Results in Physics 26 (2021) 104390

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Results in Physics
journal homepage: www.elsevier.com/locate/rinp

A mathematical model to study resistance and non-resistance strains

of influenza
Isa Abdullahi Baba a, Hijaz Ahmad b, c, *, M.D. Alsulami d, khadija M. Abualnaja e,
Mohamed Altanji f
a
Department of Mathematical Sciences, Bayero University, Kano, Nigeria
b
Department of Basic Sciences, University of Engineering and Technology, Peshawar, Pakistan
c
Section of Mathematics, International Telematic University Uninettuno, Corso Vittorio Emanuele II, 39, 00186 Roma, Italy
d
University of Jeddah, College of Sciences and Arts at Alkamil, Department of Mathematics, Jeddah, Saudi Arabia
e
Department of Mathematics and Statistics, College of Science, Taif University, P. O. Box 11099, Taif 21944, Saudi Arabia
f
Department of Mathematics, College of Science, King Khalid University, Abha 61413, Saudi Arabia

A R T I C L E I N F O A B S T R A C T

Keywords: Recently, cases of influenza virus resistance are being observed. Resistance is deadly and can cause many pan­
Equilibrium points demics in future. That is why, here we investigate the situation on which the strains exist side – by – side and the
Bilinear incidence rate difference in their mode of transmission. This paper studies two strain (resistance and non - resistance) flu model.
Basic reproduction ratio
The non-resistant strain mutates to give the resistant strain. These strains are differentiated by their incidence
Saturated incidence rate
Global stability
rates which are; bilinear and saturated for the non-resistant and saturated resistant strain respectively. This will
Lyapunov function help in studying the difference in the mode of transmission of the two strains. Equilibrium solutions are
computed and Lyapunov functions are used to show their global stability. It is clear from the analysis that disease
– free equilibrium is globally asymptotically stable if max{RR , RN } < 1. On the other hand endemic equilibrium is
globally asymptotically stable if min{RR , RN } > 1. Any strain with biggest basic reproduction ratio out performs
the other. In order to support the analytic results some numerical simulations are carried out.

Introduction
Influenza virus causes Influenza. It is characterized by a serious
cytopathogenic respiratory disease which is infectious in nature [1].
Based on matrix protein (M) and nucleoprotein (NP) differences, it
subdivide into A, B, and C [2].
Type A and B infects humans and animals. Type A being the most
severe is further divided according to hemagglutinin and neuraminidase
proteins found on the surface of the virus. There is H1 to H16 of hem­
agglutinin and N1 to N9 of neuraminidase. The nomenclature of Influ­
enza A depends on the combination of the various hemagglutinin and
neuraminidase. For example H1N1 virus means influenza A that has an
H1 protein and N1 protein. On the other hand, type C affects only
humans. Its spread is not usually epidemic that is why it is hardly
differentiated from common cold [3].
Another mode of characterization of influenza A and B is through
strains. New Influenza strain appears through either antigenic drift or
antigenic shift [4]. Antigenic drift happens over time through gradual
changes in the virus. New strains are produced which is hardly recog­
nized by antibodies. Contrastingly, antigenic is characterized by rapid
change in the virus which gives rise to an entirely new strain. While
Influenza A can undergo either of the changes, Influenza B only un­
dergoes antigenic drift [5].
New Influenza strain is hardly prevented by vaccination. This can be
observed from the 2009 H1N1 influenza pandemic. Therefore, in order
to prevent the escalation of influenza epidemic, antiviral is needed
[5–7]. Nowadays, influenza virus resistance cases are discovered.
Example is the H3N2 virus resistance to Aminoadamantanes and H1N1
virus resistance to Oseltamivir [8–10]. Resistance is deadly and can
cause many pandemics in future [9].
General, transmission rate of a new strain of is believed to be very
little when compared with the original strain. This phenomenon is
linked with the fact that mutation minimizes viral strength [10–15].
However, it was found in the case of H1N1 influenza virus resistance to
Oseltamivir that these mutations do not necessarily effect virus trans­
mission [16–19].

