal herds. However, they took into account the disease induced mortality rate in the model. Qualitative behavior of the
fractional order SRIC model was investigated and numerical simulations of the fractional order SRIC model were provided
to demonstrate the effectiveness of the proposed method by using implicit Euler’s method.
In [62], the authors assumed that the Salmonella infection spreads in animal herds which are grouped as four com-
partments, according to their infection status: S(t ) is the proportion of susceptible individuals at time t (individuals that
do not have the bacterial infection), I (t ) is the proportion of infected individuals (that have the bacterial infection), R(t ) is
the proportion of recovered individuals (that recovered from the infection and have temporary immunity), and C (t ) is the
proportion of cross-immune individuals at time t. The total number of animals in the herd is given by N = S + I + R + C.
They considered that initially all the animals are susceptible to the infection. Once infected, a susceptible individual leaves
the susceptible compartment and enters the infectious compartment where it then becomes infectious. The infected ani-
mals pass into the recovered compartment. The individuals who have recovered from the disease have temporary immunity
and grouped into C (t ) compartment. Therefore, the disease transmission model consists of nonnegative initial conditions
together with system of equations as follows:
dS(t )
= μN + ηC (t ) − (β I (t ) + μ )S(t ),
dt
dI (t )
= β S(t )I (t ) + σ βC (t )I (t ) − (θ + m + μ )I (t ), (21)
dt
dR(t )
= (1 − σ )β C (t )I (t ) + θ I (t ) − (μ + δ )R(t ),
dt
dC (t )
= δ R(t ) − β C (t )I (t ) − (η + μ )C (t ),
dt
where parameter μ denotes the mortality rate in every compartment and is assumed to be equal to the rate of newborns
in the population. β is the contact rate and also called transmission from susceptible to infected. η−1 is the cross immune
period, θ −1 is the infectious period, δ −1 is the total immune period, and σ is the fraction of the exposed cross immune
individuals who are recruited in a unit time into the infective subpopulation [60], [63]. The disease induces mortality rate
is noted by m.
Although a large number of work have been done in modeling the dynamics of epidemiological diseases, it has been
restricted to integer-order (delay) differential equations. In recent years, it has turned out that many phenomena in different
fields can be described very successfully by models using fractional order differential equations (FODEs). The author in
[62] introduced fractional order into model aboved. They assumed that s(t ) = S(Nt ) , i(t ) = I (Nt ) , r (t ) = RN
(t ) (t )
, c (t ) = C N , where
N is the total number of population, and the fractional model takes the form as follows:
C α1
0 Dt s (t ) = μ + ηc(t ) − (β i(t ) + μ )s(t ),
289
C α2
0 Dt i (t ) = β s(t )i(t ) + σ β c(t )i(t ) − (θ + m + μ )i(t ), (22)
C α3
0 Dt r (t ) = (1 − σ )β c(t )i(t ) + θ i(t ) − (μ + δ )r (t ),
C α4
0 Dt c (t ) = δ r (t ) − β c(t )i(t ) − (η + μ )c(t ).
The researchers provided a fractional order SIRC epidemic model with Salmonella bacteria infection and derived the suffi-
cient conditions to preserve the asymptotic stability of infection-free and endemic steady states. The fractional order dy-
namical models are more suitable to model biological systems with memory than their integer-orders and the presence of
a fractional differential order into a corresponding differential equation leads to a notable increase in the complexity of the
observed behavior and enlarges the stability region of the solutions.
3.4. Mathematical modeling of H1N1 epidemics(SEIR MODEL)
The pandemic virus A(H1N1)/09 is a flu virus of swine, avian, and human origin that was first identified in April 2009 in
Mexico and the USA [64]. The virus soon spread to the rest of the world and on June 11, 2009; the WHO declared the new
influenza A(H1N1) a pandemic [64]. The transmission of the virus AH1N1 is only possible through effective contacts of a
susceptible individual with an infectious individual. Typical interventions to control the spread include quarantine, isolation,
travel restrictions, closing of public places, fear-based self-quarantine, and cancelation of events [64]. These interventions
have economic costs to individuals and society related to lost work, increased school absenteeism, and decreased business
revenues [65,66]. A pandemic influenza A(H1N1) vaccine became available in the USA in October 2009 [67]. Every year,
approximately 36,0 0 0 people die from seasonal influenza or flu-related causes only in the USA [67]. Additionally, since
there are thousands deaths worldwide due to the A(H1N1)/09 virus, it is important to understand the dynamics regarding
the evolution of the A(H1N1)/09 virus.
In order to study the dynamics of H1N1 influenza virus spread, several models have been presented. For instance, the
classical SIR epidemiological model with a seasonal forced function has been used to model the influenza A(H1N1)/09 virus
spread in the US population [68]. The classical SEIR model has been used to predict the infected individuals, hospital bed
shortage, and effectiveness of vaccination in a city of Japan and mixed with statistical methods in order to forecast the
prevalence of A(H1N1) in Singapore [65,69]. However, when considering influenza, the SEIR model, which is an immediate
extension of the original SIR model, is more realistic. The SEIR model introduces a fourth compartment corresponding to
the incubation (disease latency) stage when a person is infected but still not infectious enough to be able to transmit it.
The SEIR model has been applied in epidemics that include a latency and recovery periods such dengue, influenza, rabies,
and tuberculosis [44,70–73]. For instance, the SEIR model has been used to describe real data of tuberculosis, and the least
squares fitting has been used for estimating the model parameters [72]. Furthermore, the SEIR model has been used to
explore effective control and prevention measures for the human rabies in China, where it is one of the major public health
problems [73].
In [74], the authors proposed the population scaled fractional SEIR using Caputo derivatives of order α . The proposed
model was then fitted to the known real data related to H1N1 infected cases. The SEIR epidemiological model considers that
the total population N (t ) is divided into four subpopulations: S(t ) susceptible, E (t ) people incubating the virus, infectious
I (t ), and recovered R(t ) subpopulations. In addition, the newborn children become susceptible at a rate μ (birth rate), and
individuals leave the system by death at a rate d. An individual in S(t ) flows to E (t ) because people in I (t ) transmit A(H1N1)
virus by effective contacts at rate β . Finally, they consider that once an individual is recovered, he or she acquires permanent
immunity [67]. The other parameters of the model are ρ , recovery rate from the infection and latent individuals become
infected at rate . The population-scaled SEIR model (without loss of generality) with constant population size (d = μ ) is
given by [74]:
dS(t )
= μ − β S(t )I (t ) − μS(t ),
dt
dE (t )
= β S(t )I (t ) − (μ + )E (t ), (23)
dt
dI (t )
= E (t ) − (μ + ρ )I (t ),
dt
dR(t )
= ρ I (t ) − μR(t ).
dt
Then, the authors considered the SEIR fractional model using Caputo derivatives of order α as follows [74]:
C α
0 Dt S (t ) = μα − β α S(t )I (t ) − μα S(t ),
C α
0 Dt E (t ) = β α S(t )I (t ) − (μα + α )E (t ), (24)
C α
0 Dt I (t ) = α E (t ) − (μα + ρ α )I (t ),
C α
0 Dt R (t ) = ρ α I (t ) − μα R(t ).
In the fractional model, the next state depends not only upon its current state but also upon all of its historical states.
The authors tested the proposed SEIR fractional order model with real data. The parameter values of the model were esti-
290
mated minimizing the mean square error between the fractional model outputs and the real data of influenza A(H1N1). The
proposed fractional model epidemic peak adjusts better to the peak of the real data and gives better results in terms of the
mean square error then with the classical SEIR model. This fact is important from a health point of view since it translates
to a longer period with a high number of infected individuals, which can affect the health system. It is concluded that the
fractional order epidemic model produces numerical results that agree very well with the real data of influenza A(H1N1)
and provides useful information for the understanding, prediction, and control of the transmission of different epidemics
are in many cases a more powerful approach to epidemiological models, because one can choose the order α of fractional
differentiation that best corresponds to real data.
3.5. Mathematical modeling of measles epidemics(SEIR MODEL)
Measles is a higher contagious viral disease caused by infection of Paramyxovirus, generally of the genus Morbillivirus. It
is a serious disease of childhood that can lead to complications and death. For example, measles caused about 7500 deaths
in the United States in 1920 and still causes about 1 million deaths worldwide each year [75]. Measles vaccinations are given
to children between 6 and 18 months of age, but the optimal age of vaccination for measles seems to vary geographically.
Its incubation period is located somewhere between 9 and 12 days and its infectivity period between 4 and 9 days. Measles
is highly present in early childhood and its epidemics are commonly related to aggregation of children at schools or child-
care centres. It is recommended to get vaccinated against it at around 18 months of age and have a booster at 4 to 5 years
of age. The disease is particularly characterized by its low mortality and high morbidity. Measles will continue to circulate
in a community with a higher number of susceptible hosts by birth of children. However, in communities which generate
insufficient new hosts, measles will die out. This theory was introduced in 1957 by Bartlett [76], who brought out the critical
population size for a community and referred it to be the minimum number supporting measles.
In [77], the authors formulated the system modeling the fractional temporal spread of measles in a human population.
In the model, a population supposed constant is divided into different classes, disjoint and based on their disease status.
At time t , S = S(t ) is the fraction of population representing individuals susceptible to measles, E = E (t ) is the fraction
of population representing individuals exposed to measles, I = I (t ) is the fraction of population representing individuals
infectious with measles, and R = R(t ) is the fraction of population representing individuals that recovered from measles.
They assumed that all recruitment is done by birth into the class of susceptible and occurs at constant birth rate b. The rate
constant for nondisease related death is μ; thus μ 1
is the average lifetime. They used the standard mass balance incidence
expressions β (t )SI to indicate successful transmission of measles due to effective contacts dynamics in the population by
infectious individuals. Once infected, a fraction of exposed people becomes infectious with a constant rate σ , so that σ1 is
the average incubation period. Some infectious individuals will recover after a treatment or a certain period of time at a
rate constant ζ , making ζ1 the average infectious period. The formulated fractional temporal SEIR measles model is given by
[77]:
C α
0 Dt S = b − (β (t )I + μ )S,
C α
0 Dt E = β (t )SI − (σ + μ )E, (25)
C α
0 Dt I = σ E − (ζ + μ )I,
C α
0 Dt R = ζ I − μR.
This model was solved by predictor corrector scheme of Adams Bashforth Moulton type [77]. The authors had started
by showing nonnegativity of solutions to the fractional metapopulation model which defined as system of differential equa-
tions generated by discrete spatial models with continuous time and have been thoroughly analyzed in numeral articles
[78,79] thereby addressing the problem of its well posedness. They had also shown that the disease-free equilibrium of the
model is linearly stable if the spectral radius (the basic reproduction number) R0 ≤ 1 and unstable if R0 ≥ 1. They simulated
numerical data based on online magazine Otago Daily Time. Numerical simulations shown that, even in fractional dynamics
of measles in metapopulation, the epidemic will not occur in communities which generate insufficient new hosts, which is
in accordance with the theory of Bartlett. This work generalizes the preceding ones with the inclusion of the fractional dy-
namics to a combined SEIR and metapopulation model, giving at the same time one of the multiple applications of fractional
differential equations.
In 2018, a fractional temporal SEIR measles mode was considered. The model consists of four coupled time fractional
ordinary differential equations. The time-fractional derivative is defined in the Caputo sense. In this model, the population
is spatially spread into four patches representing four cities. The authors considered the set P = {A, B, W, D} representing
four patches. The mcxy is the rate of travel from city x to city y in compartment c with c = S, E, I, R which represents the
transfer rate of individuals in the compartment c of city x moving to the same compartment c in city y. It is clear that
mcxx = 0, for all x ∈ P and c ∈ {S, E, I, R}. The basic metapopulation model is given by [80]
dSx
= bx − (βx (t )Ix + μx )Sx + Sy mSyx − Sx mSxy ,
dt
y∈P y∈P
dEx
= βx (t )Sx Ix − (σx + μx )Ex + Ey mEyx − Ex mExy , (26)
dt
y∈P y∈P
291
dIx
= σx Ex − (ξx + μx )Ix + Iy mIyx − Ix mIxy ,
dt
y∈P y∈P
dRx
= ξx Ix − μx Rx + Ry mRyx − Rx mRxy .
dt y∈P y∈P
The fractional temporal model is formulated by the following differential equations with the fractional derivative in the
sense of Caputo.

