A nonlinear Dynamics of Coronavirus (CoV) Model and
Stability Analysis
Manar A. Alqudah
Department of Mathematical Science, Princess Nourah Bint Abdulrahman University P.O.
Box 84428, Riyadh 11671, Saudi Arabia.
maalqudah@pnu.edu.sa, manarqudah@yahoo.com
Abstract—In this paper we introduced new mathematical
model of coronavirus (CoV ) as a system of non linear differential
equations, we found the Jacobian matrix , the equilibrium
points. Studied the local stability analysis of free disease and
the endemic equilibrium points by the help of basic reproduction
number, and established global stability of positive interior
endemic point using suitable Lyapunov function.
1.Introduction
Coronavirus (CoV) is a newly discovered infectious disease
with rapid speared. This disease first reported in Saudi Arabia
in 2012 and transported to many countries in Asia, Europe, US,
and North Africa as discussed in [1] . Coronavirus transmission
of human-to-human is by direct transmission through dribble
produced during sneezing or coughing and indirect
transmission through touching surfaces and devices polluted
with the virus, and then touch the mouth, nose or eyes.
According to the discovered cases, the symptoms of the disease
include fever, cough, shortness of breath, and diarrhea. In
advanced cases, the infected patient has severe pneumonia
which lead to death. The rapid growth in number of CoV cases
set up a global alert to people and government, and world
health organization. Actions were taken to get CoV spread
under control since 2015 [1]. TV stations, posters and
newspapers campaigned to realize the public on CoV
prevention. Sterilizer was splashed in many public places.
People who have had direct or indirect contact with probable
CoV- infected cases have been quarantined in their homes or in
hospitals. The study of CoV transmission dynamics by
mathematical models is very important to analyze the spread
and control of the disease. Researchers studied severe acute
respiratory syndrome (SARS) rather than CoV such as in [2]
Bck Choi and A.W,Pak discussed a simple approximate
mathematical model for public health practitioners to predict
the number of SARS cases death, [3] studied a discrete
epidemic model for SARS transmission and control in China,
in [4] they wrote a discrete mathematical model to represent
candidate genes associated with susceptibility for SARS-
coronavirus. In [5] numerical study of SARS epidemic model
with the inclusion of diffusion in the system was studied.
Reference [ 6] studied learning during a crisis: The SARS
epidemic in Taiwan. In [7] wrote on the role of super spreading
in Middle East respiratory syndrome coronavirus (MERS-
CoV) transmission. [8], and [9] determined (MERS-CoV)
modeling Transmission in Korea, while in [10] a comparison
This preprint research paper has not been peer reviewed. Electronic copy available at: https://ssrn.com/abstract=3267150
of incubation period distribution of human infections with
MERSCoV in South Korea and Saudi Arabia was done. In [11]
investigated of nonlinear epidemiological models for analyzing
and controlling the MERS outbreak in Korea.
It is pointed that the clinical screening of infectives has
essential effect on the spread of CoV. Persons who are unaware
of their infection due to unknown the symptoms of CoV
disease. Moreover those who are aware of their infection may
not always provision while contacting with others. Therefore
random screening of infectives who unaware that they are
infected letting such people to take preventive measures like
masks use so the riskof spreading the infection is reduced.
In this paper we introduced new mathematical model of
coronavirus (CoV ) as a system of non -linear differential
equations, we found the Jacobian matrix , the equilibrium
points. Studied the local stability analysis for each equilibrium
points by the help of basic reproduction number, and
established global stability of positive interior endemic point
using suitable Lyapunov function under sufficient conditions.
This paper organized as follows: In section 2 we introduced
a mathematical model of CoV. In section 3 we showed the
positively solutions of the model and in section 4 we found the
equilibrium points and analyzed their stability also in section 5
we proved the global stability of the endemic point and finally
in section 6 we wrote the conclusion.
2. Mathematical model of Coronavirus (CoV)
The model consist of four populations; 𝑆(𝑡) is the
susceptible or CoV negative individuals, A1 (t) is the
unaware corona infected individuals, A2 (t) is the aware
corona infected individuals and C(t) is the individuals with
CoV . The aware infected population includes of individuals
that have contracted the virus and are known to be infected
after random medical screening. The schematic representation
of the individual flow between the different populations is
shown in the following discussion:
2.1 Susceptible individuals, 𝑆(𝑡).
The susceptibles are consist of individuals that have not
infected but may get infected through the contacts with
infectives. The rate of all recruited of all individual per year to
be susceptible is λ and the natural death rate is
𝛽 per year. Suscetibles are lost from this class after contacts
 with unware infectives 𝐴1 and with aware infectives 𝐴2 at a equations shows that The solution (𝑆(𝑡), 𝐴1 (𝑡), 𝐴2 (𝑡), 𝐶(𝑡))
rates 𝛼1 and 𝛼2 respectively. always positive for 𝑡 ≥ 0.