* Corresponding author.
E-mail address: hijaz555@gmail.com (H. Ahmad).

https://doi.org/10.1016/j.rinp.2021.104390
Received 19 January 2021; Received in revised form 24 May 2021; Accepted 25 May 2021
Available online 29 May 2021
2211-3797/© 2021 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
I. Abdullahi Baba et al. Results in Physics 26 (2021) 104390

Mathematical modeling helps in studying the dynamics of a given

epidemic disease [26–41]. For any epidemic, the important questions
that need answers are: what causes the epidemic, and how can the
population be prevented? Epidemiological models answer these type of
questions [20–22]. That is why, in order to analyze the situation in
which the two strains can coexist and the difference in their mode of
transmission, we employ the use of mathematical modeling. An impor­
tant element in mathematical modeling is the Incidence rate. Its’ sig­
nificance in epidemiology can’t be over emphasized.
This paper studies two strains of influenza and their possible coex­
istence in a population. Different incidence rates were considered for
these strains. This is due to the fact that the mutated strain will have a
minimal effect. We assume saturated and bilinear incidence rates for the
resistant and non-resistant strains respectively. Saturated incidence rate
grasps the negotiating alteration and swarming impact of the infected
people and hinders the unboundedness of the interconnection rate by
Fig. 1. Schematic diagram of model (1).
fitting parameters, which was reused in several epidemic issues [24,25].
The paper follows the following format; in the first section, the
introduction is given. Second section takes care of the model construc­ Mathematical analysis
tion. Detail analysis of the model is given in the third section. Numerical
simulations and conclusion are given in the fourth and fifth sections The following lemma is presented first;
respectively. Lemma 1. S +IR +IN +R = dbis an invariant manifold of system (1), which
is attracting in the fourth quadrant.
Model construction
Proof. Summing equations in (1), we have
An epidemic model with two – strain and four compartments is dN βSIR βSIR
considered. Let S(t) – susceptible, IR (t) - infective resistant, IN (t) - = b − dS − αSIN − + αSIN − (d + μ)IN + − (d + γ)IR
dt 1 + kIR 1 + kIR
infective non-resistant, and R(t) - removed individuals at time t, repre­ + μIN + γIR − dR,
sent the compartments. Table 1 gives the meaning of parameters and
Fig. 1 consists of the schematic diagram of the model. dN
We assume that; = b − dN.
dt
For N(t0 ) ≥ 0, we have
(i) people become susceptible through birth or immigration only
(ii) co – infection is not possible b
N(t) = + ce− dt ,
(iii) there is immunity d

The disease dynamics can clearly be studied using the system of now at t0 = 0,
equations below; b
N(t0 ) = + c,
dS βSIR d
= b − dS − αSIN − , ( )
dt 1 + kIR
b b − dt
∴N(t) = + N(t0 ) − e .
dIN d d
= αSIN − (d + μ)IN ,
dt Thus lim N(t) = db,
t→∞
dIR βSIR Since, N = S +IR +IN +R, then we can consider,
= − (d + γ)IR , (1)
dt 1 + kIR dS βSIR
= b − dS − αSIN − ,
dR dt 1 + kIR
= μIN + γIR − dR.
dt dIN
= αSIN − (d + μ)IN ,
where, N = S + IR + IN + R. dt

dIR βSIR
= − (d + γ)IR .
dt 1 + kIR

Table 1
Parameters description of the model.
Parameter Description
Equilibrium solutions
B Recruitment into susceptible class
1 Death rate
d
We get the following solutions after equating (1) to zero and solving
В Rate of infection by resistant strain the system simultaneously;
α Rate of infection by non – resistant strain
1 Rate at which individuals with resistant strain become removed from
(i) Disease free equilibrium
γ the population
1 Rate at which individuals with non - resistant strain become removed ( )
b
μ from the population E0 = , 0, 0
k Mutation effect on the resistant strain
d

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I. Abdullahi Baba et al. Results in Physics 26 (2021) 104390

