Electronic Journal of Differential Equations, Vol. 2017 (2017), No. 121, pp. 1–18.

ISSN: 1072-6691. URL: http://ejde.math.txstate.edu or http://ejde.math.unt.edu

DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL

HAIJIAO LI, SHANGJIANG GUO

Communicated by Zhaosheng Feng

Abstract. This article concerns the SIRC epidemiological model for influenza
A, which efficiently describes the mechanism of disease spreading, including
the susceptible (S), the infected (I) and the recovered (R), along with a cross-
immune class (C) that recovers after being inflected by different strains of the
same viral subtype. The dynamics of the model is completely determined by
the basic reproduction number R0 . If R0 ≤ 1, the disease-free equilibrium
of the SIRC model is globally asymptotically stable, which means influenza
A will die out. Otherwise, the SIRC model may have exactly one endemic
equilibrium which is globally asymptotically stable under certain parametric
conditions. Also, numerical simulations are given to support our analytical
results.

1. Introduction
Influenza [7], a member of the family Orthomyxoviridae, is a RNA virus which
can give rise to epidemic disease between mankind and animals. In general, in-
fluenza is primarily divided into A, B and C types and every type contains a wide
variety of subtypes according to hemagglutinin (HA) and neuraminidase (NA) dif-
ferences. From an epidemiologic standpoint, influenza A is the most common and
the most terrible virus among three types, and can result in the highest pathogenic-
ity because of the easiest way to generate variation. What’s worse, the virus
has brought about more than century pandemic influenza in the past years. The
pathogenicity of influenza B virus is the same as type A, but performed studies are
shown that type B virus does not contribute to century pandemic. Last, influenza C
virus just leads to unconspicuous or feeble respiratory infection and almost doesn’t
incur a pandemic either.
In this article, we pay attention to influenza A virus whose surface often has a
tiny variation, which is referred to as drift. That is, the virus camouflages itself by a
subtle change, and it thereby can elude identificaton by the human immune system.
As a result of the drift, all kinds of flu strains appear every year. Therefore, human
annually need to take a vaccine against influenza for prevention. On the other hand,
shift means influenza A takes place genetic mutations causing a new “subtype”. In
this case, it can lead to outbreaking a global pandemic influenza. For example,

2010 Mathematics Subject Classification. 34D20, 92D30.

Key words and phrases. SIRC model; cross-immunity; global stability;
basic reproduction number.
c 2017 Texas State University.
Submitted May 18, 2016. Published May 4, 2017.
1
2 H. LI, S. GUO EJDE-2017/121

Spanish outbroke H1N1 influenza virus in 1918-1919 about the death toll up to
20-40 million [24]. In 1957-1958, Asia influenza erupted due to the result of H2N2
virus. Furthermore, influenza A virus which threats the lives of even the healthiest
individuals brings serious economic loss for many countries. Some research data
indicate the direct economic loss up to 10-30 billion dollars in America, and the
potential economic losses at 10-15 billion dollars [23]. Consequently, devoting to
studying the spread of influenza A is extremely indispensable.
Mathematically modelling, as a bridge, plays a crucial role in understanding of
the spread of the epidemic. Researchers transform their focus from considering
threshold value of pathophoresis to prevent epidemic propagation by taking some
strategies for control [2]. The model of influenza is parallel to the traditional stan-
dard SIR model in which the crowd are segmented into three compartments: sus-
ceptible (S), infectious (I), recovered (R). A number of compartmental models have
been established based on this idea [26]. Nonetheless, some scholars indicate that
the traditional SIR model is not adequate to describe actual situation of influenza
spreading because every type can evolve different subtypes. Hence, Andreasen
et al. [1] initially considered the dynamics of system with multiple virus strains
consisting of partial cross-immunity [22], concluding that the system exists stable
equilibrium when the number of strains are less than or equal to three. However,
in the work of Lin et al. [13], they demonstrated that oscillations can be sustained
under a linear chain of three cocirculating influenza A strains. These researchers
only consider a special case where cross-protection is symmetric to analyze complex
system because the analysis and computation of multiple viral strains are much in-
tractable. Recently, Minayev and Ferguson [18] proposed a deterministic model
of multi-strain pathogens with symmetric equilibrium, self-organized strain struc-
tures, regular periodic and chaotic regimes, which is determined by cross-immune
response function. In addition to these properties, Kooi et al. [11] revealed bifurca-
tion analysis, Lyapunov exponent calculation as well as quantitative and qualitative
results by numerical simulations in three multi-strain compartment models. Nuño
et al. [21] developed a general multiple strains pathogens model with all kinds of
cross-immunity structures. They illustrated the weaker cross-immunity structures
are more likely to appear instability in the strain coexistence mode. For seasonal
influenza, there is another case where strong and weak cross-immunity can result
in coexistence with the following pandemic. On the contrary, the intermediate level
one may take the place of the seasonal subtype. Chung and Liu [6] extended the
result of Nuño et al. [20] and elucidated the local asymptotic stability of a two-
strain influenza model. Also, the stability may be lost when two strains are far
apart. All the above published works didn’t analyze global asymptotical stability
of models with cross-immune class. In this paper, we investigate a SIRC model
with cross-immune class proposed by Casagrandi et al. [5], which is represented by
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 3