2.2. Unaware CoV-infected individuals, A1 (t).
The unaware infected individuals are consist of individuals 4. Equilibrium Points and Stability Analysis
that have infected but are not aware of their infection as they
In this section we discussed the existence of model
not developed disease symptoms. it has a natural death rate 𝛽
equilibrium points of the form (𝑆, 𝐴1 , 𝐴2 , 𝐶)
and developing clinical CoV at a rate 𝛿1 . The unware infectives
are assumed to become aware after screening at a rate 𝜃. 𝛾1 is Theorem 2 The model (1) has two equilibrium points
the rate of infected individual after interaction may remain given by the following:
unaware and join the unaware infectives class 𝐴1. The unaware λ
corona infected persons are detected by clinical test of screened 𝑃1 ( , 0,0,0) corresponding to the free disease case and
𝛽
CoV positive through nonlinear term 𝐴1 𝐴2 at rate 𝑘.
𝑃2 (𝑆 ∗ , 𝐴1∗ , 𝐴∗2 , 𝐶 ∗ )
2.3. Aware CoV- infected individuals, 𝐴2 (𝑡). 𝜆 𝛿1 𝐴1 + 𝛿2 𝑓(𝐴1 )
=( , 𝐴 , 𝑓(𝐴1 ), )
This population is created by the screening of (𝛼1 𝐴1 + 𝛼2 𝑓(𝐴1 ) ) + 𝛽 1 𝜇+𝛽
class 𝐴1 with rate 𝜃. This class interact with susceptible and
some of them becomes aware after the interaction and directly corresponding to endemic case.
join this class at rate 𝛾2 , also this population has natural death Proof. To find the equilibrium points, we solved the
rate 𝛽 and developing clinical CoV at a rate 𝛿2 . following system for (𝑆, 𝐴1 , 𝐴2 , 𝐶):
2.4. Individuals with CoV, 𝐶(𝑡). 𝜆 − (𝛼1 𝑆𝐴1 + 𝛼2 𝑆𝐴2 ) − 𝛽𝑆 = 0
This population is created when the infective population 𝛼1 𝑆𝐴1 + 𝛾1 𝑆𝐴2 − (𝜃 + 𝛿1 + 𝛽)𝐴1 − 𝑘𝐴1 𝐴2 = 0
𝐴1 (𝑡) and 𝐴2 (𝑡) develop clinical CoV symptoms at a rate 𝛿1
and 𝛿2 , respectively. This population has natural death rate 𝛽 𝛾2 𝑆𝐴2 + 𝜃𝐴1 − (𝛿2 + 𝛽)𝐴2 + 𝑘𝐴1 𝐴2 = 0
and clearance rate from the virus 𝜇 . 𝛿1 𝐴1 + 𝛿2 𝐴2 − (𝜇 + 𝛽)𝐶 = 0
Taking into account the above considerations, the model 𝜆
we get the equilibrium point trivially 𝑃1 ( , 0,0,0) if
dynamics is assumed to be the following nonlinear ODE’s: 𝛽
𝐴1 = 𝐴2 = 𝐶 = 0 which called the free disease point.