⎡ ⎤
αS 0 [ ]
d+μ 0
F=⎣ βS βkSIN ⎦, V =
(ii) Non-resistant equilibrium 0 −
1 + kIN (1 + kIN )2
0 d+γ
( )
d + μ bα − d 2 − d μ Then,
E1 = , ,0 ,
α α(d + μ) ⎡ ⎤
b
2
which exists when bα − d − dμ ≥ 0, and this is the same as bα
≥ 1. ⎢αd 0 ⎥
d(d+μ) ⎢
F(E0 ) = ⎣ ⎥,
b⎦
0 β
(iii) Resistant equilibrium d
( )
d + γ + bk bβ − d2 − dγ and,
E2 = , 0, ,
dk + β dγk + d2 k + βd + βγ ⎡ αb ⎤
0
bβ
⎢ d(d + μ) ⎥
which only exists if bβ − d2 − dγ ≥ 0, and this is the same as d(d+γ) ≥ 1. FV − 1 (E0 ) = ⎢
⎣
⎥
βb ⎦
0
d(d + γ)
(iv) Endemic equilibrium
( ) The dominant eigenvalue of FV − 1 (E0 ) is the basic reproduction
d + μ − (d2 k + dkμ + βd − αd − αγ + βμ − bkα) βd + βμ − αd − αγ number, and is given by;
E3 = , , ,
α (d + μ)αk (d + γ)αk ( )
R0 = ρ FV − 1 .
which only exists if, This implies R0 = RN = d(d+ μ), orR0 = RR = d(d+γ).
αb βb

d2 k + dkμ + βd − αd − αγ + βμ − bkα ≤ 0, (*) The portrait of R0 is given in Figs. 2 and 3 below;

andβd + βμ − αd − αγ ≥ 0.(**) Stability analysis

From (*)
Here, global stability analyses of the equilibrium solutions are car­
[dk(d + μ) − bkα ] + [β(d + μ) − α(d + γ)] ≤ 0. ried out by Lyapunov function technique. Let us prove the following
theorems;
This is equivalent to; d(d+
αb
μ) ≥ 1, and d(d+γ) ≤ d(d+μ).
βb αb

From (**), Theorem 1. E0 is globally asymptotically stable if max{RR , RN } < 1 and

unstable otherwise.
β(d + μ) ≥ α(d + γ).
Proof. Consider the Lyapunov function defined as;
This implies d(d+γ)
βb αb
≥ d(d+ μ).
V = (S − S0 lnS) + IR + IN + C,
From (*) and (**), endemic equilibrium E3 exists only if
βb αb whereC = − S0 +S0 lnS0 . Then
= ≥ 1. ( )
d(d + γ) d(d + μ) S0
V̇ = 1 − Ṡ + I˙R + I˙N
S
Basic reproduction ratio

The method of next generation matrix (NGM) is used here to obtain

the basic reproduction ratio. Let

Fig. 2. Portrait of.R0 = RN

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I. Abdullahi Baba et al. Results in Physics 26 (2021) 104390

Fig. 3. Portrait of.R0 = RR

( )( )
S0 βSIR ( ) ( )
= 1− b − dS − αSIN − + (αS S S1 − αb + d 2 + d μ
S 1 + kIR ≤ dS1 2 − − + (αS − (d + μ))
( ) S1 S α(d + μ)
βSIR ( )
− (d + μ)IN ) + − (d + γ)IR β(d + μ)
1 + kIR + IR − (d + γ)
α
( ) ( )
dS0 2 αS0 βS0 By the relation between geometric and arithmetic means, it is clear
= dS0 − dS − + (d + μ)IN − 1 + (d + γ)IR − 1
S d+μ (d + γ)(1 + kIR ) that V̇ ≤ 0if,
− αb + d2 + dμ < 0andβ(d+
α − (d +γ) < 0.
μ)
( )
S S0 This implies RN > 1and RN > RR .
≤ dS0 2 − − + (d + μ)IN (RN − 1) + (d + γ)IR (RR − 1).
S0 S
Theorem 3. E2 is globally asymptotically stable if RR > 1and RR >
By the relation between geometric and arithmetic means and b(dk+β) b(dk+β)
, RN > d(d+γ+bk).
considering d(d+γ+bk)

max{RR , RN } < 1, we have the proof. Proof. Consider the following Lyapunov function