the following system of four ordinary differential equations,

dS(t)
= γ(1 − S) − βSI + ηC,
dt
dI(t)
= βSI + µβCI − (γ + α)I,
dt (1.1)
dR(t)
= (1 − µ)βCI + αI − (γ + δ)R,
dt
dC(t)
= δR − βCI − (γ + η)C,
dt
with initial conditions:
(S(0), I(0), R(0), C(0))T ∈ R4+ := (S, I, R, C)T ∈ R4 : S ≥ 0, I ≥ 0, R ≥ 0, C ≥ 0


and positive real parameters γ, β, η, µ, α, and δ. The parameters α, δ and η

are the inverses of the average time spent by the individuals in each of the three
compartments I, R, and C, respectively. The parameter γ denotes the mortality
rate in every compartment and is assumed to equal to the rate of newborn in the
population. The parameter µ is interpreted as the average reinfection probability
of a cross-immune subject, whereas the parameter β is the contact rate. The state
space of model (1.1) is R4+ . The novelty of this model is that it takes into account the
presence of cross-immune (C) subjects, i.e., subjects that are temporarily immune.
It efficiently describes the mechanism for influenza A virus spreading. In this paper,
we shall not only consider existence, number, and local asymptotical stability of
equilibrium for the model, but also verify the globally asymptotical stability. By
analyzing the SIRC model, we can gain the law of development of influenza A.
In some sense, this paper puts forward an important theoretical approach and
decision-making basis in order to prevent influenza A spreading.
Let
β
R0 =
γ+α
which is called the basic reproduction number [3, 10] or the contact number that
represents the average number of secondary infections from a single infections host.
We can prove that the dynamics of model (1.1) is completely determined by the
threshold value R0 . If R0 ≤ 1 then the disease-free equilibrium E0 is globally
asymptotically stable and hence the disease will die out (see Theorem 4.2). If
R0 > 1 then the unique endemic equilibrium E ∗ is globally asymptotically stable
so that the disease always persists at the unique endemic level (see Theorem 6.3).
Thus, we can conclude that the spread of the disease should be controlled by way
of suitable protection measures of the society to reduce the value of β (transmission
rate of disease) when susceptible individuals contact with infected individuals. This
can be done by adopting some strategies to detect early cases among the passengers
coming from the infected countries and individuals should follow simple steps like
cough etiquettes, stay away from persons coughing or sneezing, avoid gathering and
so on. Disease spreading can also be kept under control by increasing α (recovery
rate of the infected population). It is recommended that if one feels any respiratory
distress, one should report to a nearby hospital immediately. The global stability
of E0 when R0 ≤ 1 can be routinely proved by using a well-known Lyapunov
function, but the global stability of E ∗ when R0 > 1 has been an open problem in
4 H. LI, S. GUO EJDE-2017/121

the literature due to the high dimensionality for the model. Our proof is based on
a theoretical approach developed in [14, 15].
From a mathematical viewpoint, it is interesting to notice that, in the absence
of cross-immunity (µ = 1), the two classes S and C are immunologically indistin-
guishable, since
d(S + C)
= γ[1 − (S + C)] − β(S + C)I + δR.
dt
Consequently, in the limit of µ → 1, the SIRC model reduces to the following
classical SIRS model
dS(t)
= γ(1 − S) − βSI + δR,
dt
dI(t)
= βSI − (γ + α)I, (1.2)
dt
dR(t)
= αI − (γ + δ)R.
dt
Thus, our results generalize some earlier results on the SIRS model. In this paper,
we shall prove the global stability of a unique endemic equilibrium of (1.2) when
the basic reproduction number R0 is greater than 1.
This article is organized as follows. The positively invariant set is shown in
section 2. Section 3 is devoted to the existence of equilibrium including a disease-
free equilibrium and a unique endemic equilibrium. The stability of the disease-
free equilibrium and the endemic equilibrium is presented in sections 4 and 6,
respectively. Section 5 is devoted to the persistence of the model and the work of
numerical simulation reveals in section 7. Finally, this paper ends up with a brief
conclusion in section 8.

2. Positively invariant set

This section is devoted to proving the positivity and boundedness of solutions
of model (1.1) with initial conditions (S(0), I(0), R(0), C(0))T ∈ R4+ . We first
introduce the following lemma.
Lemma 2.1 ([25]). Suppose Ω ⊂ R × Cn is open, fi ∈ C(Ω, R), i = 1, 2, 3 . . . n.
If fi |xi (t)=0,Xt ∈Cn+0 ≥ 0, Xt = (x1t , x2t , . . . , xnt )T , i = 1, 2, 3 . . . n, then Cn+0 is the
invariant domain of the following equations
dxi (t)
= fi (t, Xt ), t ≥ σ, i = 1, 2 . . . n.
dt
Theorem 2.2. Each solution (S(t), I(t), R(t), C(t)) of model (1.1) with the non-
negative initial conditions is non-negative for all t > 0.
Proof. Let X = (S, I, R, C)T and f (X) = (f1 (X), f2 (X), f3 (X), f4 (X))T then we
can rewrite model (1.1) as
Ẋ = f (X)
where    
f1 (X) γ(1 − S) − βSI + ηC
f2 (X)  βSI + µβCI − (γ + α)I 
f (X) = 
f3 (X) = (1 − µ)βCI + αI − (γ + δ)R .
  

f4 (X) δR − βCI − (γ + η)C

EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 5

Note that
dS(t) dI(t)
|S=0 = r + ηC > 0, |I=0 = 0,
dt dt
dR(t) dC(t)
|R=0 = (1 − µ)βCI + αI ≥ 0, |C=0 = δR ≥ 0.
dt dt
Then it follows from Lemma 2.1 that R4+ is invariant set. 

