16
Wang and Jia Advances in Difference Equations (2019) 2019:433 https://doi.org/10.1186/s13662-019-2352-5 RESEARCH Open Access Stationary distribution of a stochastic SIRD epidemic model of Ebola with double saturated incidence rates and vaccination Panpan Wang 1 and Jianwen Jia 1* * Correspondence: [email protected] 1 School of Mathematical and Computer Science, Shanxi Normal University, Linfen, China Abstract In this paper, a stochastic SIRD model of Ebola with double saturated incidence rates and vaccination is considered. Firstly, the existence and uniqueness of a global positive solution are obtained. Secondly, by constructing suitable Lyapunov functions and using Khasminskii’s theory, we show that the stochastic model has a unique stationary distribution. Moreover, the extinction of the disease is also analyzed. Finally, numerical simulations are carried out to portray the analytical results. MSC: Primary 37H10; 60H10; secondary 92C60; 92D30 Keywords: Stochastic SIRD model; Ebola virus; Extinction; Stationary distribution 1 Introduction Ebola virus is a potent virus which causes Ebola hemorrhagic fever in humans and pri- mates. It is a very rare virus. After discovering its existence in southern Sudan and the Ebola region of Congo in 1976, it attracted widespread attention in the medical commu- nity. Ebola virus has a high mortality rate between 50 percent and 90 percent. It is mainly transmitted by contacting with the blood, body fluids, and infected corpses of animals or human. For the spread of Ebola virus, on the basis of models (see e.g. Refs. [16]), we di- vide the total group into four categories: susceptible group S, infected group I , recovered group R, and infected corpse group D. The infected corpse can spread disease through contacting with the susceptible, and its infection rate is higher than that of an infected individual. Considering the above discussion, the deterministic SIRD epidemic model is formulated as follows: dS dt = A β 1 S(t)I (t) 1+α 1 I (t) β 2 S(t)D(t) 1+α 2 D(t) μS(t )– qS(t ), dI dt = β 1 S(t)I (t) 1+α 1 I (t) β 2 S(t)D(t) 1+α 2 D(t) –(ρ + μ + δ)I (t ), dR dt = ρ I (t )+ qS(t )– μR(t ), dD dt =(μ + δ)I (t )– γ D(t ), (1.1) where A is a constant input rate, β 1 and β 2 represent the transmission coefficient. Func- tions β 1 S(t)I (t) 1+α 1 I (t) and β 2 S(t)D(t) 1+α 2 D(t) represent two different types of saturated incidence rates. μ is © The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, pro- vided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Page 1: StationarydistributionofastochasticSIRD … · 2019. 10. 15. · WangandJia AdvancesinDifferenceEquations20192019:433 Page3of16 Thispaperisarrangedasfollows.InSect.2,westudytheexistenceofanergodicsta

Wang and Jia Advances in Difference Equations (2019) 2019:433 https://doi.org/10.1186/s13662-019-2352-5

R E S E A R C H Open Access

Stationary distribution of a stochastic SIRDepidemic model of Ebola with doublesaturated incidence rates and vaccinationPanpan Wang1 and Jianwen Jia1*

*Correspondence:[email protected] of Mathematical andComputer Science, Shanxi NormalUniversity, Linfen, China

AbstractIn this paper, a stochastic SIRD model of Ebola with double saturated incidence ratesand vaccination is considered. Firstly, the existence and uniqueness of a globalpositive solution are obtained. Secondly, by constructing suitable Lyapunov functionsand using Khasminskii’s theory, we show that the stochastic model has a uniquestationary distribution. Moreover, the extinction of the disease is also analyzed. Finally,numerical simulations are carried out to portray the analytical results.