Theorem 2. If RN > 1 and RN > RR ,then E1 is globally asymptotically V = (S − S2 lnS) + (IR − IR2 lnIR )+IN + C,
stable.
whereC = − S2 +S2 lnS2 − IR2 +IR2 lnIR2 . Then
Proof. Consider the Lyapunov function defined as; ( ) ( )
S2 IR2 ˙
V = (S − S1 lnS) + (IN − IN1 lnIN )+IR + C, V̇ = 1 − Ṡ + 1 − I R + I˙N
S IR
Where C = − S1 +S1 lnS1 − IN1 +IN1 lnIN1 . Then, ( )( ) ( )( )
( ) ( ) S2 βSIR IR2 βSIR
S1 IN1 ˙ = 1− b − dS − αSIN − + 1− − (d + γ)IR
V̇ = 1 − Ṡ + 1 − I N + I˙R S 1 + kIR IR 1 + kIR
S IN + αS − (d + μ)IN
( )( ) ( )
S1 βSIR IN1 ( ) (
= 1− b − dS − αSIR − + 1− (αS − (d + μ)IN )
S 1 + kIR IN dS2 2 βS2
( ) = 2dS2 − dS − + IN (αS2 − (d + μ) ) + IR − (d + γ) + IR2 (d
βSIR S 1 + kIR
+ − (d + γ)IR )
1 + kIR βS
+ γ) −
1 + kIR
dS1 2 ( ) ( ) ( )
= 2dS1 − dS − + IN (αS1 − (d + μ) ) + IN1 ( − αS + (d + μ))
S
( ) =dS2 2− S
S2
− SS2 + IN α(d+γ+bk)
dk+β
− (d + μ) + IR β(d+γ+bk)
dk+β
− (d + γ) +
βS1
+ IR
1 + kIR
− (d + γ) ( )( )
βS − bβ+d2 +dγ
1+kIN
− (d + γ) dγk+d2 k+βd+βγ
( ) ( )
S S1 (d + μ)
= dS1 2 − − +IN α − (d + μ) − IN1 (αS − (d + μ)) By the relation between geometric and arithmetic means, it is clear
S1 S α
⎛ ⎞ V̇ ≤ 0if,
(d+μ)
⎜β α ⎟ d + γ + bk d + μ d + γ + bk d + γ
+ IR ⎝ − (d + γ) ⎠ < , and < .
1 + kIR dk + β α dk + β β

4
I. Abdullahi Baba et al. Results in Physics 26 (2021) 104390

b(dk+β) b(dk+β)
This implies RN > d(d+γ+bk) , andRR > d(d+γ+bk) ,
and − bβ +d2 +dγ < 0 which implies RR > 1.
Theorem 4. If RR = RN > 1, then E3 is globally asymptotically stable.
Proof. Consider the Lyapunov function define as;
V = (S − S3 lnS) + (IR − IR3 lnIR ) + (IN − IN3 lnIN ) + C,
where C = − S3 +S3 lnS3 − IR3 +IR3 lnIR3 − IN3 +IN3 lnIN3 . Then
( ) ( ) ( )
S3 IR3 ˙ IN3 ˙
V̇ = 1 − Ṡ + 1 − IN + 1 − IN
S IR IN
( )( ) ( )(
S3 βSIR IN3
= 1− b − dS − αSIN − + 1− αS
S 1 + kIR IN
( )( )
IR3 βSIR Fig. 5. Dynamics of.E1
− (d + μ)IN ) + 1 − − (d + γ)IR
IR 1 + kIR