𝑑𝑆 The second point is the endemic equilibrium point has the

= λ − (𝛼1 𝑆𝐴1 + 𝛼2 𝑆𝐴2 ) − 𝛽𝑆, form (𝑆, 𝐴1 , 𝐴2 , 𝐶), such that
𝑑𝑡
𝛿1 𝐴1 + 𝛿2 𝐴2 𝜆
𝑑𝐴1 𝐶= 𝑎𝑛𝑑 𝑆=
= 𝛼1 𝑆𝐴1 + 𝛾1 𝑆𝐴2 − (𝜃 + 𝛿1 + 𝛽)𝐴1 𝜇+𝛽 (𝛼1 𝐴1 + 𝛼2 𝐴2 ) + 𝛽
𝑑𝑡
− 𝑘𝐴1 𝐴2 , (𝟏) Which are two implicit equations between 𝐴1 , 𝐴2 . To find
𝑑𝐴2 𝐴1 , 𝐴2 we write from the second equation of model (1)
= 𝛾2 𝑆𝐴2 + 𝜃𝐴1 − (𝛿2 + 𝛽)𝐴2 + 𝑘𝐴1 𝐴2 , substitute S to get:
𝑑𝑡
𝑑𝐶 𝜆
= 𝛿1 𝐴1 + 𝛿2 𝐴2 − (𝜇 + 𝛽)𝐶, (𝛼1 𝐴1 + 𝛾1 𝐴2 ) − (𝜃 + 𝛿1 + 𝛽)𝐴1
𝑑𝑡 (𝛼1 𝐴1 + 𝛼2 𝐴2 ) + 𝛽
− 𝑘𝐴1 𝐴2 = 0 (𝟐)
𝑆(0) = 𝑆0 > 0, 𝐴1 (0) = 𝐴10 ≥ 0, 𝐴2 (0) = 𝐴20 ≥ 0, 𝐶(0)
= 𝐶0 ≥ 0. And from the third equation of model (1), we have:
Further assume that all of the parameters of the model are 𝜆
𝛾2 𝐴2 ( ) + 𝜃𝐴1 − (𝛿2 + 𝛽)𝐴2 + 𝑘𝐴1 𝐴2
nonnegative. 𝛼1 𝐴1 + 𝛼2 𝐴2 + 𝛽
=0 (𝟑)
3. Positively of solutions
Simplifying (2), (3) to get:
Theorem 1 The solution (𝑆(𝑡), 𝐴1 (𝑡), 𝐴2 (𝑡), 𝐶(𝑡)) of the
model (1) with the above initial conditions, remain positive for 𝜆(𝛼1 𝐴1 + 𝛾1 𝐴2 ) − (𝛼1 𝐴1 + 𝛼2 𝐴2 + 𝛽)(𝜃 + 𝛿1 + 𝛽)𝐴1
all 𝑡 ≥ 0. − 𝑘(𝛼1 𝐴1 + 𝛼2 𝐴2 + 𝛽)𝐴1 𝐴2
Proof. From the second equation of model (1) we have: =0 (𝟒)

𝑑𝐴1 and,
= 𝛼1 𝑆𝐴1 + 𝛾1 𝑆𝐴2 − (𝜃 + 𝛿1 + 𝛽)𝐴1 − 𝑘𝐴1 𝐴2
𝑑𝑡 𝜆𝛾2 𝐴2 + (𝛼1 𝐴1 + 𝛼2 𝐴2 + 𝛽)𝜃𝐴1 − (𝛼1 𝐴1 + 𝛼2 𝐴2 +
≥ −(𝜃 + 𝛿1 + 𝛽)𝐴1 , 𝛽)(𝛿2 + 𝛽)𝐴2 + 𝑘(𝛼1 𝐴1 + 𝛼2 𝐴2 + 𝛽)𝐴1 𝐴2 =
0 (𝟓)
Then 𝐴(𝑡) ≥ 𝑐1 𝑒 −(𝜃+𝛿1+𝛽)𝑡 > 0. Such that 𝑐1 is the
Another simplification:
constant of integration. A similar manner of the other

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 −𝛼1 (𝜃 + 𝛿1 + 𝛽)𝐴1 2 − 𝑘𝛼1 𝐴1 2 𝐴2 − 𝑘𝛼2 𝐴1 𝐴2 2 J
𝜆
( , 0, 0, 0)
𝛽
− (𝛼2 (𝜃 + 𝛿1 + 𝛽) + 𝑘𝛽)𝐴1 𝐴2 𝜆 𝜆
+ ( 𝜆𝛼1 − 𝛽(𝜃 + 𝛿1 + 𝛽))𝐴1 + 𝜆𝛾1 𝐴2 −𝛽 −𝛼1 ( ) −𝛼2 ( ) 0