Theorem 2.3. D = {(S, I, R, C)T ∈ R4+ : 0 ≤ S + I + R + C ≤ 1} is a positively

invariant set and also a globally attractive set of model (1.1).
Proof. Consider the total population N (t) = S(t) + I(t) + R(t) + C(t). Direct
calculation leads to
dN
= γ − γN. (2.1)
dt
Solving this equation, we obtain
N (t) = 1 − (1 − N (0))e−γt .
It is straight forward to show that N (t) ≤ 1 if N (0) ≤ 1. This means that the
set D is a positively invariant set for model (1.1). If N (0) > 1 then it turns out
that limt→∞ N (t) = 1. Thereby the set D is the globally attractive set for model
(1.1). 
Remark 2.4. In view of the above two theorems, we see that the positively in-
variant set D can attract every solution with initial conditions starting in its state
space R4+ . Namely, every trajectory of model (1.1) with the initial conditions in
R4+ eventually stays in D.

3. Existence of equilibria
In this section, we consider the existence, type, and number of the equilib-
ria. Obviously, model (1.1) has two equilibria: one is disease-free equilibrium
E0 = (1, 0, 0, 0) which exists for all parameter values; and the other is the endemic
equilibrium E ∗ = (S ∗ , I ∗ , R∗ , C ∗ ), which is a positive solution of the following
equation
γ(1 − S ∗ ) − βS ∗ I ∗ + ηC ∗ = 0,
βS ∗ I ∗ + µβC ∗ I ∗ − (γ + α)I ∗ = 0,
(3.1)
(1 − µ)βC ∗ I ∗ + αI ∗ − (γ + δ)R∗ = 0,
δR∗ − βC ∗ I ∗ − (γ + η)C ∗ = 0.
It follows from the third and forth equations of (3.1) that
δαI ∗
C∗ = . (3.2)
(δµ + γ)βI ∗ + (γ + δ)(γ + η)
Next, substituting (3.2) in the second equation of (3.1), we obtain
γ+α µδα
S∗ = − ∗
· I ∗. (3.3)
β (δµ + γ)βI + (γ + δ)(γ + η)
Combining (3.2) with (3.3) and then substituting them in the first equation of (3.1),
we have
aI ∗2 + bI ∗ + d = 0, (3.4)
6 H. LI, S. GUO EJDE-2017/121

where
a = β 2 (γ + α)(δµ + γ) − β 2 µδα = β 2 (γδµ + γ 2 + αγ) > 0,
b = βγ(γ + α)(δµ + γ) + β(γ + α)(γ + δ)(γ + η)
− γβµδα − γβ 2 (δµ + δ) − βηδα,
d = γ(γ + α)(γ + δ)(γ + η) − γβ(γ + δ)(γ + η).
Therefore, we have the following result.
Theorem 3.1. If R0 ≤ 1, model (1.1) always has a disease-free equilibrium E0 =
(1, 0, 0, 0). If R0 > 1, the model has exactly one endemic equilibrium E ∗ =
(S ∗ , I ∗ , R∗ , C ∗ ).
Proof. It is not difficult to observe that model (1.1) has a disease-free equilib-
rium E0 (1, 0, 0, 0). Now, we consider the existence of the endemic equilibrium
E ∗ (S ∗ , I ∗ , R∗ , C ∗ ) when R0 > 1. It follows from R0 > 1 that d < 0 and hence
that (3.4) has exactly one positive solution I ∗ , which, together with (3.2), implies
that C ∗ is positive. Similarly, from the first and forth equations of (3.1), we see
that both S ∗ and R∗ are positive. Therefore, model (1.1) has exactly one endemic
equilibrium E ∗ when R0 > 1. 

4. Stability of disease-free equilibrium

This section is devoted to the local and global stability of the disease-free equi-
librium.
Theorem 4.1. The disease-free equilibrium E0 (1, 0, 0, 0) is locally asymptotically
stable if R0 < 1. If R0 > 1 then E0 is unstable and all solutions starting from
sufficiently close to E0 in D ultimately leave away from E0 , except those starting
on S-axis close to E0 along this.
Proof. The Jacobian matrix of (1.1) at E0 is
 
−γ −β 0 η
 0 β − (γ + α) 0 0 
 .
 0 α −(γ + δ) 0 
0 0 δ −(γ + η)
Its characteristic equation is
(λ + γ)[λ − (β − (γ + α))](λ + γ + δ)(λ + γ + η) = 0.
If R0 < 1 then all the characteristic roots are less than 0. That is, E0 is locally
asymptotically stable. If R0 > 1 then there exists a characteristic value β−(γ+α) >
0. Therefore, E0 is unstable. Moreover, the trajectory starting from sufficiently
close to E0 will be away from a neighborhood of E0 except that those are on
the S-axis, where model (1.1) can translate into dS(t) dt = γ(1 − S(t)) and hence
limt→∞ S(t) = 1. This completes the proof. 
Next we will prove that E0 is globally asymptotically stable by means of Lya-
punov function.
Theorem 4.2. The disease-free equilibrium E0 for (1.1) is globally asymptotically
stable when R0 ≤ 1.
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 7