C α
0 Dt Sx = bx − (βx (t )Ix + μx )Sx + Sy mSyx − Sx mSxy ,
y∈P y∈P

C α
0 Dt Ex = βx (t )Sx Ix − (σx + μx )Ex + Ey mEyx − Ex mExy , (27)
y∈P y∈P

C α
0 Dt Ix = σx Ex − (ξx + μx )Ix + Iy mIyx − Ix mIxy ,
y∈P y∈P

C α
0 Dt Rx = ξx Ix − μx Rx + Ry mRyx − Rx mRxy .
y∈P y∈P
where is the Gamma function. This fractional measles model was used to construct the analytical technique and predictor-
corrector scheme. The authors also explored the average error estimates for the measles model to verify with the theoretical
analysis. They used the GMMP scheme (Gorenflo-Mainardi-Moretti-Paradisi) [81] to show the accuracy of the analytical
solution for the time coupled fractional differential equations. The best features of the techniques proposed in this work are
that they can be easily extended to other fractional epidemic models. The authors limited the discussions on the effect of
differential order but put more effort into constructing a simple and effective analytical technique that can be easily applied
to other fractional models. In some circumstances, the solutions from the derived techniques can also help to understand
the underlying mechanisms that influence the epidemic pattern. It can be concluded that the analytical technique presented
in this paper is reliable and yet an alternative for the analytical evaluation to other time fractional differential equations
models.
3.6. Mathematical modeling of an anti-SARS vaccine (SVEIR MODEL)
The World Health Organization (WHO) reported the emergence of a new respiratory disease known as severe acute
respiratory syndrome (SARS) in March 2003. The disease, caused by a coronavirus, spread rapidly across Asia, Europe and
North America, with the highest prevalence in Asia. SARS resulted in about 900 deaths and 8000 infections globally.
Owing to the rapid transmissibility of the virus and the fear of a large epidemic, the WHO spearheaded an international
effort to combat the spread of SARS. Absent a definitive anti-SARS treatment or vaccine, these efforts were based on the
quarantine of suspected cases and isolation of individuals infected with SARS-CoV to stop them from infecting others. Many
advances have been made towards the design of a vaccine for SARS, and some vaccines are undergoing clinical trials. This is
a welcome development since, historically, vaccines have been and continue to be very useful in preventing illness or death
of millions of individuals.
Over the past few decades, a large number of simple compartmental mathematical models of the general form SVI or
SVIR (where S, V, I and R denote the populations of susceptible, vaccinated, infectious and recovered individuals) have been
used in the literature to assess the impact or potential impact of imperfect vaccines for combatting the spread of some
human diseases. While in some of these studies the vaccine is only given to people newly recruited into the population,
such as newborns (cohort vaccination), in many others, a proportion of susceptible individuals is continuously vaccinated.
In other studies, such as Arino et al. [82], both cohort and continuous vaccination are provided. Gandon et al. [83] provided
a nice study on some of the epidemiological and evolutionary consequences associated with the use of imperfect vaccines
using an SVI model with two infected components (unvaccinated infected and vaccinated infected individuals). Their study,
which is based on an imperfect vaccine which may decrease probability of infection and/or may decrease the growth rate
of parasites within the host, shows that eradication success depends on the type of vaccine and vaccine coverage used. The
model constructed in the current paper is an extension of the standard SVIR models, including a new compartment for the
latent class (an essential feature of the SARS transmission dynamics).
The development of the mathematical model in [84] is based on subdividing a given SARS-affected community into five
compartments: susceptible, S(t ), vaccinated, V (t ), asymptomatic, E (t ), symptomatic, I (t ), and recovered, R(t ), individuals.
The total population size is N (t ) = S(t ) + V (t ) + E (t ) + I (t ) + R(t ). The rates of change of the populations in each compart-
ment are represented by the following equations:
dS
= − β SI − ξ S − μS,
dt
dV
= ξ S − (1 − τ )β V I − μV,
dt
292
dE
= β SI + (1 − τ )β V I − α E − μE, (28)
dt
dI
= α E − δ I − dI − μI,
dt
dR
= δ I − μR.
dt
In [85], Wei et al. proposed a new SVEIR epidemic disease model with time delay
dS
= μ − μS(t ) − β S(t )I (t ),
dt
dV
= −β1V (t )I (t ) − γ1V (t ) − μV (t ),
dt
dE
= β S(t )I (t ) + β1V (t )I (t ) − β e−μτ S(t − τ )I (t − τ ) − β1 e−μτ V (t − τ )I (t − τ ) − μE (t ), (29)
dt
dI
= β e−μτ S(t − τ )I (t − τ ) + β1 e−μτ V (t − τ )I (t − τ ) − γ I (t ) − μI (t ) − α I (t ),
dt
dR
= γ1V (t ) + γ I (t ) − μR(t ).
dt
They analyzed the dynamic behavior of the model under pulse vaccination. Pulse vaccination is an effective strategy for the
elimination of infectious disease. Using the discrete dynamical system determined by the stroboscopic map, they obtain an
infection-free periodic solution. They also showed that the infection-free periodic solution is globally attractive when some
parameters of the model under appropriate conditions. The permanence of the model was investigated analytically.
In [86], the authors proposed a fractional-order mathematical 5D dynamical system modelling an SVEIR model of in-
fectious disease transmission in a chemostat is proposed. The model developed here has five components, S, V, E, I and R
known as SVEIR model of infectious disease transmission in a chemostat. The population are classified as Susceptible indi-
viduals (S), Vaccinated individuals (V ), Exposed individuals (E), Infected individuals (I), and Recovered individuals (R) and
modelled by the following five-dimensional dynamical system of Fractional Differential Equations (FDEs) with the Caputo
fractional derivative:
C α
0 Dt S = D(Sin − S ) − (mS + p)S − μ(I )S,
C α
0 Dt V = pS − (D + mV )V − θ μ(I )V,
C α
0 Dt E = μ(I )(S + θ V ) − (D + mE + ε )E, (30)
C α
0 Dt I = ε E − (D + mI + γ )I,
C α
0 Dt R = γ I − (D + mR )R,
where p, θ , 1/ε and 1/γ are the vaccination rate, the vaccination factor reducing the risk of infection after vaccination,
the average latency time spent in compartment E before moving to compartment I and the average duration elapsed in
compartment I before recovery (R), respectively. mS , mV , mE , mI and mR are the mortality rates of susceptible, vaccinated,
exposed, infected and recovered individuals, respectively. μ represents the saturated incidence rate. A profound qualitative
analysis was given and the analysis of the local and global stability of equilibrium points was carried out.
3.7. Mathematical modeling of HIV/AIDS epidemics (SIJA MODEL)
Human immunodeficiency virus (HIV), which leads to acquired immunodeficiency syndrome (AIDS), is a pandemic which
is almost very dangerous and fatal if untreated and uncontrolled. Over 35 million people have died from AIDS-related ill-
nesses since the start of the epidemic in 1981. Viral transmission typically occurs following exposure to cell-associated virus
through: (1) contaminated blood products or syringes, (2) sexual intercourse and (3) mother to child in utero, during birth,
or through breastfeeding. An individual may advance through several infective stages before developing full blown AIDS
[87]. Virus number in the blood is a major indicator of the disease stages. Sometimes these stages are meant to correspond
to CD4+ T-cell count ranges. In a normal healthy individual’s peripheral blood, the level of CD4+ T-cells is between 800 and
1200/mm3 and once this number reaches 200 or below in an HIV infected patient, the person is classified as having AIDS.
Without drug treatment, HIV-1 infection is nearly uniformly fatal within 5–10 years. With drug therapies, such as HAART
(highly active antiretroviral therapy), treated individuals can live longer free of HIV-related symptoms [88].
Mathematical models have been used extensively in research into the epidemiology of HIV/AIDS to help improve our
understanding of the major contributing factors to the pandemic. From the initial models of May and Anderson [89–91],
various refinements have been added into modelling frameworks, and specific issues have been addressed by researchers
[92–95]. The book [96] by Castillo-Chavez contains a review of HIV/AIDS modeling papers including single-group models,
multiple-group models, and epidemiologic-demographic models. It also contains papers on AIDS models with HIV class age,
variable infectivity, distributions for the AIDS incubation period, heterogeneity, and structured mixing.
293
To construct the model, the authors in [97] first divided the total population into a susceptible class of size S and an
infectious class before the onset of AIDS and a full-blown AIDS group of size A which is removed from the active population.
Based on the facts that the infectious period is very long (≥ 10 years), the researchers further considered several stages of
the infectious period. For simplicity, they only consider two stages according to clinic stages and papers [88,95] i.e., the
asymptomatic phase (I) and the symptomatic phase (J). Thus, they first considered the following model [97]:
RL α
0 Dt S (t ) = μK − cβ (1 + bJ )S − μS,
RL α
0 Dt I (t ) = cβ (1 + bJ )S − (μ + k1 )I + γ J, (31)
RL α
0 Dt J (t ) = k1 I − (μ + k2 + γ )J,
RL α
0 Dt A (t ) = k2 J − (μ + d )A,
where, μK is the recruitment rate of the population, μ is the number of death rate constant. c is the average number of
contacts of an individual per unit of time. β and bβ are probability of disease transmission per contact by an infective in
the first stage and in the second stage, respectively. k1 and k2 are transfer rate constant from the asymptomatic phase I
to the symptomatic phase J and from the symptomatic phase to the AIDS cases, respectively. γ is treatment rate from the
symptomatic phase J to the asymptomatic phase I. d is the disease-related death rate of the AIDS cases.
In [98], Kheiri and Jafari presented a fractional order model of the transmission dynamics HIV/AIDS with random testing
and contact tracing in Cuba, that is the generalization, to fractional order, of the model given by Mastroberardino et al.
[99]:
C α
0 Dt S (t ) = − (ε1 u1 β + (1 − u1 )β )X S − μS,
C α
0 Dt X (t ) = (ε1 u1 β + (1 − u1 )β )X S − κ X Y − (μ + γ + κ )X, (32)
C α
0 Dt Y (t ) = κ X Y + κ − (μ + (ε2 u2 γ + (1 − u2 )γ ))Y,
C α
0 Dt Z (t ) = γ X + (ε u γ + (1 − u )γ )Y − μ Z,
2 2 2
where 0 ≤ α ≤ 1. The model parameters are:

-: constant recruitment rate of susceptible population;
-β : recruitment rate of new members of HIV-infected population infected by sexual transmission with X;
-γ : rate at which HIV-infected population develops AIDS;
-κ : rate at which undiagnosed HIV-infected population is diagnosed through contact tracing;
-κ : rate at which undiagnosed HIV-infected population is diagnosed through random testing;
-μ: mortality rate of the adult population;
-μ : mortality rate of the population with AIDS;
-u1 : the proportion of susceptible individuals that use condom;
-u2 : the proportion of diagnosed HIV-infected population that are under ART treatment;
-ε1 : efficacy of u1 ;
-ε2 : efficacy of u2 .
The stability of the equilibria of the model are discussed using the stability theorem and using the fractional La-Salle
invariance principle for fractional differential equations (FDEs). In this model, the susceptible population are transmitted to
the undiagnosed HIV infected population by a mass action term. The undiagnosed HIV-infected population are infected by
sexual transmission and move to the diagnosed class in two ways: one is through a mass action term that represents contact
tracing, and the other is through a linear term that represents random or voluntary testing. In addition, it is assumed that
the diagnosed HIV-infected population and the AIDS people can not transmit the infection due to the Cuban health care
system [99]. It is worth noting that 99% of the infection is done in Cuba via sexual contact [100], so infection by nonsexual
transmission is neglected.
Kheiri and Jafarin [98] presented a general formulation for a FOCP, in which the state and co-state equations are given in
terms of the left fractional derivatives. This approach simplifies the use of fractional numerical methods to solve the state
and co-state equations. For numerical simulation of the FOCP, they developed the Forward-Backward sweep method (FBSM)
using the Adams-type predictor-corrector method. They considered the control parameters of the model as time dependent
controls and formulate an optimal control problem. Conditions for fractional optimal control of the disease are derived and
analyzed. The state and co-state equations were characterized by left fractional derivatives and the numerical method is
used to numerically compute the solutions of the optimality system. Also, the efficacy of the fractional derivative order α
(0.6 ≤ α ≤ 1) on the HIV/AIDS epidemic model and the controls was investigated.
3.8. Mathematical modeling of smoking epidemics (POSQL MODEL)
Smoking is the major problem in the entire world effecting healthy community. Smoking effects different organs of hu-
man body caused more than one million deaths in the world. A chance of heart attack in smoker is 70% more as compared
to nonsmoker. Similarly, the incident rate of lung cancer of smoker is 10% more than nonsmoker. The main effects of short
term smoking are coughing, stained teeth, high blood pressure and bad breath. The major effects of long term smoking
are gum disease, stomach ulcer, lung cancer, heart disease, throat cancer and mouth cancer in the recent years. The life of
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smoker is also 12–13 years shorter than non-smoker. According to the reports of world health organization (WHO) smoking
kills many individual in the entire world. Every scientist, doctor and mathematician tries to control the effect of smoking.
The lot of smoking models are presented by the researchers. Erturk et al. examined the smoking model related with Caputo
fractional derivative [101]. Zaman studied the optimal control of the smoking models and present the qualitative analysis of
dynamics of smoking [102,103]. Analysis of cigarette smoking and lung cancer is presented in [104]. Garsow et al. [105] de-
scribed the mathematical analysis of tobacco use their decline. Some more interesting studies about dynamics of smoking
is discussed in [106–109].
The concept of mathematical modeling has been prolonged to define the stability and qualitative features of giving up
smoking models from 20 0 0. Smoking model is divided into five subdepartment like potential smoker P (t ), the occasional
smoker O(t ), smoker S(t ), temporarily quit smoker Q (t ) and permanently quit smoker L(t ). The proposed smoking model
in the form of system of nonlinear differential equation is given by [110]:
dP
= − β P S − μP,
dt
dO
= β PS − α1 O − μO,
dt
dS
= α1 O + α2 SQ − (μ + γ )S, (33)
dt
dQ
= −α2 SQ − μQ + γ (1 − δ )S,
dt
dL
= δγ S − μL.
dt
In this model, is represent the recruitment rate in P, β is the effective contact rate between S and P, μ is the natural death
rate, α1 is the rate at which occasional smokers become regular smokers, α2 and γ represents the contact rate between
smokers and temporary quitters who revert back to smoking and the rate of quitting smoking respectively, (1 − δ ) is the
fraction of smokers who temporary quit smoking (at the rate γ ), δ is the remaining fraction of smoking which represents
permanently quit smoking.
The fractional smoking model in the sense of Caputo fractional derivatives could be described as follows [110]:
C φ1
0 Dt P (t ) = − β PS − μP,
C φ2
0 Dt O (t ) = β PS − α1 O − μO,
C φ3
0 Dt S (t ) = α1 O + α2 SQ − (μ + γ )S, (34)
C φ4
0 Dt Q (t ) = −α2 SQ − μQ + γ (1 − δ )S,
C φ5
0 Dt L (t ) = δγ S − μL.
In this study smoking epidemic model has been investigated as follows:
(i) Laplace Adomian decomposition method for mathematical models based on system of fractional order differential
equations is more powerful approach to compute the convergent solutions.
(ii) The convergence analysis is also provided to demonstrate the efficiency of the method.
(iii) The constructed series by Laplace Adomian decomposition method for smoking model show a good agreement to
control the bad impact of smoking for different time period and to eradicate a death killer factor in the world.
(iv) Introduced the stability analysis theory and sensitivity analysis of mathematical epidemic models in the nonlinear
system which represent both the local and global behavior of smoking dynamics.
(v) Estimated the parameter that characterize the behavior of disease and present numerical simulations.
The pivotal aim of the resent work is to obtain an approximated analytical solution for the fractional smoking epidemic
model with the aid of a novel technique called q-homotopy analysis transform method (q-HATM) [111]. The considered
nonlinear mathematical model has been effectively employed to elucidate the evolution of smoking in a population and its
impact on public health in a community. The researchers found some new approximate solutions in a series form, which
converges rapidly, and the proposed algorithm provides auxiliary parameters, which are very reliable and feasible in con-
trolling the convergence of obtained approximate solutions. Further, they presented novel simulations for all cases of results
to validate the applicability and effectiveness of proposed scheme. The outcomes of the study reveal that the q-HATM is
computationally very effective to analyse nonlinear fractional differential equations arises in daily life problems.
3.9. Mathematical modeling of shigellosis and norovirus outbreak (SEIAR MODEL)
Shigellosis (bacillary dysentery), the result of infection with Shigella, is an enteric infectious disease responsible for ap-
proximately 1,10 0,0 0 0 deaths per year worldwide [112]. As approximately two-thirds of those who die from shigellosis are
children under 5 years of age, it is one of the most common diarrhea-related causes of morbidity and mortality in children in
295
developing countries [113]. Shigellosis epidemics usually occur in areas with crowding and poor sanitary conditions, where
person-to-person transmission or contamination of food or water by the organism is common [114–119]. In China, many
private wells supplying water to schools are built in close proximity to sources of pollution, including toilets, septic tanks,
sewer ditches, and lakes and ponds into which sewage is discharged. As water from these wells is often not treated before
being piped into schools, waterborne outbreaks of Shigella frequently occur [117], with devastating effects on students, their
families, and schools.
Many outbreak control strategies developed by primary-level health departments in China are empirically-driven. This
can be attributed to a lack of data regarding the rate of morbidity in the absence of intervention, making it difficult to
estimate whether the efficacy of a single or combined intervention could be decreased if implemented using traditional
methods. In these circumstances, researchers often perform mathematical modeling to estimate the total attack rate (TAR),
an indicator of the extent of an outbreak [120–124]. A bacillary dysentery model with seasonal fluctuation was formulated
and studied by Bai et al. [125].
Fortunately, a waterborne pathogen model termed the Susceptible-Infectious-Recovered-Water (SIRW) model can be used
to examine disease outbreaks that occur via multiple transmission pathways [126], such as shigellosis. The SIRW model is a
simple ordinary differential equation model that extends the classic SIR framework by adding a compartment (W ) that tracks
the pathogen concentration in water. Infected individuals shed the pathogen into water compartments, and new infections
arise both through exposure to contaminated water as well as by the classic SIR person-person transmission pathway. The
researchers developed a SEIARW model to examine the efficacy of different intervention strategies in controlling an outbreak
of shigellosis at a primary school in Changsha City, China.
In [127], the authors gave the development of the SEIARW model, where individuals were characterized according to their
epidemiological status as susceptible (S), exposed (E, infected but not yet fully contagious), infectious (I), asymptomatic
(A), and recovered (R); W denotes the reservoir (water) compartment. The susceptible individuals become infected (i.e.,
move from S to E) by contact with either infected/asymptomatic individuals or contaminated water at rates of β SI, β kSA
and βW SW respectively, where β and βW are the probability of transmission per contact, k is the relative transmissibility
of asymptomatic to symptomatic individuals. As exposed individuals become infectious after an incubation period, they
move from E to I at a rate of (1 − p)ωE and E to A at a rate of pωE , where 1/ω is the incubation period of the disease
and p is the proportion of asymptomatic individuals. After the infectious period has passed, infectious and asymptomatic
individuals may move to R at a rate of γ I and γ A respectively, where 1/γ and 1/γ are the infectious period of the I and A.
Infectious and asymptomatic individuals can in turn contaminate the water compartment by shedding the pathogen into W
at a shedding rate of μI and μ A, where μ and μ are the shedding coefficients. The pathogen in W will subsequently leave
the water compartment at a rate of εW, where 1/ε is the lifetime of the pathogen. The corresponding model equations are
as follows:
dS
= −β S(I + kA ) − βW SW,
dt
dE
= β S(I + kA ) + βW SW − ωE,
dt
dI
= (1 − p)ωE − γ I, (35)
dt
dA
= pωE − γ A,
dt
dR
= γ I + γ A,
dt
dW
= μI + μ A − εW.
dt
A disease with similar epidemic models above called Norovirus which is one of the most important pathogens of infec-
tious diarrhea and outbreaks of all ages [128–130]. In the United States, Norovirus causes approximately 21 million cases
each year [129], 71,0 0 0 hospitalizations [131], and 80 0 deaths [129,132]. In developing countries, there are frequent out-
breaks of medical institutions and schools [133], which have a great impact on the health of residents. The disease is mainly
transmitted through the fecal-oral route, and the infection dose is very low. Ingestion of 18 viruses at a time can cause
infection [134]. Therefore, it is easy to cause transmission, usually by human contact, and water or Food spread. School
outbreaks can also lead to absenteeism or even suspension of classes, affecting normal teaching order and increasing the
burden of family care for children. Therefore, in-depth study of the dynamic characteristics of Norovirus infectious diarrhea
outbreaks, and the evaluation of the effects of various types of prevention and control measures have important public
health significance.
Based on the natural history of Norovirus-infected diarrhea, the researchers established the integer order SEIAR model of
Norovirus transmission in schools. Taking an outbreak event in a city in 2007 as an example, the dynamic characteristics of
Norovirus were studied and the key prevention and control was quantitatively evaluated. But the results which demonstrated
the effect of match could be improved further to reflect the spread of Norovirus, especially the transmission speed before
the intervention.
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The SEIAR model is the most common method for studying the dynamic characteristics of some infectious disease, such
as Norovirus, influenza, worm propagation The classical model of the SEIAR model considers that the total human population
N is divided into five subpopulations: S(t ) susceptible humans, E (t ) exposed humans (infected but not yet fully contagious),
I (t ) infected humans, A(t ) asymptomatic humans, R(t ) recovered (or removed) humans. Hence, the classical model consists
of five ordinary differential equations for the five independent functions of the form [135]:
dS
= −β S(I + κ A ),
dt
dE
= β S(I + κ A ) − μω E − (1 − μ )ωE,
dt
dI
= (1 − μ )ωE − γ I, (36)
dt
dA
= μω E − γ A,
dt
dR
= γ I + γ A.
dt
Based on the integer order SEIAR model, we propose the following fractional SEIAR model using the Caputo fractional
derivative with order αi (i = 1, 2, · · · , 5):
λα1 C0Dtα1 S = −β S(I + κ A ),