𝛽 𝛽
=0 (𝟔) 𝜆 𝜆
0 𝛼1 ( ) − (𝜃 + 𝑚1 ) 𝛾1 ( ) 0
= 𝛽 𝛽
and,
𝜆
0 𝜃 𝛾2 ( ) − 𝑚2 0
𝛼1 𝜃𝐴1 2 + 𝑘𝛼1 𝐴1 2 𝐴2 + 𝑘𝛼2 𝐴1 𝐴2 2 𝛽
− (𝛼1 (𝛿2 + 𝛽) − 𝑘𝛽 − 𝛼2 𝜃)𝐴1 𝐴2 + 𝛽 𝜃𝐴1 [ 0 𝛿1 𝛿2 −(𝜇 + 𝛽)]
+ ( 𝜆𝛾2 − 𝛽(𝛿2 + 𝛽)) 𝐴2 − 𝛼2 (𝛿2 + 𝛽)𝐴2 2 ,to find the corresponding characteristic equation we
=0 (𝟕) compute
Adding equations (6) and (7) to get: 𝑑𝑒𝑡(𝐽(𝑃1 ) − 𝑟𝐼) = 0 , so the eigenvalues are:
2
−𝛼1 (𝛿1 + 𝛽)𝐴1 − (𝛼2 (𝛿1 + 𝛽) + 𝛼1 (𝛿2 + 𝛽)) 𝐴1 𝐴2 + (𝜆𝛼1 𝑟1 = −𝛽 , 𝑟2 = −(𝜇 + 𝛽) which have negative sign since
− 𝛽(𝛿1 + 𝛽))𝐴1 𝛽, 𝜇 > 0.
+ ( 𝜆(𝛾1 + 𝛾2 ) − 𝛽(𝛿2 + 𝛽))𝐴2 𝜆 𝜆
− 𝛼2 (𝛿2 + 𝛽) 𝐴2 2 = 0 (𝟖) 𝑟3 = 𝛼1 ( ) − (𝜃 + 𝑚1 ) and 𝑟4 = 𝛾2 ( ) − 𝑚2 , to get
𝛽 𝛽
negative sign eigenvalues we must have for 𝑟3 𝑎𝑛𝑑 𝑟4 :
Let 𝑚1 = 𝛿1 + 𝛽, 𝑚2 = 𝛿2 + 𝛽 so:
𝜆
−𝛼1 𝑚1 𝐴1 2 −(𝛼2 𝑚1 + 𝛼1 𝑚2 ) 𝐴1 𝐴2 + (𝜆𝛼1 − 𝛽𝑚1 )𝐴1 < 𝑚𝑎𝑥 { 𝜃+𝑚
𝛼1
1 , 𝑚2 },
𝛾2
hence we choose 𝑅0 =
𝛽
+ ( 𝜆(𝛾1 + 𝛾2 ) − 𝛽𝑚2 )𝐴2 − 𝛼2 𝑚2 𝐴2 2 𝜆
( the basic reproduction number) and we get
𝜃+𝑚 𝑚
=0 𝛽𝑚𝑎𝑥{ 𝛼 1 , 𝛾 2 }
1 2
the result.
For simplicity letting 𝛼2 𝑚1 + 𝛼1 𝑚2 = 0; implies:
2 2 The stability of the point P2 (S ∗ , A∗1 , A∗2 , C ∗ ) is examined
(𝐴1 + 𝑎2)2 − 𝑎4 = (𝛼𝛼21)2[(𝐴2 + 𝑏2)2 − 𝑏4 ] (𝟗) by finding the Jacobian matrix:
Such that :
𝛽𝑚2 + 𝜆𝛼2
𝑎=( ),
𝛼1 𝑚2 −𝛽 − 𝐽11 −𝐽12 −𝐽13 0
𝛽𝑚2 − 𝜆(𝛾1 + 𝛾2 ) 𝐽21 𝐽22 𝐽23 0
𝑎𝑛𝑑 𝑏=( ), ∗
𝐽 =[ ],
𝛼2 𝑚 2 𝐽31 𝐽32 𝐽33 0
0 𝛿1 𝛿2 −(μ + 𝛽)
𝛼1 𝑎 2 𝑎2 𝛼 𝑏2 𝑏
So, 𝐴2 = √(𝐴1 + ) − + ( 2)2 − . λ
𝛼2 2 4 𝛼1 4 2 Where 𝐽11 = 𝛼1 𝐴1 + 𝛼2 𝑓(𝐴1 ), 𝐽12 = 𝛼1 ( ),
𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 )+𝛽
𝜆
𝐽13 = 𝛼2 ( ),
That is 𝐴2 = 𝑓(𝐴1 ), is positive iff 𝐴1 > 0, thus: 𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 )+𝛽