Proof. Consider a Lyapunov function V = V (S, I, R, C) defined by

1
V = (S − 1 + I + R + C)2 .
2
The time derivative of V along a solution of (1.1) is
dV
= −γ(S − 1 + I + R + C)2 ≤ 0.
dt
We see that dVdt =0 if and only if S + I + R + C = 1. Consequently, the maximal
invariant set in {(S, I, R, C)T ∈ R4+ : dV T 4
dt = 0} is in {(S, I, R, C) ∈ R+ : S + I +
R + C = 1}. Therefore, to prove that the disease-free equilibrium E0 of (1.1) is
globally asymptotically stable, it suffices to show that the equilibrium (0, 0, 0) of
the following model is globally asymptotically stable:
dI(t)
= βI(1 − I − R − C) + µβCI − (γ + α)I,
dt
dR(t)
= (1 − µ)βCI + αI − (γ + δ)R, (4.1)
dt
dC(t)
= δR − βCI − (γ + η)C.
dt
Again define a Lyapunov function by
1 k1 k3
V1 = (R + C)2 + R2 + k2 I + C 2 ,
2 2 2
where
µ α 2γ + η
k1 = , k2 = , k3 = .
1−µ (1 − µ)β δ
Using a similar argument as above, we have
dV1
= (R + C)(Ṙ + Ċ) + k1 RṘ + k2 I˙ + k3 C Ċ
dt
= −k2 βI 2 − (γ + k1 (γ + δ))R2 − (γ + η + k3 (γ + η))C 2 + k2 (β − (γ + α))I
+ (−µ + k1 (1 − µ))βCIR + (α + k1 α − k2 β)IR + (−(2γ + η) + k3 δ)RC
− (µ + k3 )βC 2 I + (α + k2 (µ − 1)β)CI.
Therefore,
dV1 α 2 µ(γ + δ) 2 2γ + η 2
=− I − (γ + )R − (γ + η)(1 + )C
dt 1−µ 1−µ δ
α 2γ + η
+ (β − (γ + α))I − (µ + )βC 2 I.
(1 − µ)β δ
Since R0 ≤ 1, we obtain
dV1
≤ 0.
dt
Obviously, (4.1) implies that the largest invariant set in the set of dV dt = 0 is
1

(0, 0, 0). By LaSalle’s invariant principle [12, 16], we conclude that model (4.1) is
global asymptotically stable at (0, 0, 0). 
Remark 4.3. From the perspective of epidemiological significance, Theorem 4.2
demonstrates that the disease ultimately dies out regardless of the initial values of
model (1.1) when R0 ≤ 1.
8 H. LI, S. GUO EJDE-2017/121

Take µ = 1, then (1.1) can reduce to the classical SIRS model of the form (1.2).
Hence, we can deduce that the disease-free equilibrium G0 = (1, 0, 0) of (1.2) is
globally asymptotically stable when R0 ≤ 1. Namely, we have the following result.
Corollary 4.4. The disease-free equilibrium for model (1.2) is globally asymptoti-
cally stable when R0 ≤ 1.
In fact, it is straightforward to show that the disease-free equilibrium G0 =
(1, 0, 0) is locally asymptotically stable. We can also illustrate that G0 is globally
asymptotically stable by considering the following Lyapunov function
1 2γ γ
V2 = (S − 1 + I + R)2 + I + R2 .
2 β α
5. Persistence
In the section, we will establish the persistence theorem of disease when R0 > 1.
Persistence implies that the infected individuals will persist in the future. In this
paper, we first use the definition given by Butler and Waltman [4]. That is, model
(1.1) is said to be uniformly persistent if there exists a positive number b such that
n o
min lim inf (S(t)), lim inf (I(t)), lim inf (R(t)), lim inf (C(t)) = b (5.1)
t→∞ t→∞ t→∞ t→∞
for every trajectory with positive initial conditions.
For a region E, denote by ∂E and E̊ the boundary and the interior of E, re-
spectively. Denote by ∂F the restriction of the flow F to ∂E and note that ∂E
is, in general, not positively invariant. Let N be the maximal invariant set of ∂E.
Suppose N is a closed invariant set and there exists a cover {Nα }α∈A of N , where
A is a nonempty index set. Nα ⊂ ∂E, N ⊂ ∪α∈A Nα and Nα (α ∈ A) are pairwise
disjoint closed invariant sets. Furthermore, we propose the following hypotheses:
(H1) All Nα are isolated invariant sets of the flow F;
(H2) Nα (α ∈ A) is acyclic, that is, any finite subset of Nα (α ∈ A) does not
form a cycle;
(H3) Any compact subset of ∂E contains, at most, finitely many sets of Nα
(α ∈ A).
The following lemma plays an important role in analyzing the uniformly persistence.
Lemma 5.1 ([9]). Let E be a closed positively invariant subset of X on which a
continuous flow F is defined. Suppose there is a constant α > 0 such that F is
point dissipative on S[∂E, α] ∩ E̊ and the assumptions (H1)–(H3) hold. Then the
flow F is uniformly persistent if and only if W + (Nα ) ∩ S[∂E, α] ∩ E̊ = ∅ for all
α ∈ A, where W + (Nα ) = {y ∈ X| Λ+ (y) ⊂ Nα }.
Theorem 5.2. Model (1.1) is uniformly persistent in D̊ if and only if R0 > 1.
Proof. It is easy to prove the necessity by means of Theorems 4.1 and 4.2 because
the asymptotical stability of E0 excludes all kinds of persistence. Now, we prove
the sufficiency of this theorem by using Lemma 5.1. Choose X = R4 and E = D.
We only need to prove that model (1.1) satisfies all the conditions of Lemma 5.1.
Note that the maximal invariant set on the boundary ∂D only contains a point
E0 which is isolated. Then the assumptions (H1)–(H3) are satisfied. By Lemma
5.1, we observe that the uniform persistence of model (1.1) is equivalent to the
instability of the disease-free equilibrium. Thereby, the proof is complete. 
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 9

Remark 5.3. It follows from Theorem 5.2 that the uniform persistence of model
(1.1) in the bounded set D̊ is equivalent to the existence of a compact attractor
K ⊂ D̊.