λα2 C0Dtα2 E = β S(I + κ A ) − μω E − (1 − μ )ωE,
λα3 C0Dtα3 I = (1 − μ )ωE − γ I, (37)
λα4 C0Dtα4 A = μω E − γ A,
λα5 C0Dtα5 R = γ I + γ A,
where some new parameters λαi (i = 1, 2, · · · , 5 ) are introduced, which have dimension of (days )αi −1 on the left sides of
the equations to preserve units. This ensures that both sides of the equations have the same dimension (days )−1 .
In this paper, we will use the single-term and multi-term fractional order SEIAR model to describe the outbreak of
norovirus with the fractional derivatives in the sense of Caputo in sections 6 and 7. These fractional SEIAR models have
different values of fractional order. In order to obtain the numerical solution of the fractional equations, the GMMP scheme
is used as an implicit difference scheme. The Newton method is used to solve this implicit difference scheme which can be
considered as a nonlinear equations. Furthermore, the corresponding inverse problem of parameter estimation is investigated
by the modified hybrid Nelder-Mead simplex search and particle swarm optimization algorithm [136]. Using the statistics
from the norovirus outbreak in a middle school in China in 2007 [135], the parameters of the single-term and multi-term
fractional order SEIAR model can be determined, respectively, and both the numerical results of two fractional order SEIAR
models are in good agreement with the real data details in sections 6 and 7.
4. Numerical methods for the fractional order differential equation
There are various numerical methods which have been applied to solve the fractional order equations, including the
Power Series Method [27], the Predictor Corrector Method [27,29], the Mellin Transform Method [137], and others. In this
paper, we applied the GMMP scheme (Gorenflo-Mainardi-Moretti-Paradisi) [81] and Newton method to solve the equations
mentioned above, which is much more efficient than other numerical methods. For the sake of simplicity, we consider the
equations as form:
λ Ca Dtα x(t ) = f (t , x(t )) (38)