𝛿1 𝐴1 +𝛿2 𝑓(𝐴1 ) 𝜆 𝐽21 = 𝛼1 𝐴1 + 𝛾1 𝑓(𝐴1 ),

𝐶= 𝑎𝑛𝑑 𝑆=
𝜇+𝛽 (𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 ) )+𝛽 𝜆
are also positive solutions, hence we get the endemic point 𝐽21 = 𝛼1 ( ) − (𝜃 + 𝑚1 ) − 𝑘𝑓(𝐴1 )
𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 )+𝛽
𝜆 𝛿1 𝐴1 + 𝛿2 𝑓(𝐴1 ) (10)
𝑃2 ( , 𝐴1 , 𝑓(𝐴1 ), ) 𝜆
(𝛼1 𝐴1 + 𝛼2 𝑓(𝐴1 ) ) + 𝛽 𝜇+𝛽 𝐽23 = 𝛾1 ( ) − 𝑘𝐴1 ,
𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 )+𝛽
= 𝑃2 (S ∗ , A∗1 , A∗2 , C ∗ )
Theorem 3 The free disease case 𝑃1 is asymptotically 𝐽31 = 𝛾2 𝑓(𝐴1 ), 𝐽32 = 𝜃 + 𝑘𝑓(𝐴1 ), and
stable if 𝑅0 < 1 and unstable if 𝑅0 > 1. 𝐽33 = 𝛾2 (
𝜆
) − 𝑚2 + 𝑘𝐴1 .
𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 )+𝛽
Proof The Jacobian matrix corresponding to system (1) is
given by: Clearly J11 , J12 , J13 , J21 , J31 , and J32 are all positive, and
for J22 , J23 , and J33 to be positive the condition:
J=
−(𝛼1𝐴1 + 𝛼2 𝐴2) − 𝛽 −𝛼1𝑆 −𝛼𝟐 𝑆 0 𝜆
> 𝜃 + 𝑚1 + 𝑚2 + 𝑘𝐴1 + 𝑘𝑓(𝐴1 ).
𝛼1𝐴1 + 𝛾1 𝐴2 𝛼𝟏 𝑆 − (𝜃 + 𝑚1) − 𝑘𝐴2 𝛾1 𝑆 − 𝑘𝐴1 0 𝛼1 𝐴1 +𝛼2 𝑓(𝐴1 )+𝛽
𝛾𝟐 𝐴𝟐 𝜃 + 𝑘𝐴2 𝛾𝟐 𝑆 − 𝑚2 + 𝑘𝐴2 0 (11)
[ 0 𝛿1 𝛿2 −(𝜇 + 𝛽)]
The characteristic equation corresponding to J ∗ takes the
So, the Jacobian matrix at the free disease point is: form:
(𝛽 + 𝜇 + 𝑟)(𝑟 3 + 𝑎1 𝑟 2 + 𝑎2 𝑟 + 𝑎3 )
= 0 , hence the first eigenvalue is ∶

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 𝑟1 = −(𝜇 + 𝛽) < 0 and the other eigenvalues are the roots ≤ (𝛼𝑆̅ −( 𝛿 + 𝛽) )(𝐴1 + 𝐴2 ).
of the function
So,
𝑓(𝑟) = 𝑟 3 + 𝑎1 𝑟 2 + 𝑎2 𝑟 + 𝑎3 = 0,
(𝐴1 + 𝐴2 )(𝑡) ≤ 𝑐2 𝑒 −(𝛿+𝛽−𝛼𝑆̅)𝑡 .
where
Thus, 𝑙𝑖𝑚𝑡→∞ 𝑠𝑢𝑝 (𝐴1 + 𝐴2 )(𝑡) ≤ 0, 𝑎𝑛𝑑
𝑎1 = (𝛽 + 𝐽11 ) − (𝐽22 + 𝐽33 ),
𝑙𝑖𝑚𝑡→0 𝑠𝑢𝑝 (𝐴1 + 𝐴2 )(𝑡) ≤ 𝑐2 = 𝐴10 + 𝐴20 .