6. Stability of the endemic equilibrium

This section concerns the stability of the endemic equilibrium E ∗ (S ∗ , I ∗ , R∗ , C ∗ )
when R0 > 1.
Theorem 6.1. E ∗ (S ∗ , I ∗ , R∗ , C ∗ ) is locally asymptotically stable when R0 > 1.
Proof. Let N (t) = S(t) + I(t) + R(t) + C(t). It is easy to see that Ṅ (t) = γ − γN (t).
By a change of variables, we see that model (1.1) is equivalent to the model
Ṅ = γ − γN,
Ṡ = γ(1 − S) − βSI + ηC,
(6.1)
˙
I = βSI + µβCI − (γ + α)I,
Ċ = δ(N − S − I − C) − βCI − (γ + η)C .
By Theorem 3.1 model (6.1) has a unique endemic equilibrium (N ∗ , S ∗ , I ∗ , C ∗ ),
where N ∗ = S ∗ + I ∗ + R∗ + C ∗ . Now, it suffices to verify that (N ∗ , S ∗ , I ∗ , C ∗ )
is locally asymptotically stable to show that E ∗ (S ∗ , I ∗ , R∗ , C ∗ ) of model (1.1) is
locally asymptotically stable.
The Jacobian matrix of model (6.1) at (N ∗ , S ∗ , I ∗ , C ∗ ) is
 
−γ 0 0 0
 0 −γ − βI ∗ −βS ∗ η 
 ∗ ∗ ∗ ∗
.
 0 βI βS + µβC − (γ + α) µβI 
∗ ∗
δ −δ −δ − βC −δ − βI − (γ + η)
Since βS ∗ + µβC ∗ − (γ + α) = 0, its characteristic equation is
(λ + γ)(d0 λ3 + d1 λ2 + d2 λ + d3 ) = 0,
where
d0 = 1, d1 = δ + βI ∗ + γ + η + γ + βI ∗ ,
d2 = µβI ∗ (δ + βC ∗ ) + (γ + βI ∗ )(δ + βI ∗ + γ + η) + βI ∗ βS ∗ + δη,
d3 = (γ + βI ∗ )µβI ∗ (δ + βC ∗ ) + βI ∗ βS ∗ (βI ∗ + γ + η) + βI ∗ η(δ + βC ∗ )
+ δ(1 − µ)βI ∗ βS ∗ .
Therefore, the conclusion of this theorem is verified if the real parts of all solutions
of d0 λ3 + d1 λ2 + d2 λ + d3 = 0 are negative. From above, we have d0 > 0, d1 > 0,
d2 > 0, d3 > 0, and
d1 d2 − d0 d3 =(γ + βI ∗ )(δ + η + γ + βI ∗ )(δ + η + γ + βI ∗ + γ + βI ∗ )
+ µβI ∗ (δ + βC ∗ )(δ + η + γ + βI ∗ ) + δη(δ + γ + η + γ + βI ∗ )
+ δµβI ∗ βS ∗ + βI ∗ βS ∗ (γ + βI ∗ ) − βI ∗ βC ∗ η.
It follows from the second of model (6.1) that
ηβC ∗ = −γβ + γβS ∗ + βS ∗ βI ∗ .
We get
βI ∗ βS ∗ (γ + βI ∗ ) − βI ∗ βC ∗ η = γββI ∗ ,
10 H. LI, S. GUO EJDE-2017/121

namely, d1 d2 − d0 d3 > 0. By applying the Routh-Hurwitz criterion, we can verify

that (N ∗ , S ∗ , I ∗ , C ∗ ) is locally asymptotically stable. 

Next, we consider the global asymptotical stability of the endemic equilibrium

E ∗ . The routine technique of the global asymptotical stability of endemic equilib-
rium is based on Lyapunov function and the Poincaré-Bendixson trichotomy. Here
we will utilize another method, which is developed by Li and Muldowney [14, 15].
Let x 7→ f (x) ∈ Rn be a C 1 function for x in an open set D ⊂ Rn . Consider the
differential equation
ẋ = f (x). (6.2)
Denote by x(t, x0 ) the solution to (6.2) such that x(t, x0 ) = x0 , and introduce the
following two assumptions:
(H3) There exists a compact absorbing set K ⊂ D;
(H4) Equation (6.2) has a unique equilibrium x in D.
Let A ba an n × n matrix, A[2] is called the second additive compound matrix
of A, which is an (n2 ) × (n2 ) matrix. For instance, when n = 3,
 
a11 + a22 a23 −a13
f (x) =  a32 a11 + a33 a12  .
−a31 a21 a22 + a33
For the detailed discussions of compound matrix and their properties we refer the
reader to [8, 19]. Let x 7→ P (x) be a (n2 ) × (n2 ) matrix-value function that is C 1
for x ∈ D. Assume that P −1 (x) exists and is continuous in x ∈ K, where K is the
compact absorbing set. A quantity q 2 is defined as
1 t
Z
q 2 = lim sup sup µ(B(x(s, x0 )))ds,
t→∞ x0 ∈K t 0

where
∂f [2] −1
B = Pf P −1 + P P ,
∂x
and the matrix Pf is obtained by replacing each entry pij of P by its derivative in
the direction of f , pijf . The quantity µ(B) is Lozinskiĭ measure of B with respect
to a vector norm | · | in RN , N = (n2 ) × (n2 ), defined by
|I + hB| − 1
µ(B) = lim ,
h→0+ h
see [17]. The following global stability result is [14, Theorem 3.5].