where x(t ) = λ = (λα1 , λα2 , λα3 , λα4 , λα5 and
(S(t ), E (t ), I (t ), A(t ), R(t ))T , )T C Dα
denotes the Caputo fractional derivative. In
a t
order to obtain the numerical solution of the fractional differential equations, we discrete in time using the uniform grids
with 0 < α < 1, that is t j = a + jh, j = 0, 1, 2, · · · , N, Nh = t − a. As we know, the Riemann-Liouville and Grünwald-Letnikov
fractional derivatives can be approximated using the following formula,
1 α 1 α
N N
RL α α
a Dt x (t ) = GL
a Dt x (t ) = lim α
ck x(tN−k ) ≈ α ck x(tN−k ), (39)
h→0 h h
k=0 k=0
and the Caputo fractional derivatives can be approximated by the following relation

n−1
1 α (t − a ) j x( j ) (a )
N
C α
a Dt x (t ) ≈ α ck x(tN−k ) − , (40)
h j!
k=0 j=0

where ckα = (−1 )k αj are binomial coefficients.
297
This method was first introduced by Gorenflo in [81] and is known as the GMMP scheme in [138]. Based on the GMMP
scheme, we can present the numerical techniques for simulating fractional order differential equations. In order to explain
this method, the fractional order nonlinear Eq. (37) can be written as:
λ Ca Dtα x(t ) = f (t, x(t )), 0 ≤ t ≤ T ,

x(k ) (a ) = x0(k ) , k = 0, 1, · · · , n − 1. (41)
It follows from formula (40) that

n−1

N
(t − a ) j x( j ) (a )
λ ckα x(tN−k ) − = hα f (tN , x(tN )), (42)
j!
k=0 j=0
i.e,

n−1
n−1
(t − a ) j x( j ) (a ) N (t − a ) j x( j ) (a )
x(tN ) = hα λ f (tN , x(tN )) + − ckα x(tN−k ) − . (43)
j! j!
j=0 k=1 j=0
In particular, if 0 < α ≤ 1, the above formula (43) can be written as follows:

N
x(tN ) = hα λ f (tN , x(tN )) + x(a ) − ckα [x(tN−k ) − x(a )]. (44)
k=1
Based on the Grünwald-Letnikov formula, we can present an implicit difference scheme (44) which can be considered as
an equation with respect to an unknown variable x(tN ). Then, we can use the Newton method to solve the value of x(tN )
by the Eq. (44).
The Newton method is an effective method of solving nonlinear equations. For the nonlinear equations F (x ) = 0, the
Newton method is expressed as:
xn+1 = xn − JF (xn )−1 F (xn ), n = 0, 1, 2, · · · , (45)

where JF (xn ) is the Jacobian matrix at xn . The LU factorization of JF (xn ) can be used to solve the above equations for def-
initeness in the description of Newton algorithm, and any other appropriate factorization such as QR or Cholesky can be
used as well. The inputs of the algorithm are the initial iterate x0 , the nonlinear map F, and a termination tolerances ε . The
details of the Newton algorithm are:
Step i: Compute and factor the Jacobian matrix JF (x0 ) = LU,
Step ii: Solve the linear equation LUs = −F (x0 ), x = s + x0 ,
Step iii: While the x satisfies the condition x − x0 > ε , then
(iii.a) Let x0 = x, then factor the Jacobian matrix JF (x0 ) = LU,
(iii.b) Solve the linear equation LUs = −F (x0 ), x = s + x0 ,
(iii.c) Compute and evaluate x − x0 . If x − x0 > ε , goto step (iii.a).
Then we can get the output x = x(tN ), i.e., the solution of the Eq. (44). In this paper, we use the GMMP scheme and
Newton method to obtain the numerical solution of the fractional systems.
5. The technique for parameter estimation in fractional order non-linear systems
An exploration using a model reflecting the behaviour of a real system is known as the forward problem, whereas the
process of fitting model parameters to a measurement or measurements is known as the inverse problem. It is difficult
to estimate parameters of fractional order nonlinear model. This problem will become more difficult when the range of
the parameters is large and the function f is highly non-linear with respect to the unknown parameters in the fractional
nonlinear model. To improve the fitting process and its robustness and avoid being trapped in a local minimum, strict
procedures can be followed, which involve narrowing the search space. Therefore, the search for a global minimum has
been formulated as a constrained optimisation problem. To analyse the reliability of our model in a quantitatively correct
way, parameters need to be globally determined.
In this section, a feasible and reliable parameter estimation technique is presented for the purpose of obtaining the global
minimum to the optimisation problem. A technique is proposed for estimating parameters in a fractional order nonlinear
model. The fractional order nonlinear system (41) can be written as a model with m unknown parameters:
λ Ca Dtα x(t ) = f (t, x(t ), P ), 0 ≤ t ≤ T ,

x(k ) (a ) = x0(k ) , k = 0, 1, · · · , n − 1, (46)
where x = (x1 , x2 , x3 , x4 , x5 )T
are state variables and f = ( f1 , f2 , · · · , fn )T
are n-dimensional vector functions, and every
fi (i = 1, 2, · · · , n ) may be nonlinear with respect to the unknown parameters P = ( p1 , p2 , · · · , pm )T , m is the number of
parameters.
298
In the following, we will introduce the method of parameter estimation with a modified hybrid Nelder-Mead simplex
search and particle swarm optimization [136]. Both the hybrid Nelder-Mead simplex search (NMSS) ([139]) and the particle
swarm optimisation (PSO) ([140]) have been widely used in solving challenging optimisation problems which are widely
used for identifying parameter. However, the literature shows that the practical use of NMSS and PSO are both limited,
since NMSS is likely to be trapped in a local optima and PSO has a slow convergence rate. Interestingly, the combined use
of NMSS and PSO has been demonstrated to be outperform both NMSS and PSO in terms of solution quality and convergence
rate.
In the NMSS-PSO parameter estimation process, the role assigned to NMSS and PSO is different due to their different
functionalities. The NMSS focuses on exploitation and PSO focuses on exploration. The combination of the two methods
makes full use of the merits of each method. Specifically, NMSS is used to exploit the current solution space and PSO focuses
on the exploration of the unknown space. The obvious distinctions between NMSS and PSO mainly exist in their choice of
initial points and the manner with which they proceed towards the solution: NMSS uses predetermined initial points and
moves towards points with better objective function values, while PSO uses a set of random initial points and through
iterations moves away from points with worse objective function values. The PSO proceeds by moving towards those points
which have better function values, while the NMSS evolves by moving away from a point which has the worst performance.
The modified hybrid Nelder-Mead simplex search and particle swarm optimization (MH-NMSS-PSO) method has been used
to estimate parameters for integer and fractional model, which takes the best advantages of both the NMSS method and the
PSO method. In the following, we will use the MH-NMSS-PSO method to conduct the parameter estimation for fractional
order nonlinear models. Taking the better characteristics of each method, we propose the MH-NMSS-PSO method as follows.
Suppose that P = ( p1 , p2 , · · · , pm )T ∈ , where = [ p(1min ) , p(1max ) ] × [ p(2min ) , p(2max ) ] × · · · × [ p(mmin ) , p(mmax ) ] is a bounded
domain.
Let x(t j ) be one of numerical solutions of Eq. (46) with the given parameters P = ( p1 , p2 , · · · , pm ) ∈ which is obtained
by the GMMP scheme and Newton method, the approximation of the unknown parameter vector P ∗ = ( p∗1 , p∗2 , · · · , p∗2 ) is
determined by the root-mean-square error (rMSE)