𝑎2 = 𝐽22 𝐽33 + 𝐽31 𝐽13 + 𝐽12 𝐽21 − [(𝛽 + 𝐽11 )(𝐽22 + 𝐽33 ) + (14)
𝐽23 ], (𝟏𝟐)
That is the populations 𝐴1 (𝑡), 𝑎𝑛𝑑 𝐴2 (𝑡) are become at
𝑎3 = (𝛽 + 𝐽11 )[𝐽22 𝐽33 − 𝐽23 ] + 𝐽12 [𝐽31 𝐽23 − 𝐽21 𝐽33 ] + the end either CoV individuals 𝐶(𝑡) or cure of the disease to
𝐽13 [𝐽21 𝐽32 − 𝐽22 𝐽31 ]. be susceptible individuals, 𝑆(𝑡).
Here And,
𝑎𝑖 > 0 (𝑖 = 1,2,3) if 𝑑𝐶
(𝐽22 + 𝐽33 ) < (𝛽 + 𝐽11 ) < 𝐽22𝐽33+𝐽(𝐽3122𝐽13+𝐽+𝐽3312) 𝐽21−𝐽23 , 𝐽𝐽23 < 𝐽22 < 𝐽21𝐽31𝐽32, = 𝛿1 𝐴1 + 𝛿2 𝐴2 − (𝜇 + 𝛽)𝐶
33 𝑑𝑡
and
(13)
≤ 𝛿 ′ (𝐴1 + 𝐴2 ) − (𝜇 + 𝛽)𝐶
𝐽31 𝐽23 > 𝐽21 𝐽33 and if 𝑎1 𝑎2 − 𝑎3 > 0
≤ 𝛿 ′ 𝑐2 − (𝜇 + 𝛽)𝐶
the Routh-Hurwitz criteria conditions are hold. Thus the ′
endemic equilibrium P2 is locally asymptotically stable. Thus, Thus, 𝑙𝑖𝑚𝑡→∞ 𝑠𝑢𝑝 𝐶(𝑡) ≤ 𝐶̅ = 𝛿𝜇+𝛽
𝑐2
.

Theorem 4 The endemic point 𝑃2 is locally asymptotically

stable if 𝐽11 , 𝐽12 , 𝐽13 , 𝐽21 , 𝐽31 , 𝐽32 , 𝐽22 , 𝐽23 , 𝑎𝑛𝑑 𝐽33 are defined
by equation (10), and the conditions (13) are hold where
𝑎1 , 𝑎2 , and 𝑎3 have been defined in (12). Theorem 6 The endemic point 𝑃2 is globally
asymptotically stable if the following conditions are satisfied
in 𝛷.
5. Global stability of the endemic point (𝛼1 + 𝛼2 )(2𝑐2 + 𝑆 ∗ ) + 2𝛽 > 𝜋1 + 𝛾2 ,
In this section we studied the global stability about the (15)
endemic point 𝑃2 , by discussing the bound of the dependent
2𝛾1 𝐴∗2 + 𝛼1 𝑆 ∗ > 𝜋1 + 𝜋2 + 𝛿1 ,
variables 𝑆(𝑡), 𝐴1 (𝑡), 𝐴2 (𝑡), 𝑎𝑛𝑑 𝐶(𝑡). For this we find the
(16)
region of attraction in the following lemma.
Lemma 5 The set 2𝜃𝐴1∗ + 𝛼2 𝑆 ∗ > 𝜋1 + 𝛾2 + 𝛿2 , 𝑎𝑛𝑑 𝜇 + 𝛽 > 𝛿1+2 𝛿2,
(17)
̅ 0 ≤ 𝐴1 (𝑡) +
𝛷 = {(𝑆, 𝐴1 , 𝐴2 , 𝐶) ∈ 𝑅+4 : 0 ≤ 𝑆(𝑡) ≤ 𝑆,
𝐴2 (𝑡) ≤ 𝑐2 , 0 ≤ 𝐶(𝑡) ≤ 𝐶̅ } is the region of attraction for the where 𝜋1 = 𝛼1 + 𝛾1 𝑐2 𝐴1∗ and 𝜋2 = 𝛾1 𝑆 ∗ 𝐴1∗ + 𝜃𝐴∗2 .