Lemma 6.2. Assume that D is simple connected and that assumptions (H3) and
(H4) hold. Then the unique equilibrium x̄ of (6.2) is global stable in D if q 2 < 0.

Theorem 6.3. If R0 > 1 then the endemic equilibrium E ∗ of (1.1) is globally

asymptotically stable when η < γ and δ − η + α + β < γ.

Proof. From the discussions of Theorem 3.1 and Remark 5.3, we conclude that
model (1.1) satisfies the assumptions (H3) and (H4) in D. From the proof of
Theorem 2.3, we have limt→∞ N (t)=1. Thus, we just need to consider the following
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 11

limiting equation of model (1.1):

Ṡ = γ(1 − S) − βSI + ηC,
I˙ = βSI + µβCI − (γ + α)I, (6.3)
Ċ = δ(1 − S − I − C) − βCI − (γ + η)C.
Let f = (f1 , f2 , f3 )T , where f1 , f2 and f3 represent the right-hand sides of model
(6.3), respectively. Furthermore, let x = (S, I, C)T , then the Jacobian matrix
associated with a general solution x(t) of model (6.3) is
 
−γ − βI −βS η
∂f
=  βI βS + µβC − (γ + α) µβI .
∂x
−δ −δ − βC −δ − βI − (γ + η)
The second additive compound matrix of ∂f
∂x is
 
g11 µβI −η
∂f [2] 
= −δ − βC g22 −βS  ,
∂x
δ βI g33
where
g11 = −γ − βI + βS + µβC − (γ + α),
g22 = −γ − βI − δ − βI − (γ + η),
g33 = βS + µβC − (γ + α) − δ − βI − (γ + η).
Set the function P (x) = P (S, I, C) = diag( SI , SI , SI ), then we have
Ṡ I˙ Ṡ I˙ Ṡ I˙
Pf P −1 = diag( − , − , − ).
S I S I S I
Therefore,
∂f [2] −1
 
−1 B11 B12
B = Pf P +P P = ,
∂x B21 B22
where
Ṡ I˙
B11 = g11 + − , B12 = (µβI, −η),
S I !
I˙
T g22 + ṠS − −βS
B21 = (−δ − βC, δ) , B22 = I
I˙
.
βI g33 + ṠS − I

Let (u, v, w) denote the vector in R3 , we consider the following norm in R3 ,

|(u, v, w)| = max{|u|, |v| + |w|},
and let µ1 denote the Lozinskiĭ measure with respect to this norm. Using the
method of estimating µ1 in [17], we have
µ1 (B) ≤ sup{g1 , g2 },
where g1 = µ1 (B11 ) + |B12 |, g2 = µ1 (B22 ) + |B21 |, and |B12 |, |B21 | are matrix
norms with respect to the L1 vector norm and µ1 denote the Lozinskiǐ measure
with respect to the L1 norm. From (6.1), it implies that
I˙
= βS + µβC − (γ + α).
I
12 H. LI, S. GUO EJDE-2017/121

Therefore,
Ṡ
µ1 (B11 ) = − γ − βI, |B12 | = max{µβI, η}, |B21 | = 2δ + βC,
S
Ṡ
µ1 (B22 ) = − γ + max{−δ − βI − η − βS − µβC + α, βS − δ − βI − η}.
S
Thus, we have
Ṡ Ṡ
g1 = − γ + max{(µ − 1)βI, −βI + η} < − γ + η,
S S
Ṡ
g2 = − γ + max{δ − βI − η − βS + (1 − µ)βC + α, βS + δ − βI − η + βC}
S
Ṡ
< − γ + δ − η + max{α + βC, βS + βC}
S
Ṡ
< − γ + δ − η + α + β.
S
This leads to
Ṡ
µ1 (B) ≤ − γ + max{η, δ − η + α + β},
S
where ω = max{η, δ − η + α + β} < γ. Consequently,
1 t
Z
1 S(t)
µ1 (B)ds ≤ log − (γ − ω),
t 0 t S(0)
which yields q2 < 0. The proof is complete. 

Remark 6.4. Theorems 5.2 and 6.3 describe that the disease always persists and
becomes endemic at an endemic level, no matter how small size the initial value of
infections has. To eradicate the disease, what we need to do is to reduce the key of
threshold value R0 to below 1.
In view of Theorem 6.3, we can obtain the global asymptotical stability of en-
demic equilibrium E ∗ of model (1.1) when R0 > 1, η < γ and δ−η+α+β < γ. In the
following theorem, we shall see that the constraint that η < γ and δ−η+α+β < γ is
not necessary if we consider the global asymptotical stability of endemic equilibrium
of model (1.2), which can be regarded as a special case of model (1.1).
Theorem 6.5. If R0 > 1 then the unique endemic equilibrium of (1.2) is globally
asymptotically stable.
Proof. It is easy to see that if R0 > 1 then model (1.2) has a unique endemic
equilibrium G∗ = (S1∗ , I1∗ , R1∗ ), where
γ+α (γ + δ)(β − γ − α) α(β − γ − α)
S1∗ = , I1∗ = , R1∗ = .
β (γ + δ + α)β (γ + δ + α)β
Meanwhile, we further see that G∗ is locally asymptotically stable. Next, we show
that G∗ is globally asymptotically stable by considering the following Lyapunov
function
1 I k5
V3 = (S − S1∗ + I − I1∗ + R − R1∗ )2 + k4 (I − I1∗ + I1∗ log ∗ ) + (S − S1∗ + I − I1∗ )2 ,
2 I1 2
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 13