N 2
j=0 x(t j ) − x j
g(P ∗ ) = min g(P ) = min , (47)
P∈ p∈ N+1
where x j are real data.
The MH-NMSS-PSO method tries to find a potential global minimum g(P ∗ ) in the equation with the parameters P ∈ .
The MH-NMSS-PSO method takes the advantages of both the NMSS method and the PSO method to conduct the inverse
problem. It starts with (3m + 1 ) initial particles, which is constructed in two parts. Firstly, the predetermined points is em-
ployed to form an initial simplex of (m + 1 ) particles which is used in the NMSS method, and the 2m paticles are randomly
generated in the PSO method. Then, we sotred the total (3m + 1 ) particles from smallest to largest by the function values
g(P ) in Eq. (47). In the following, the best (m + 1 ) particles are handled by the NMDD method, while the last 2m particles
are adjusted by the PSO method. Then the algorithm for the MH-NMSS-PSO method is summarised as follows:
Step 1: Initialization. Generate a population of size 3m + 1.
For the minimization of the functions g(P ) of m variables (unknown parameters), create (m + 1 ) vertex points Pi =
( p1,i , p2,i , · · · , pm,i ) ∈ , (i = 1, 2, · · · , m + 1 ) to form an initial m-dimensional simplex. Evaluate the function value at each
extreme point (or vertex) of the simplex, i.e. m + 1 particles are constructed via the standard starting point used in
the NMSS, and a step size of ( p(jmax ) − p(jmin ) )/(m + 1 ) at each coordinate direction to form an initial simplex for the
NMSS part, i.e. p j,i = p(jmin ) + (i − 1 ) × ( p(jmax ) − p(jmin ) )/(m + 1 ), ( j = 1, 2, · · · , m; i = 1, · · · , m + 1 ). 2m particles are ran-
domly generated in each dimension for the PSO part, Pi = ( p1,i , p2,i , · · · , pm,i ) ∈ , (i = m + 2, · · · , 3m + 1 ), where p j,i =
p(jmin ) + Rand × ( p(jmax ) − p(jmin ) )( j = 1, 2, · · · , m; i = m + 2, · · · , 3m + 1 ) and Rand is a random number in the range (0,1).
Moreover, the particle’s initial velocities in each dimension are selected by the following:
V j,i = (V j(max ) − Vi(min ) )/L j ( j = 1, 2, · · · , m; i = m + 2, · · · , 3m + 1 ), (48)
where L j ( j = 1, 2, · · · , m ) are selected integers.
Step 2: Evaluation and ranking: evaluate the objective function value g(P ) of each particle. Rank them based on the
objective function value;
g( p1 ) ≤ g( p2 ) ≤ · · · ≤ g( p3m+1 ). (49)
Step 3: NMSS method: apply the NMSS method to the best m + 1 particles and replace the (m + 1 )th particle with the
update as follows:
(3.1) Calculate P0 , the center of gravity of all points except Pm+1 , i.e. P0 = ( p1,0 , p2,0 , · · · , pm,0 ) ∈ , where p j,0 =
m
p j,i
i=1
m ( j = 1, 2, · · · , m ).
(3.2) Reflection: In each iteration, determine Pm+1 , Pm and P1 vertices, indicating the highest, the second highest and the
lowest function values that occur, respectively. Let g(Pm+1 ), g(Pm ) and g(P1 ) represent the corresponding observed function
values. Compute the reflected point
Pr = (1 + κ )P0 − κ Pm+1 , (50)
299
where κ is the reflection coefficient (κ > 0 ) using the suggested value κ = 1 [139]. Pr = ( p1,r , p2,r , · · · , pm,r ) ∈ , p j,r =
(1 + κ ) p j,0 − κ p j,m+1 ( j = 1, 2, · · · , m ). If g(P1 ) ≤ g(Pr ) ≤ g(Pm ), then Pr replaces Pm+1 , else go to step (3.3).
(3.3) Expansion: If g(Pr ) ≤ g(P1 ), then compute the expanded point
Pe = γ Pr + (1 − γ )P0 , (51)
where γ is the expansion coefficient using the suggested value γ = 2 [139]. Pe = ( p1,e , p2,e , · · · , pm,e ), p j,e = γ p j,r + (1 −
γ ) p j,0 ( j = 1, 2, . . . , m ). If g(Pe ) ≤ g(P1 ), then Pe replaces Pm+1 , otherwise Pr replaces Pm+1 . Else continue at step (3.4).
(3.4) Contraction: if g(Pr ) > g(Pm ), then if g(Pr ) ≤ g(Pm+1 ), then Pr replaces Pm+1 , compute the contracted point
Pc = β Pm+1 + (1 − β )P0 . (52)
where β (0 < β < 1 ) is the expansion coefficient using the suggested value β = 0.5 [139]. Pc = ( p1,c , p2,c , · · · , pm,c ), p j,c =
β p j,m+1 + (1 − β ) p j,c ( j = 1, 2, · · · , m ). If g(Pc ) ≤ g(Pm+1 ), then Pc replaces Pm+1 . Else go to step (3.5).
(3.5) Shrink: For all but the best point, replace the point with
Pi = σ Pi + (1 − σ )P1 , (53)
where σ is the shrinkage coefficient with the suggested value σ = 0.5 and Pi denotes the vertex point for i = 2, 3, · · · , m + 1.
Step 4: Particle swarm optimization: apply the PSO operator for updating the last 2m particles with the worst objective
function value as follows:
(4.1) Velocity and position update. Assign the best positions P bi = Pi (i = m + 2, · · · , 3m ) (initialize randomly all particles
positions in step 1 and the global best location Pg = Pm+2 . The particles velocity and position are updated by the following
equations:
new
V j,i = ω × V j,iold + C1 × Rand1 × (Pb j,i − Pj,iold ) + C2 × Rand2 × (Pg j − Pj,iold ),
new old new
Pj,i = Pj,i + V j,i , j = 1, 2, · · · , m; i = m + 2, · · · , 3m + 1,
where C1 and C2 are two pre-determined positive constants, ω is an inertia weight and Rand1 and Rand2 are random num-
bers in the range (0, 1 ). Considering the ranges of the search space in different dimensions, we use C1 = 0.8, C2 = 0.3 and
ω = [0.5 + (Rand/2.0 )] in our case.
(4.2) Imposed boundaries. The absorbing walls are imposed to drive particles to the pre-determined parameter domains
[141]. Thus, it avoids physically impossible solutions by assuming the velocity in a certain dimension is zero when a particle
hits the boundary placed on that parameter.
(4.3) PSO iteration. Return to step 4 and start a new PSO iteration until it reaches the largest PSO iteration time Siter .
Step 5: Evaluate and rank again for all 3m + 1 particles. Discriminate the stopping criterion: if Sc < ε , where ε is a small
error parameter, the loop will stop. The criterion is defined by