Table 2
dS3 2
= 2dS3 − dS − + IN (αS3 − (d + μ) ) + IN3 ((d Parameter values as used in the simulation.
S
( ) ( ) Parameter Fig. 4 Fig. 5 Fig. 6 Fig. 7
βS3 βS
+ μ) − α S ) + I R − (d + γ) + IR3 (d + γ) −
1 + kIR 1 + kIR b 1.00 1.00 1.00 1.00
d 0.20 0.20 0.20 0.20
α 0.15 0.60 0.15 0.60
( ) ( 2 ) μ 0.80 0.20 0.80 0.20
S S3 d k + dkμ + βd − αd − αγ + βμ − αbk
≤ dS3 2− − +(αS − (d + μ)) β 0.10 0.10 0.52 0.60
S3 S αk(d + μ)
( ) ( )( ) γ 0.75 0.75 0.22 0.20
β(d + μ) βS − βd − βμ + αd + αγ
+ IR − (d + γ) + − (d + γ) k 0.10 0.10 0.00 0.00
α 1 + kIR αk(d + γ)
RN 0.75 7.50 0.75 7.50
RR 0.53 0.53 6.20 7.50
By the relation between geometric and arithmetic means, it is clear
V̇ ≤ 0if ,
Numerical simulations
d2 k + dkμ + βd − αd − αγ + βμ − αbk ≤ 0, (*)

α − (d +γ) ≤ 0, (**) and − βd − βμ + αd + αγ ≤ 0.(***)

β(d+μ)
This section consists of the numerical simulations. It can be seen that
From (*) the results support the analytic results. From Fig. 2 it is clear that both
strains die out, reason being max{RR , RN } < 1 (RN = 0.75, andRR =
RN ≥ 1andRN ≥ RR . 0.53). For Fig. 3 resistant strain dies out with RR = 0.53 and non-
From (**) resistant strain persists with RN = 7.5 and in Fig. 4 non-resistant strain
diminish with RN = 0.75and resistant strain persists withRR = 6.2.
RN ≥ RR . Finally in Fig. 5 the two strains persist withRN = RR = 7.5. Parameter
From (***) values for the numerical simulations are given in Table 2.

RR ≥ RN . Conclusion
From (*), (**)and(***), we get
Recently, cases of influenza virus resistance are being observed.
RN = RR = 1. Resistance is deadly and can cause many pandemics in future. That is
why, in this paper we analyze the possible coexistence for the two strains
and the difference in their mode of transmission. Two strain influenza
model is constructed in which one strain mutates to give the other. We
attribute bilinear and saturated incidence rates to non-resistant and