MSC: Primary 37H10; 60H10; secondary 92C60; 92D30

Keywords: Stochastic SIRD model; Ebola virus; Extinction; Stationary distribution

1 IntroductionEbola virus is a potent virus which causes Ebola hemorrhagic fever in humans and pri-mates. It is a very rare virus. After discovering its existence in southern Sudan and theEbola region of Congo in 1976, it attracted widespread attention in the medical commu-nity. Ebola virus has a high mortality rate between 50 percent and 90 percent. It is mainlytransmitted by contacting with the blood, body fluids, and infected corpses of animals orhuman. For the spread of Ebola virus, on the basis of models (see e.g. Refs. [1–6]), we di-vide the total group into four categories: susceptible group S, infected group I , recoveredgroup R, and infected corpse group D. The infected corpse can spread disease throughcontacting with the susceptible, and its infection rate is higher than that of an infectedindividual.

Considering the above discussion, the deterministic SIRD epidemic model is formulatedas follows:

⎧⎪⎪⎪⎪⎪⎨

⎪⎪⎪⎪⎪⎩

dSdt = A – β1S(t)I(t)

1+α1I(t) – β2S(t)D(t)1+α2D(t) – μS(t) – qS(t),

dIdt = β1S(t)I(t)

1+α1I(t) – β2S(t)D(t)1+α2D(t) – (ρ + μ + δ)I(t),

dRdt = ρI(t) + qS(t) – μR(t),dDdt = (μ + δ)I(t) – γ D(t),

(1.1)

where A is a constant input rate, β1 and β2 represent the transmission coefficient. Func-tions β1S(t)I(t)

1+α1I(t) and β2S(t)D(t)1+α2D(t) represent two different types of saturated incidence rates. μ is

© The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in anymedium, pro-vided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, andindicate if changes were made.

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 2 of 16

the natural mortality rate of S, I , and R compartments, δ is mortality due to diseases, 1γ

represents the average period of infectiousness after death in human corpses, and ρ is therecovery rate. On the basis of biological significance, all parameter values are assumed tobe positive, and the quantity of infected corpse is less than the quantity of infected indi-viduals, that is, I(t) > D(t), see [7].

Noticing that R has no influence on the transmission dynamics, we can exclude the thirdequation. Therefore, we only need to study the following subsystem:

⎧⎪⎪⎨

⎪⎪⎩

dSdt = A – β1S(t)I(t)

1+α1I(t) – β2S(t)D(t)1+α2D(t) – μS(t) – qS(t),

dIdt = β1S(t)I(t)

1+α1I(t) – β2S(t)D(t)1+α2D(t) – (ρ + μ + δ)I(t),

dDdt = (μ + δ)I(t) – γ D(t).

(1.2)

Obviously, the feasible region of system (1.2) is R3+. Referring to [8], we have the basic

production number of system (1.2), its expression is

�0 =β1Aγ + β2A(μ + δ)(μ + q)γ (ρ + μ + δ)

.

It is easy to draw two conclusions about system (1.2).

Lemma 1.1 If �0 < 1, the disease-free equilibrium E0 = ( Aμ+q , 0, 0) exists, and the E0 is glob-

ally asymptotically stable.

Lemma 1.2 If �0 > 1, the endemic equilibrium E∗ = (S∗, I∗, D∗) exists, and the E∗ is globallyasymptotically stable.

As mentioned above, we show that the epidemic model is depicted by deterministicmodel. However, epidemic models are inevitably influenced by multifarious unpredictableenvironmental noise types because of the actual situations. Owing to this reason, manyauthors have studied epidemic models with stochastic perturbations (see e.g. Refs. [9–18]). But as far as we know, the studies on the dynamics of the stochastic SIRD model ofEbola seem to be rare. In this paper, we assume that stochastic perturbations are of thewhite noise type which are directly proportional to S(t), I(t), D(t), influenced on the S(t),I(t), D(t) in system (1.2) respectively, then we build the following stochastic model:

⎧⎪⎪⎨

⎪⎪⎩

dS(t) = (A – β1S(t)I(t)1+α1I(t) – β2S(t)D(t)

1+α2D(t) – μS(t) – qS(t)) dt + σ1S(t) dB1(t),

dI(t) = ( β1S(t)I(t)1+α1I(t) + β2S(t)D(t)

1+α2D(t) – (ρ + μ + δ)I(t)) dt + σ2I(t) dB2(t),

dD(t) = ((μ + δ)I(t) – γ D(t)) dt + σ3D(t) dB3(t),

(1.3)

where σi (i = 1, 2, 3) denotes the intensities of the white noises which satisfy nonnegativity.Bi(t) (i = 1, 2, 3) is a standard Brownian motion that is defined on a complete probabilityspace (Ω , F, P) with a filtration {Ft}t∈R+ satisfying the usual conditions, that is, {Ft}t∈R+

is right continuous and F0 contains all P-null sets. Other parameters are the same as forsystem (1.2).