where k4 and k5 are positive constants to be determined later. The time derivative
of V3 along the solutions of (1.2) is
dV3 I − I1∗ ˙
= (S −S1∗ +I −I1∗ +R−R1∗ )(Ṡ + I˙ + Ṙ)+k4 ˙
I +k5 (S −S1∗ +I −I1∗ )(Ṡ + I).
dt I
Note that
γ(1 − S1∗ ) − βS1∗ I1∗ + δR1∗ = 0,
βS1∗ I1∗ − (γ + α)I1∗ = 0,
αI1∗ − (γ + δ)R1∗ = 0.
Then, we have
dV3
= (S − S1∗ + I − I1∗ + R − R1∗ )(−γ)(S − S1∗ + I − I1∗ + R − R1∗ )
dt
+ k4 (I − I1∗ )β(S − S1∗ ) + k5 (S − S1∗ + I − I1∗ )(−γ(S − S1∗ )
+ δ(R − R1∗ ) − (γ + α)(I − I1∗ ))
= −γ(1 + k5 )(S − S1∗ )2 − (γ + k5 (γ + α))(I − I1∗ )2 − γ(R − R1∗ )2
+ (−2γ + k4 β − k5 (2γ + α))(S − S1∗ )(I − I1∗ )
+ (−2γ + k5 δ)(S − S1∗ )(R − R1∗ ) + (−2γ + k5 δ)(I − I1∗ )(R − R1∗ ).
Take k4 = 2γ(δ + 2γ + α)/(δβ) and k5 = 2γ/δ, then we have
dV3 2γ 2γ
= −γ(1 + )(S − S1∗ )2 − (γ + (γ + α))(I − I1∗ )2 − γ(R − R1∗ )2 ≤ 0.
dt δ δ
Therefore, the LaSalle’s invariant principle [12, 16] implies that G∗ is globally
asymptotically stable. 

7. Numerical simulation
In this section, we aim to provide a numerical simulation to substantiate the
theoretical results established in the previous sections by using the Runge-Kutta
fourth order iterative method. Consider model (1.1) with the parameters given as
follows: γ = 0.3, η = 0.2, µ = 0.05, α = 0.5, δ = 0.5, β = 0.4.
In Figure 1, we set up two sets of initial values. One case is that S(0) =
0.3, I(0) = 0.5, R(0) = 0, C(0) = 0. Another case is that S(0) = 20, I(0) =
20, R(0) = 0, C(0) = 0. It is observed in Figure 1 that all trajectories of model
(1.1) eventually stay in the positively invariant set D regardless of whether or not
the initial values are in D and that we can obtain the pivotal threshold value
R0 = 0.5 for the choice of parameters. In this case, it follows from Theorem 3.1
that (1.1) has a unique equilibrium E0 = (1, 0, 0, 0). Theorem 4.2 means that this
disease-free equilibrium is globally asymptotically stable.
Figure 1 shows that the infected individuals are eventually eradicated from the
crowd, while the susceptible individuals will ultimately approach the maximum
value. The epidemiological implication of Figure 2(a) is that the infected population
vanish over time. In other words, the disease will die out in the long time. If we
change the value of β into 0.98, then R0 = 1.225 and hence E0 is unstable (see
Figure 2(b)).
If (γ, η, µ, α, δ, β) = (0.3, 0.2, 0.05, 0.5, 0.5, 0.9), then there exists a unique en-
demic equilibrium E ∗ which is locally asymptotically stable (see Theorem 6.1).
Figure 3 implies that the number of infected individuals persist and gradually tend
14 H. LI, S. GUO EJDE-2017/121

(a) (b)
35
S
I
30 R
1
S C
I 25
0.8 R
Populations

Populations
C
20
0.6
15

0.4
10

0.2
5

0 0
0 5 10 15 20 25 0 5 10 15 20 25 30
Time Time

Figure 1. Solution of (1.1) with γ = 0.3, η = 0.2, µ = 0.05,

α = 0.5, δ = 0.5, β = 0.4, where the initial value is (a): S(0) = 0.3,
I(0) = 0.5, R(0) = 0, C(0) = 0, and (b): S(0) = 20, I(0) = 20,
R(0) = 0.

(a) (b)

0.14 0.1

0.12
0.08
0.1

0.06
0.08
R

0.06
0.04

0.04
0.02
0.02

0 0
0.8 0.4

0.6 1 0.3 1
0.8 0.8
0.4 0.2
0.6 0.6
0.2 0.1
0.4 0.4
I 0 0.2 S I 0 0.2 S

Figure 2. Solution of (1.1) with S(0) = 0.3, I(0) = 0.5, R(0) = 0,

C(0) = 0 and γ = 0.3, η = 0.2, µ = 0.05, α = 0.5, δ = 0.5, where
(a) β = 0.4 and (b) β = 0.98.

to a positive constant when R0 = 1.125 > 1. If we take the parameters γ = 0.4,

η = 0.35, µ = 0.05, α = 0.05, δ = 0.05, β = 0.5, then all the conditions of Theorem
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 15

6.3 are satisfied, and hence that E ∗ is globally asymptotically stable. The epidemi-
ological implication of Figure 4 is that the infected individuals always exist if its
initial value is non-negative.