Fig. 4. Dynamics of.E0 Fig. 6. Dynamics of.E2

5
I. Abdullahi Baba et al.
Fig. 7. Dynamics of.E3
resistant strains respectively. Four equilibrium solutions were computed
and Lyapunov functions were used to show their global stabilities. We
were also able to show the stability depends on the magnitude the two
basic reproduction numbers obtained.
We carried out some numerical examples to support the analytic
results. It can be observed from Figs. 4 and 7 that resistant strain seize to
exist rapidly. This is can be seen as the effect of the parameter k, which
shows that the mutations reduced viral fitness.
Declaration of Competing Interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influence
the work reported in this paper.
Acknowledgment
The second and last authors extend their appreciation to the Dean­
ship of Scientific Research at King Khalid University for funding this
work through a research group program under Grant No. R.G.P.2/136/
42. This Research was supported by Taif University Researchers Sup­
porting Project Number (TURSP-2020/217), Taif University, Taif, Saudi
Arabia.
References
[1] Mohler L, Flockerzi D, Sann H, Reichl U. Mathematical model of influenza A virus
production in large scale micro carrier culture. Biotechnol Bioeng 2005;90:46–58.
[2] Tamura S, Tanimoto T, Kurata T. Mechanism of cross – protection provided by
influenza virus infection and their application to vaccines. Jpn J Infect Dis 2005;
58:195–207.
[3] Webster RG, Peiris M, Chen H, Guan Y. H5N1 Outbreaks and enzootic influenza.
Emerg Inf Dis 2016;12:3–8.
[4] Martcheva M, Iannelli M, Li XZ. Sub threshold coexistence of strains: the impact of
vaccination and mutation. Mathematical Biosciences and Engineering 2007;4:
287–317.
[5] Ward P, Small I, Smith J, Suter P, Dutkowski R. Oseltamivir (Tamiflu) and its
potential for use in the event of an influenza pandemic. J Antimicrob Chemother
2005;55:i5–21.
[6] Schünemann HJ, Hill SR, Kakad M, et al. WHO Rapid Advice Guidelines for
pharmacological management of sporadic human infection with avian influenza A
(H5N1) virus. Lancet Infect Dis 2007;7:21–31.
[7] Fiore AE, Fry A, Shay D, Gubareva L, Bresee JS, Uyeki TM. Antiviral agents for the
treatment and chemoprophylaxis of influenza — recommendations of the Advisory
Committee on Immunization Practices (ACIP). MMWR Recomm Rep 2011;60:1–24.
[8] Baranovich T, Saito R, Suzuki Y, et al. Emergence of H274Y oseltamivir-resistant A
(H1N1) influenza viruses in Japan during the 2008–2009 season. J ClinVirol 2010;
47:23–8.
[9] Monto AS, McKimm-Breschkin JL, Macken C, et al. Detection of influenza viruses
resistant to neuraminidase inhibitors in global surveillance during the first 3 years
of their use. Antimicrob Agents Chemother 2006;50:2395–402.
[10] Carr J, Ives J, Kelly L, et al. Influenza virus carrying neuraminidase with reduced
sensitivity to oseltamivir carboxylate has altered properties in vitro and is
Results in Physics 26 (2021) 104390
compromised for infectivity and replicative ability in vivo. Antiviral Res 2002;54:
79–88.
[11] Herlocher ML, Carr J, Ives J, et al. Influenza virus carrying an R292K mutation in
the neuraminidase gene is not transmitted in ferrets. Antiviral Res 2002;54:
99–111.
[12] Bouvier NM, Lowen AC, Palese P. Oseltamivir-resistant influenza A viruses are
transmitted efficiently among guinea pigs by direct contact but not by aerosol.
J Virol 2008;82:10052–8.
[13] Ives JA, Carr JA, Mendel DB, et al. The H274Y mutation in the influenza A/H1N1
neuraminidase active site following oseltamivir phosphate treatment leave virus
severely compromised both in vitro and in vivo. Antiviral Res 2002;55:307–17.
[14] Herlocher ML, Truscon R, Elias S, et al. Influenza viruses resistant to the antiviral
drug oseltamivir: transmission studies in ferrets. J Infect Dis 2004;190:1627–30.
[15] Abed Y, Goyette N, Bovin G. A reverse genetics study of resistance to
neuraminidase inhibitors in an influenza A/H1N1 virus. AntivirTher 2004;9:
577–81.
[16] Rameix-Welti MA, Enouf V, Cuvelier F, Jeannin P, van der Werf S. Enzymatic
properties of the neuraminidase of seasonal H1N1 influenza viruses provide