Compared with model (1.2), model (1.3) has the advantage of introducing stochasticperturbations, which makes the model closer to reality. Of course, the results of model(1.3) are more refined.

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 3 of 16

This paper is arranged as follows. In Sect. 2, we study the existence of an ergodic sta-tionary distribution of stochastic system (1.3). In Sect. 3, we deduce the conditions forextinction of the disease. Numerical simulations are given to support our theoretical re-sults in Sect. 4. Finally, Sect. 5 presents some conclusions.

2 Stationary distribution of system (1.3)In this section, we construct a suitable Lyapunov function to obtain the conditions of theexistence of a unique ergodic stationary distribution to system (1.3). Before this, we intro-duce the following lemma.

Lemma 2.1 ([19]) The Markov process X(t) has a unique ergodic stationary distributionπ (·) if a bounded domain Dε ⊂ Rd with regular boundary Γ exists and

(H1) there is a constant M > 0 satisfying∑d

i,j=1 aij(x)ξiξj ≥ M|ξ |2, x ∈ Dε , ξ ∈ Rd ;(H2) there exists a nonnegative C2-function V such that LV is negative for any Rd \ Dε .

Then

P{

limt→∞

1T

∫ T

0f(X(t)

)dt =

Df (x)π (dx)

}

= 1

for all x ∈ D, where f (·) is an integrable function with respect to the measure π .

Theorem 2.1 For any initial value (S(0), I(0), D(0)) ∈ �3+, there exists a unique positive

solution (S(t), I(t), D(t)) of system (1.3) for t ≥ 0, and the solution will remain in �3+ with

probability one.

The proof of this theorem is standard and we omit it.

Theorem 2.2 If

�s0 :=

β1

(μ + q + σ 212 )(ρ + μ + δ + σ 2

22 )

> 1,

then system (1.3) has a unique stationary distribution π (·), and the solution (S(t), I(t), D(t))of system (1.3) is ergodic.

Proof The diffusion matrix of system (1.3) is

A =

⎜⎝

σ 21 S2 0 00 σ 2

2 I2 00 0 σ 2

3 D2

⎟⎠ .

Let M = min(S,I,D)∈Dσ{σ 2

1 S2,σ 22 I2,σ 2

3 D2}, then we can get

3∑

i,j=1

aij(x)ξiξj = σ 21 S2ξ 2

1 + σ 22 I2ξ 2

2 + σ 23 D2ξ 2

3 ≥ M|ξ |2, (S, I, D) ∈ Dσ , ξ ∈ R3+.

Therefore, condition (H1) in Lemma 2.1 is proven.Next, the validity of condition (H2) in Lemma 2.1 will be verified.

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 4 of 16

We define a C2-function V (S, I, D): R3 → R as follows:

V (S, I, D) = M(

S +(

1 +α1

ρ + μ + δI)

+ 2D – c1 ln S – c2 ln I)

– ln S – ln D +1

m + 1(S + I + D)m+1

:= MV1 + V2 + V3 + V4, (2.1)

where M, c1, c2 will be determined later. m and δ are positive constants and satisfy thefollowing inequality:

ρ := δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)

> 0, δ = min{μ + q,ρ,γ }.

Obviously,

limk→∞,(S,I,D)∈R3\Uk

V (S, I, D) = +∞,

herein, Uk = ( 1k , k) × ( 1

k , k) × ( 1k , k). Then, V (S, I, D) is a continuous function and has a

minimum point (S0, I0, D0) in the interior of R3+. A nonnegative C2-function V (S, I, D):

R3 → R can be defined as

V (S, I, D) = V (S, I, D) – V (S0, I0, D0).