m +1 √
(ḡ − gi )2
Sc = (54)
m+1
i=1
+1 g∗i √
where ḡ = m ∗
i=1 m+1 and gi = gi = gi ( p1 , p2 , · · · , pm ). The algorithm will stop when either (54) is satisfied or the num-
ber of iterations reaches the maximum iteration count.
Step 6: Output the best estimated parameter values P = ( p1 , p2 , · · · , pm ).
This parameter estimation technique can be implemented in a straightforward manner for the purpose of solving in-
verse problems governed by fractional linear or nonlinear dynamics, since it does not require gradient computation and is
therefore derivative free. The NMSS-PSO algorithm has been outlined in detail in [136].
6. Application to parameter estimation in the fractional SEIAR model
In this section, the MH-NMSS-PSO scheme is employed to estimate the fractional orders and parameters for the
fractional-order Norovirus infection system in Section 3.9. The results can verify the efficiency of both the GMMP scheme
presented in Section 4 and the MH-NMSS-PSO presented in Section 5 for the inverse problem.
In the reference [135], they used the data about a Norovirus infectious diarrhea incident reported in a school in China.
The information includes the number of people affected, the onset time of all cases, the intervening time of the department
of the centers for disease control and prevention, the preventive and control measures, etc. The details of the outbreak are
as follows: the department of the centers for disease control and prevention of a city received a telephone report from
a middle school on March 8, saying that there were more than ten cases of vomiting, abdominal pain and diarrhea in
the school recently. The following case definitions were established: vomiting or diarrhea and other symptoms such as
abdominal pain, fever, headache and dizziness have occurred among the students and staff of the school since March 5.
There are 93 classes in 5 grades in the school, with 5225 students and 430 teachers. The number of cases reached a peak
on 8 March. After the intervention on 8 March, isolation measures were taken. The epidemic situation began to decline
gradually. The authors used the integer order SEIAR model to predict the number of the infected people with the selected
values of the parameters: β = 8.3452 × 10−4 , κ = 3.9065 × 10−11 , ω = 1, ω = 1, μ = 0.3, γ = 0.3333 and γ = 0.03846,
300
90
Real data
80 Fractional SEIAR
70
Infected humans
60
50
40
30
20
10
0
0 5 10 15 20
Time (days)
Fig. 1. Number of infected humans I (t ) in a middle school in the 2007: Comparison of numerical results of one-term fractional SEIAR model with the real
data with the estimated parameters obtained by MH-NMSS-PSO method. The root-mean-square error is rMSE = 4.0792.
and the root-mean square error between the numerical solutions of integer order SEIAR model with the real data is rMSE
= 7.9138 [135].
In this paper, we use the modified hybrid Nelder-Mead simplex search and particle swarm optimization (MH-NMSS-PSO)
algorithm to estimate the parameters of fractional SEIAR model (37) to the real data. The real data of a 2007 Norovirus out-
break in a middle school is used as the known data to perform the inverse problem of parameter estimation. The parameters
λαi (i = 1, 2, · · · , 5 ) are used to ensure that both sides of the equation have the same dimension, and these constants can be
divided throughout and combined with the parameters on the right-hand side. There are five fractional order parameters and
totally seventeen parameters that should be estimated. In this inverse procedure, the unknown parameters vector is taken
as P = (λ1 , · · · , λ5 , α1 , · · · , α5 , β , μ, κ , ω, ω , γ , γ ). Each of the parameters in the fractional order SEIAR model (37) has its
particular biological meaning and each parameter has a corresponding value range. Therefore, based on these ranges, we
select some appropriate intervals and initial velocities as follows:
0 ≤ λi = pi ≤ 2, i = 1, 2, · · · , 5, 0 ≤ α j = p j+5 ≤ 1, j = 1, 2, · · · , 5
1 × 10−4 ≤ β = p11 ≤ 1 × 10−3 , 1 × 10−11 ≤ κ = p12 ≤ 1 × 10−10
0.01 ≤ μ = p13 ≤ 0.3, 1 ≤ ω = p14 ≤ 2
1 ≤ ω = p15 ≤ 2, 0.3 ≤ γ = p16 ≤ 1
0.05 ≤ γ = p17 ≤ 0.09
and
⎧
⎪ 0.02 , i = 1, 2, · · · , 5;
⎪
⎪
⎪
⎪ 0.01 , i = 6, 7, · · · , 10;
⎪
⎨ 1 × 10−4 , i = 11;
Vi = 1 × 10−11 , i = 12;
⎪
⎪ 0.01 , i = 13;
⎪
⎪
⎪
⎪
⎩ 0.025 , i = 14, 15;
0.01 , i = 16, 17.
Using the same initial values and the time as t = 20 days, we apply the MH-NMSS-PSO to estimate model parameters
from the real data based on the numerical solution solved by the GMMP scheme. Fig. 1 shows the comparison of numerical
results of fractional SEIAR model with the real data and the calculated model parameters P ∗ are:
λ1 = 0.6182, λ2 = 0.8757, λ3 = 0.1106, λ4 = 0.9341, λ5 = 0.4627,
α1 = 0.9049, α2 = 0.6940, α3 = 0.7945, α4 = 0.6637, α5 = 0.8279,
β = 1 × 10−3 , κ = 5.6636 × 10−11 , μ = 0.0382, ω = 1.0038, ω = 1.0 0 0 0,
γ = 0.3458, γ = 0.0737.
As can be seen from Fig. 1 that, the root-mean square error between the numerical solutions of fractional SEIAR model and
the real data is rMSE = 4.0792, which suggests that both the GMMP scheme and the MH-NMSS-PSO method are valid in
301
dealing with inverse problems for the fractional SEIAR system, and the fractional SEIAR model provides better fit to the real
data than the interger order SEIAR model.
7. Application to parameter estimation in the multi-term fractional SEIAR model
7.1. Multi-term fractional order SEIAR model of norovirus outbreak
As we known, the multi-term fractional order differential equation have played an important role in capturing the be-
haviour of real materials, especially in the field of the viscoelastic mechanics. In the recent years, some studies has shown
that the multi-term fractional differential equation can also provide a better epidemic model than integer order derivative
[10]. For searching a better norovirus epidemic system which is capable of providing numerical results that agree much
better with the real data, we propose the following multi-term fractional order SEIAR model:
C ξ1 ,··· ,ξr ,ξ0
0 Dt S (t ) = −β S(I + κ A ),
C θ1 ,··· ,θr ,θ0
0 Dt E (t ) = β S(I + κ A ) − μω E − (1 − μ )ωE,
C φ1 ,··· ,φr ,φ0
0 Dt I (t ) = (1 − μ )ωE − γ I, (55)
C ϕ1 ,··· ,ϕr ,ϕ0
0 Dt A (t ) = μω E − γ A,
C ψ1 ,··· ,ψr ,ψ0
0 Dt R (t ) = γ I + γ A.
In this model,

r
C ξ1 ,··· ,ξr ,ξ0
0 Dt x (t ) = λξi · C0 Dtξi x(t ) + λξ0 · C0 Dtξ0 x(t ),
i=1

r
C θ1 ,··· ,θr ,θ0
0 Dt x (t ) = λθi · C0 Dtθi x(t ) + λθ0 · C0 Dtθ0 x(t ),
i=1

r
C φ1 ,··· ,φr ,φ0
0 Dt x (t ) = λφi · C0 Dtφi x(t ) + λφ0 · C0 Dtφ0 x(t ),
i=1

r
C ϕ1 ,··· ,ϕr ,ϕ0
0 Dt x (t ) = λϕi · C0 Dtϕi x(t ) + λϕ0 · C0 Dtϕ0 x(t ),
i=1

r
C ψ1 ,··· ,ψr ,ψ0
0 Dt x (t ) = λψi · C0 Dtψi x(t ) + λψ0 · C0 Dtψ0 x(t ),
i=1
where 0 < ξ1 < · · · < ξr < ξ0 = 1, 0 < θ1 < · · · < θr < θ0 = 1, 0 < φ1 < · · · < φr < φ0 = 1, 0 < ϕ1 < · · · < ϕr < ϕ0 = 1, 0 < ψ1 <
· · · < ψr < ψ0 = 1, and the weighted coefficients λξi , λθi , λφi , λϕi and λψi ∈ R+ are used to preserve units.
We use the GMMP scheme to discretize this multi-term fractional order nonlinear equation. For the sake of simplicity,
we discretize in time using a uniform grid t j = jh, j = 0, 1, 2, · · · , n and nh = t. The multi-term fractional order nonlinear
equation can be generally written as:
C α1 ,··· ,αr ,α0
0 Dt x (t ) = f [tn , x(tn )], 0 ≤ t ≤ T , (56)
where x = and 0 < α1 < · · · < αr < α0 = 1.
(S(t ), E (t ), I (t ), A(t ), R(t ))T
Firstly, the Caputo fractional derivative can be discretized as follows:
1 αi
n
C αi
0 Dt x (tn ) = ck [x(tn−k ) − x(0 )], i = 1, 2, · · · , r, (57)
hαi
k=0
α α
where ck i = (−1 )k i
j
are binomial coefficients. Hence, we have

r
λi
n
λ0
C α1 ,··· ,αr ,α0
0 Dt x (tn ) = ckαi [x(tn−k ) − x(0 )] + [x(tn ) − x(tn−1 )]
hαi h
i=1 k=0

n
r
λi λ0
= ckαi [x(tn−k ) − x(0 )] + [x(tn ) − x(tn−1 )]
hαi h
k=0 i=1

n
r
λi αi λ0
= ck [x(tn−k ) − x(0 )] + [x(tn ) − x(tn−1 )]
hαi h
k=0 i=1

n
λ0
= Bnk [x(tn−k ) − x(0 )] + [x(tn ) − x(tn−1 )], (58)
h
k=0
302
λ α
where Bnk = ri=1 αii ck i .
h
The discrete scheme of the multi-term fractional order equations (55) is given by
C α1 ,··· ,αr ,α0
0 Dt x (tn ) = f [tn , x(tn )], 0 ≤ t ≤ T , (59)
From the equations (58) and (59), we have