model (1), starting in the region Proof. The proof is based on constructing a suitable
𝜆 positive definite Lyapunov function about 𝑃2 ,
0 ≤ 𝑆, 𝐴1 , 𝐴2 , 𝑎𝑛𝑑 𝐶, where 𝑆̅ = , 𝑐2 = 𝐴10 + 𝐴20 ,
𝛽 1 1
𝛿′ 𝑐 𝑉(𝑆, 𝐴1 , 𝐴2 , 𝐶) = 12(𝑆−𝑆 ∗)2+ (𝐴1 − 𝐴1∗ − 𝐴1∗ 𝑙𝑛𝐴𝐴1∗ ) + (𝐴2 −
𝐶̅ = 𝜇+𝛽2, 2 1 2
1
𝐴∗2 −𝐴∗2 𝑙𝑛𝐴𝐴2∗ )+ (𝐶 − 𝐶 ∗ )2 ,
𝛿 = 𝑚𝑖𝑛{𝛿1 , 𝛿2 } , 𝛿 ′ = 𝑚𝑎𝑥{𝛿1 , 𝛿2 }, 𝛼 = 𝑚𝑎𝑥{𝛼1 , 𝛾1 + 2 2
𝛾2 }. This function is defined and continuous on 𝑡 (𝑅+4 ) and 𝑉 is
𝑑𝑆 zero at the endemic point P2 (S ∗ , A∗1 , A∗2 , C ∗ ). The time
Proof. Since = 𝜆 − (𝛼1 𝑆𝐴1 + 𝛼2 𝑆𝐴2 ) − 𝛽𝑆 derivative of 𝑉 along a solution of model (1) is given by:
𝑑𝑡

≤ 𝜆 − 𝛽𝑆. 𝑑𝑉
= (𝑆 − 𝑆 ∗ )[𝜆 − (𝛼1 𝑆𝐴1 + 𝛼2 𝑆𝐴2 ) − 𝛽𝑆] + (𝐴1 −
𝑑𝑡
Thus, 𝐴1∗ ) [𝛼1 𝑆 + 𝛾1 𝑆𝐴
𝐴1
2 − (𝜃 + 𝛿 + 𝛽) − 𝑘𝐴 ] + (𝐴 −
1 2 2
𝜆 𝐴
𝑙𝑖𝑚𝑡→∞ 𝑠𝑢𝑝 𝑆(𝑡) ≤ = 𝑆̅. 𝐴∗2 ) [𝛾2 𝑆 + 𝜃 1 − (𝛿2 + 𝛽) + 𝑘𝐴1 ]+ (𝐶 − 𝐶 ∗ )[𝛿1 𝐴1 +
𝛽 𝐴2
𝛿2 𝐴2 − (𝜇 + 𝛽)𝐶],
Now,
which can be written as:
𝑑𝐴1 𝑑𝐴2
+ = 𝛼1 𝑆𝐴1 + 𝛾1 𝑆𝐴2 − (𝛿1 + 𝛽)𝐴1 + 𝛾2 𝑆𝐴2 𝑑𝑉
= − (𝑆 − 𝑆 ∗ )[𝛼1 (𝑆𝐴1 − 𝑆 ∗ 𝐴1∗ )+𝛼2 (𝑆𝐴2 − 𝑆 ∗ 𝐴∗2 ) −
𝑑𝑡 𝑑𝑡 𝑑𝑡
∗ ∗
− (𝛿2 + 𝛽)𝐴2 𝛽(𝑆−𝑆 ∗ )]+(𝐴1 − 𝐴1∗ ) [𝛼1 (𝑆 − 𝑆 ∗ ) + 𝛾1 (𝑆𝐴2 − 𝑆 𝐴2 ) − 𝑘(𝐴 −
2
𝐴1 𝐴∗ 1
≤ 𝛼(𝐴1 + 𝐴2 )𝑆 −( 𝛿 + 𝛽) (𝐴1 + 𝐴2 )

This preprint research paper has not been peer reviewed. Electronic copy available at: https://ssrn.com/abstract=3267150
 𝐴1 𝐴∗1
𝐴∗2 )] + (𝐴2 − 𝐴∗2 ) [𝛾2 (𝑆−𝑆 ∗ ) + 𝜃 ( − ) + 𝑘(𝐴1 − 𝐴1∗ )] + [4] Hsieh YH, Chen CW, Schmitz SF, King CC, Chen
𝐴2 𝐴∗2
(𝐶 − 𝐶 ∗ )[𝛿1 (𝐴1 − 𝐴1∗ ) + 𝛿2 (𝐴2 − 𝐴∗2 ) – (𝜇 + 𝛽)(𝐶 − 𝐶 ∗ )], WJ, Wu YC, Ho MS. “Candidate genes associated with
susceptibility for SARS-coronavirus”. Bull Math Biol.vol.