0.9

0.8
S
0.7
I
Populations

0.6 R
C
0.5

0.4

0.3

0.2

0.1

0
0 2 4 6 8 10 12 14 16 18 20
Time

Figure 3. Solution of (1.1) with S(0) = 0.3, I(0) = 0.5, R(0) = 0,

C(0) = 0 and γ = 0.3, η = 0.2, µ = 0.05, α = 0.5, δ = 0.5, β = 0.9.

(a) (b)
1

0.9

0.03
0.8
S
I 0.025
0.7
R
0.02
Populations

0.6 C
0.015
R

0.5
0.01
0.4
0.005
0.3
0
0.5
0.2
0.4 1
0.3 0.8
0.1
0.2 0.6
0.1 0.4
0
0 10 20 30 40 50 60 I 0 0.2 S
Time

Figure 4. Solution of (1.1) with S(0) = 0.3, I(0) = 0.5, R(0) =

0., C(0) = 0 and γ = 0.4, η = 0.35, µ = 0.05, α = 0.05, δ = 0.05,
β = 0.5.

In what follows, we carry out sensitivity analysises for (1.1) by the change of
the recovery rate α as well as the contact rate β. In Figure 5, we study the effect
16 H. LI, S. GUO EJDE-2017/121

of parameter α on model (1.1). We see that parameter α is directly proportional

with the number of susceptible, recovered, cross-immune individuals. However, it
is inversely proportional with the number of infectious individuals, and infectious
individuals finally eradicate. It follows from Figure 5 that the threshold value R0
reduces to be less than 1 by increasing α so that the endemic equilibrium vanishes.
Therefore, model (1.1) just has a disease-free equilibrium. This means that the
larger the parameter α is, the smaller the basic reproduction number R0 is, and
hence the faster the disease die out. From a biological perspective, we should reduce
the value of R0 as possible as we can in order that the disease dies out quickly.
Finally, we examine the influence of the contact rate β. In Figure 6, we observe
that the number of infectious, recovered, cross-immune individuals are directly
proportional with the parameter β, but the number of susceptible individuals are
inversely proportional with the parameter β, and finally approach to 1. Why these
phenomena happened is that the disease-free equilibrium becomes unstable and an
endemic equilibrium appears in (1.1) when the threshold value R0 increases and
passes through 1. This implies that the larger the parameter β is, the larger the
value of R0 is, and then the higher the endemic level will be. As a result, more and
more population contacted with infected individuals will make the disease persist
at an endemic level.

0.5 α=0.005
0.8
α=0.08
0.4 α=0.9
0.6
α=0.005
S

0.3
I

0.4 α=0.08
0.2
α=0.9
0.2
0.1

0 0
0 5 10 15 20 25 30 0 1 2 3 4 5 6 7
Time Time

0.2

α=0.005 α=0.005
0.15
α=0.08 α=0.08
0.1
α=0.9 α=0.9
C
R

0.1

0.05
0.05

0 0
0 1 2 3 4 5 6 7 0 2 4 6 8 10
Time
Time

Figure 5. Sensitivity of model (1.1) for different values of α.

Conclusions. This paper presents a mathematical study on the dynamics of an

SIRC epidemiological model established by Casagrandi et al. [5]. The basic repro-
duction number R0 plays a vital role in determining the global dynamics of (1.1).
EJDE-2017/121 DYNAMICS OF A SIRC EPIDEMIOLOGICAL MODEL 17

1
β=0.02
0.8 0.5 β=0.5
β=0.9
0.4
0.6 β=0.02
S

β=0.5 0.3

I
0.4 β=0.9 0.2
0.2 0.1

0 0
0 1 2 3 4 5 6 7 0 2 4 6 8
Time Time

0.2 0.1
β=0.02
β=0.02
β=0.5
0.15
0.08 β=0.5
β=0.9
β=0.9
0.06
R

C
0.1
0.04
0.05
0.02

0 0
0 2 4 6 8 0 5 10 15
Time Time

Figure 6. Sensitivity of model (1.1) for different values of β.

It is noted that the model always has a disease-free equilibrium, which is globally
asymptotically stable when R0 ≤ 1. When R0 > 1, we apply the Routh-Hurwitz
criterion to prove that the model has a unique endemic equilibrium, which is locally
asymptotically stable. In this case, the disease-free equilibrium become unstable.
Based on Li-Muldowney’s global-stability criterion [14], we show that the unique
endemic equilibrium can be globally asymptotically stable in a feasible region, i.e.,
influenza A becomes endemic. Although we have established the global stability of
the unique endemic equilibrium E ∗ when R0 > 1, our results are obtained under
the assumptions that η < γ and δ −η +α+β < γ. From Theorem 6.5, we conjecture
that the condition that η < γ and δ − η + α + β < γ is not necessary. Therefore,
the perspective of our work is to show the assumption that R0 > 1 is a sufficient
and necessary condition ensuring the globally asymptotical stability of the unique
endemic equilibrium E ∗ .

Acknowledgments. This work has been supported by the Natural Science Foun-
dation of China (Grant No. 11671123).

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Haijiao Li
School of Business Administration, and College of Mathematics and Econometrics,
Hunan University, Changsha, Hunan 410082, China
E-mail address: [email protected]

Shangjiang Guo
College of Mathematics and Econometrics, Hunan University, Changsha, Hunan 410082,
China
E-mail address: [email protected]