n
λ0
Bnk [x(tn−k ) − x(0 )] + [x(tn ) − x(tn−1 )] = f [tn , x(tn )], (60)
h
k=0
i.e,
n
f (tn , x(tn )) Bn0 x(0 ) + λ0 h−1 x(tn−1 ) k=1 Bnk [x(tn−k ) − x(0 )]
x(tn ) = + − . (61)
Bn0 + h−1 Bn0 + λ0 h−1 Bn0 + λ0 h−1
This implicit difference scheme can also be considered as an equation with respect to an unknown variable x(tn ). The
Newton method can be used to solve for the value of x(tn ) of equation (61).
7.2. Application to parameter estimation in the multi-term fractional order SEIAR model of norovirus outbreak
In this section, we consider the following three-term fractional order SEIAR model of the Norovirus outbreak:
C ξ1 ,ξ2 ,ξ0
0 Dt S (t ) = −β S(I + κ A ),
C θ1 ,θ2 ,θ0
0 Dt E (t ) = β S(I + κ A ) − μω E − (1 − μ )ωE,
C φ1 ,φ2 ,φ0
0 Dt I (t ) = (1 − μ )ωE − γ I, (62)
C ϕ1 ,ϕ2 ,ϕ0
D
0 t A (t ) = μω E − γ A,
C ψ1 ,ψ2 ,ψ0
0 Dt R (t ) = γ I + γ A,
where
C ξ1 ,ξ2 ,ξ0
0 Dt = λ1 · C0 Dtξ1 + λ2 · C0 Dtξ2 + λ3 · C0 Dtξ0 ,
C θ1 ,θ2 ,θ0
0 Dt = λ4 · C0 Dtθ1 + λ5 · C0 Dtθ2 + λ6 · C0 Dtθ0 ,
C φ1 ,φ2 ,φ0
0 Dt = λ7 · C0 Dtφ1 + λ8 · C0 Dtφ2 + λ9 · C0 Dtφ0 ,
C ϕ1 ,ϕ2 ,ϕ0 ϕ ϕ ϕ
0 Dt = λ10 · C0 Dt 1 + λ11 · C0 Dt 2 + λ12 · C0 Dt 0 ,
C ψ1 ,ψ2 ,ψ0
0 Dt = λ13 · C0 Dtψ1 + λ14 · C0 Dtψ2 + λ15 · C0 Dtψ0 ,
and the other parameters in this model are defined as the same as those in (36). In order to make the both sides of
the equations (62) have the same dimensions about the time t, the parameters λi (i = 1, 2, · · · , 15 ) are introduced on the
left sides of the equations. The parameters λi (i = 1, 2, 3 ) have dimension of (days )ξi −1 (i = 1, 2, 0 ), and λi (i = 4, 5, 6 ) have
dimension of (days )θi −1 (i = 1, 2, 0 ), respectively, The units of the other parameters λi (i = 7, 8, · · · , 15 ) can be obtained sim-
ilarly. The introduction of these parameters ensures that both sides of the equations have the same dimensions (days )−1 .
Next, we will use the GMMP scheme to obtain the numerical solution for this three-term fractional order SEIAR model
(62), and use the modified hybrid Nelder-Mead simplex search and particle swarm optimization (MH-NMSS-PSO) algorithm
to find a suitable set of fractional orders and parameters, with which the three-term fractional SEIAR model (62) can fit
the real data. As mentioned above for the one-term fractional order SEIAR model (37), each of the parameters in the three-
term SEIAR model (62) has its particular biological meaning and each parameter has a corresponding value range. Therefore,
based on these ranges, we select some appropriate intervals and initial velocities as follows:
0 ≤ λi = pi ≤ 2, i = 1, 2, · · · , 15, 0 ≤ ξ j = p j+15 ≤ 1, j = 1, 2
0 ≤ θk = pk+17 ≤ 1, k = 1, 2, 0 ≤ φl = pl+19 ≤ 1, l = 1, 2
0 ≤ ϕm = pm+21 ≤ 1, m = 1, 2, 0 ≤ ψn = pn+23 ≤ 1, n = 1, 2
1 × 10−4 ≤ β = p26 ≤ 1 × 10−3 , 1 × 10−11 ≤ κ = p27 ≤ 1 × 10−10
0.01 ≤ μ = p28 ≤ 0.3, 1 ≤ ω = p29 ≤ 2, 1 ≤ ω = p30 ≤ 2
0.3 ≤ γ = p31 ≤ 1, 0.05 ≤ γ = p32 ≤ 0.09
and
⎧
⎪ 0.02 , i = 1, 2, · · · , 15;
⎪
⎪
⎪
⎪ 0.01 , i = 16, 17, · · · , 25;
⎪
⎨ 1 × 10−4 , i = 26;
Vi = 1 × 10−11 , i = 27;
⎪
⎪ 0.01 , i = 28;
⎪
⎪
⎪
⎪ 0.025 , i = 29, 30;
⎩
0.01 , i = 31, 32.
303
90
Real data
80 Multi-term fractional SEIAR
70
Infected humans
60
50
40
30
20
10
0
0 5 10 15 20
Time (days)
Fig. 2. Number of infected humans I (t ) in a middle school in the 2007: Comparison of numerical results of three-term fractional SEIAR model with the
real data with the estimated parameters obtained by MH-NMSS-PSO method. The root-mean-square error is rMSE = 2.6041.
Again, using the same initial values and the time as t = 20 days, we apply the MH-NMSS-PSO to estimate model pa-
rameters from the real data based on the numerical solution solved by the GMMP scheme. Fig. 2 shows the comparison of
numerical results of three-term fractional SEIAR model with the real data and the calculated model parameters P ∗ are:
λ1 = 0.0049, λ2 = 1.7476, λ3 = 0.0450, α4 = 2.5174 × 10−4 ,
λ5 = 0.0017, λ6 = 1.9998, λ7 = 0.0038, α8 = 7.8341 × 10−4 ,
λ9 = 0.0377, λ10 = 0.4703, λ11 = 1.9955, λ12 = 0.2186,
λ13 = 0.0095, λ14 = 0.1828, λ15 = 0.8119, ξ1 = 0.6236,
ξ2 = 0.8553, θ1 = 0.6023, θ2 = 0.60 0 0, φ1 = 0.9577,
φ2 = 0.9495, ϕ1 = 0.7814, ϕ2 = 0.9898, ψ1 = 0.6093,
ψ2 = 0.9324, β = 6.2302 × 10−4 , κ = 1.003 × 10−11 , μ = 0.2113,
ω = 1.0018, ω = 1.0012, γ = 0.3026, γ = 0.0524,
As can be seen from Fig. 2 that, the root-mean square error between the numerical solutions of three-term fractional SEIAR
model and the real data is rMSE = 2.6041, which implies that the three-term fractional SEIAR model can provide better fit
to the real data than the integer order and single-term fractional models.
8. Conclusion
In this paper, we reviewed the fractional epidemic model and proposed a general fractional-order epidemic models sys-
tem and a multi-term fractional-order SEIAR Model of Norovirus system based on the Caputo fractional derivative. We use
the modified hybrid Nelder-Mead simplex search and particle swarm optimization (MH-NMSS-PSO) algorithm to estimate
the parameters for fractional differential equations and the multi-term fractional differential equations. Based on the numer-
ical solutions obtained by the GMMP scheme and Newton method, the MH-NMSS-PSO is used to estimate parameters for the
single-term and multi-term fractional-order equations. Numerical results show that the GMMP scheme and MH-NMSS-PSO
are efficient and valid and the fractional models provide an excellent fit to the real data. Furthermore, the multi-term frac-
tional SEIAR model provides better fit to the real data than the integer order and single-term fractional SEIAR models. This
study also demonstrates that the general fraction model mentioned in this paper can predict the number of the infectious
people accurately and help the concerned bodies such as policy makers, stake holders and healthy professionals in making
well informed decisions in preventing or controlling a potential outbreak in their community, the fractional epidemic mod-
els can be a powerful tool that allow us to optimize the use of limited resources of simply to target control measures more
efficiently and help us to understand the global dynamics of the spread of infectious disease.
Acknowledgements
This work is supported by the Scholarship of Overseas Studies in the Education Bureau of Fujian Province, the Young and
Middle-aged Scholars’ Educational Science & Technology Research Project of Fujian Province of China (Grant No. JAT200937),
304
the National Natural Science Foundation of China (Grant No. 11772046), and the Australian Research Council via the Discov-
ery Projects DP 180103858 and DP 190101889.
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Applied Mathematical Modelling 97 (2021) 281–307

Contents lists available at ScienceDirect

Applied Mathematical Modelling

Review of fractional epidemic models

Deﬁnition 1. The fractional integral a Dt−α of function f (t ) is deﬁned as follows:

Deﬁnition 2. The Caputo derivative with order α of function f (t ) is given as

where n − 1 < α < n, n ∈ Z + .

Deﬁnition 3. The Riemann-Liouville derivative with order α of function f (t ) is deﬁned as

where n − 1 < α < n, n ∈ Z + .

Deﬁnition 4. The Grünwald-Letnikov derivative with order α of function f (t ) is deﬁned as follows:

where n − 1 < α < n.

3. Model formulation review

3.1. Mathematical modeling of dengue epidemics (SIR-SI MODEL)

C α1 ,··· ,αr ,α0 βh b

Year Author Model Contribution

3.2. Mathematical modeling of leptospirosis epidemics (SIR-SI MODEL)

3.3. Mathematical modeling of salmonella bacterial infection epidemics(SIRC MODEL)

3.4. Mathematical modeling of H1N1 epidemics(SEIR MODEL)

3.5. Mathematical modeling of measles epidemics(SEIR MODEL)

3.6. Mathematical modeling of an anti-SARS vaccine (SVEIR MODEL)

3.7. Mathematical modeling of HIV/AIDS epidemics (SIJA MODEL)

where 0 ≤ α ≤ 1. The model parameters are:

3.8. Mathematical modeling of smoking epidemics (POSQL MODEL)

3.9. Mathematical modeling of shigellosis and norovirus outbreak (SEIAR MODEL)

λα1 C0Dtα1 S = −β S(I + κ A ),

4. Numerical methods for the fractional order differential equation

λ Ca Dtα x(t ) = f (t , x(t )) (38)

λ Ca Dtα x(t ) = f (t, x(t )), 0 ≤ t ≤ T ,

In particular, if 0 < α ≤ 1, the above formula (43) can be written as follows:

xn+1 = xn − JF (xn )−1 F (xn ), n = 0, 1, 2, · · · , (45)

5. The technique for parameter estimation in fractional order non-linear systems

λ Ca Dtα x(t ) = f (t, x(t ), P ), 0 ≤ t ≤ T ,

6. Application to parameter estimation in the fractional SEIAR model

7. Application to parameter estimation in the multi-term fractional SEIAR model

7.1. Multi-term fractional order SEIAR model of norovirus outbreak

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