insights for the emergence of natural resistance to oseltamivir. PLoS Pathog 2008;
4:e1000103.
[17] Baz M, Abed Y, Simon P, Hamelin ME, Boivin G. Effect of the neuraminidase
mutation H274Y conferring resistance to oseltamivir on the replicative capacity
and virulence of old and recent human influenza A(H1N1) viruses. J Infect Dis
2010;201:740–5.
[18] Matsuzaki Y, Mizuta K, Aoki Y, et al. A two-year survey of the oseltamivir-resistant
influenza A(H1N1) virus in Yamagata, Japan and the clinical effectiveness of
oseltamivir and zanamivir. Virol J 2010;7:53.
[19] Bloom JD, Gong LI, Baltimore D. Permissive secondary mutations enable the
evolution of influenza oseltamivir resistance. Science 2010;328:1272–5.
[20] Lipsitch M, Riley S, Cauchemez S, Ghani AC, Ferguson NM. Managing and reducing
uncertainty in an emerging influenza pandemic. N Engl J Med 2009;361:112–5.
[21] Kaymakamzade B, Baba IA, Hincal E. Global stability analysis of Oseltamivir -
resistant influenza virus model. Procedia Comput Sci 2016;102:333–41.
[22] Baba IA, Hincal E. Global stability analysis of two strain epidemic model with
bilinear and non - monotone incidence rates. Eur Phys J Plus 2017;132:208.
[24] Gomes MGM, Margheri A, Medley GF, Rebelo C. Dynamical behaviour of
epidemiological models with sub-optimal immunity and nonlinear incidence. Math
Biosci 2005;51:414–30.
[25] Liu X, Yang L. Stability analysis of an SEIQV epidemic model with saturated
incidence rate. Nonlinear Anal Real World Appl 2005;13:2671–9.
[26] Baba IA, Nasidi BA, Baleanu D. Optimal Control Model for the Transmission of
Novel COVID – 19. Computers, Materials and Continua 2021;66(3):3089–106.
[27] Baba IA, Yusuf A, Nisar KS, Abdel-Aty A, Nofal TA. Mathematical Model to Assess
the Imposition of Lockdown During COVID- 19 Pandemic. Results Phys 2020;20:
103716.
[28] Sohail A, Iftikhar M, Arif R, Ahmad H, Gepreel KA, Iftikhar S. Dengue control
measures via cytoplasmic incompatibility and modern programming tools. Results
Phys 2021;21:103819.
[29] Baba IA, Baba BA, Esmaili P. A Mathematical Model to Study the Effectiveness of
Some of the Strategies Adopted in Curtailing the Spread of COVID – 19. Comput
Math Methods Med 2020;6:5248569. https://doi.org/10.1155/2020/5248569.
[30] Javeed S, Anjum S, Alimgeer KS, Atif M, Khan MS, Farooq WA, et al.. A Novel
Mathematical Model for COVID-19 with Remedial Strategies. Results in Physics,
2021. p.104248.
[31] Baba IA, Baleanu D. Awareness as the Most Effective Measure to Mitigate the
Spread of COVID-19 in Nigeria. Computers, Materials and Continua 2020;65(3):
1945–57.
[32] Ahmed I, Baba IA, Yusuf A, et al. Analysis of Caputo fractional – order model for
COVID – 19 with lockdown. Adv Diff Eq 2020;2020:394.
[33] Baba IA, Ghanbari B. Existence and uniqueness of solution of a fractional order
tuberculosis model. European Physical Journal Plus 2019;134(10).
[34] Baba IA, Abdulkadir RA, Esmaili P. Analysis of tuberculosis model with saturated
incidence rate and optimal control. Physica A 2019;540:123237.
[35] Ahmad H, Seadawy AR, Khan TA, Thounthong P. Analytic approximate solutions
for some nonlinear Parabolic dynamical wave equations. Journal of Taibah
University for Science 2020;14(1):346–58.
[36] Baba I. A. A fractional order bladder cancer model with BCG treatment effect.
Computational and Applied Mathematics (2019). 38 (37). 10.1007/s40314 – 019 –
0810 – z .
[37] Atangana A. Modelling the spread of COVID-19 with new fractal-fractional
operators: Can the lockdown save mankind before vaccination? Chaos, Solitons
Fractals 2020;136:109860.
[38] Atangana E, Atangana A. Facemasks simple but powerful weapons to protect
against COVID-19 spread: Can they have sides effects? Results Phys 2020:103425.
[39] Panda SK. Applying fixed point methods and fractional operators in the modelling
of novel coronavirus 2019-nCoV/SARS-CoV-2. Results Phys 2020;19:103433.
[40] Khan M.A., Atangana A., Alzahrani E. et al. The dynamics of COVID-19 with
quarantined and isolation. Adv Differ Equ (2020). 425 (2020). https://doi.org/
10.1186/s13662-020-02882-9.
[41] Khan MA, Atangana A. Modeling the dynamics of novel coronavirus (2019-nCov)
with fractional derivative. Alexandria Eng J 2020;59(4):2379–89.