≤ −[𝛼1 𝐴1 + 𝛼2 𝐴2 + 𝛽](𝑆 − 𝑆 ∗ )2 − 𝛾1 𝐴∗2 (𝐴1 − 𝐴1∗ )2
− 𝜃𝐴1∗ (𝐴2 − 𝐴∗2 )2 − (𝜇 + 𝛽)(𝐶 − 𝐶 ∗ )2 72(1), pp122-32, Jul (2010).
− [𝛼1 𝑆 ∗ − (𝛼1 + 𝛾1 𝐴2 𝐴1∗ )](𝑆 − 𝑆 ∗ )(𝐴1
− 𝐴1∗ ) − [𝛼2 𝑆 ∗ − 𝛾2 ](𝑆 − 𝑆 ∗ )(𝐴2 − 𝐴∗2 ) [5] Afia Naheed, Manmohan Singh, David Lucy.
+ [𝛾1 𝑆 ∗ 𝐴1∗ + 𝜃𝐴∗2 ](𝐴1 − 𝐴1∗ )(𝐴2 − 𝐴∗2 ) “Numerical study of SARS epidemic model with the inclusion
+ 𝛿1 (𝐴1 − 𝐴1∗ )(𝐶 − 𝐶 ∗ ) of diffusion in the system”. Applied Mathematics and
+ 𝛿2 (𝐴2 − 𝐴∗2 )(𝐶 − 𝐶 ∗ ),
Computation, vol. 229 , pp 480–498, (2014).
By equation(14) we have:
≤ −[(𝛼1 + 𝛼2 )𝑐2 + 𝛽](𝑆 − 𝑆 ∗ )2 −𝛾1 𝐴∗2 (𝐴1 − 𝐴1∗ )2 [6] Daniel Bennett. Chun-Fang Chiang, Anup Malani.
− 𝜃𝐴1∗ (𝐴2 − 𝐴∗2 )2 − (𝜇 + 𝛽)(𝐶 − 𝐶 ∗ )2 “Learning during a crisis: The SARS epidemic in Taiwan”.
(𝑆−𝑆 ∗ )2 +(𝐴1 −𝐴∗1 )2
− [𝛼1 𝑆 ∗ − (𝛼1 + 𝛾1 𝑐2 𝐴1∗ )] 2
Journal of Development Economics, vol. 112, pp1-18, Jan
∗ (𝑆−𝑆 ∗ )2 +(𝐴2 −𝐴∗2 )2
− [𝛼2 𝑆 − 𝛾2 ] (2015).
2
(𝐴 ∗ )2 ∗ )2
+ [𝛾1 𝑆 ∗ 𝐴1∗ + 𝜃𝐴∗2 ] 1 −𝐴1 +(𝐴2 −𝐴2 [7] A J Kucharski1, C L Althaus,“The role of super
2
(𝐴 −𝐴∗ )2 +(𝐶−𝐶 ∗ )2 spreading in Middle East respiratory syndrome coronavirus
+ 𝛿1 1 1 2 (MERS-CoV) transmission”. Euro Surveill., vol. 20(25) pp 14-
(𝐴2 − 𝐴∗2 )2 + (𝐶 − 𝐶 ∗ )2 18, Jun (2015).
+ 𝛿2 .
2 [8] Ying-Hen Hsieh, “2015 Middle East Respiratory
𝑑𝑉 Syndrome Coronavirus (MERS-CoV) nosocomial outbreak in
Now, is negative definite under the conditions (15), South Korea: insights from modeling”. PeerJ, DOI
𝑑𝑡
(16), and (17). Finally 𝑃2 (𝑆 ∗ , 𝐴1∗ , 𝐴∗2 , 𝐶 ∗ ) is globally 10.7717/peerj.1505, Nov (2015).
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Sun, Zhen Jin, “Modeling the Transmission of Middle East
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In this paper we introduced new mathematical model of 21, (2015).
coronavirus (CoV ) as a system of four non -linear ODE’s, we [10] Victor Virlogeux, Vicky J. Fang, Minah Park,
found the Jacobian matrix , the equilibrium points. Studied the JosephT.Wu & Benjamin J. Cowling. “Comparison of
local stability analysis for each equilibrium points by the help incubation period distribution of human infections with MERS-
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Hyun Kim , et al. “ Investigation of nonlinear epidemiological
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