Making use of Itô’s formula, we get

LV1 = A –β1SI

1 + α1I–

β2SD1 + α2D

– μS – qS

+α1β1SI

(ρ + μ + δ)(1 + α1I)+

α1β2SD(ρ + μ + δ)(1 + α2D)

– α1I + 2(μ + δ)I – 2γ D

– c1AS

+ c1β1I

1 + α1I+ c1

β2D1 + α2D

+ c1(μ + q) +c1

2σ 2

1

– c2β1S

1 + α1I– c2

β2SDI(1 + α2D)

+ c2(ρ + μ + δ) +c2

2σ 2

2

≤ –α1I – 1 – c1AS

– c2β1S

1 + α1I+ 1 + A +

α1Sρ + μ + δ

[β1I

1 + α1I+

β2D1 + α2D

]

+ 2(μ + δ)I + c1

[β1I

1 + α1I+

β2D1 + α2D

]

+ c1(μ + q) +c1

2σ 2

1

+ c2(ρ + μ + δ) +c2

2σ 2

2

≤ –3(Aβ1c1c2)13 + c1

(

μ + q +σ 2

12

)

+ c2

(

ρ + μ + δ +σ 2

22

)

+ 1 + A

+α1S

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2(μ + δ)I + c1

(β1

α1+

β2

α2

)

. (2.2)

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 5 of 16

Choosing

c1 =A

μ + q + σ 212

, c2 =A

ρ + μ + δ + σ 222

,

we have

LV1 ≤ – 3[

A3β1

(μ + q + σ 212 )(ρ + μ + δ + σ 2

22 )

] 13

+ 3A + 1 +α1S

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2(μ + δ)I +A

μ + q + σ 212

(β1

α1+

β2

α2

)

= – 3A((�S

0) 1

3 – 1)

+ 1 +α1S

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2(μ + δ)I

+A

μ + q + σ 212

(β1

α1+

β2

α2

)

:= – λ + 1 +α1S

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2(μ + δ)I +A

μ + q + σ 212

(β1

α1+

β2

α2

)

,

where λ = 3A((�S0) 1

3 – 1) > 0.Applying Itô’s formula, we have

LV2 = –AS

+β1I

1 + α1I+

β2D1 + α2D

+ (μ + q) +σ 2

12

≤ –AS

+β1

α1+

β2

α2+ (μ + q) +

σ 21

2,

LV3 = –(μ + δ)ID

+ γ +σ 2

32

,

and

LV4 = (S + I + D)m(A – μS – qS – ρI – γ D)

+m2

(S + I + D)m–1(σ 21 S2 + σ 2

2 I2 + σ 23 D2)

≤ (S + I + D)m[A – δ(S + I + D)

]+

m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)(S + I + D)m+1

= A(S + I + D)m –[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

(S + I + D)m+1

= F –ρ

2(S + I + D)m+1

≤ F –ρ

2(Sm+1 + Im+1 + Dm+1),

where

F = sup(S,I,D)∈R3

+

{

A(S + I + D)m –ρ

2(S + I + D)m+1

}

< ∞.

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 6 of 16

Therefore,

LV ≤ –Mλ + M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

–AS

+β1

α1+

β2

α2+ (μ + q + γ ) – (μ + δ)

ID

+σ 2

1 + σ 23

2

+ F –ρ

2(Sm+1 + Im+1 + Dm+1). (2.3)

We can choose a positive constant M such that

–Mλ + E ≤ –2,

herein,

E = sup(S,I,D)∈R3

+

{

M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F –

ρ

2(Sm+1 + Im+1 + Dm+1)

}

.

Now, we construct the following bounded closed set:

Dε ={

(S, I, D) ∈ R3+ : ε ≤ S ≤ 1

ε, ε ≤ I ≤ 1

ε, ε2 ≤ D ≤ 1

ε2

}

,

where ε > 0 is a sufficiently small constant. In the set R3+ \ Dε , we can choose ε sufficiently

small and the following conditions hold:

–Aε

+ G ≤ –1, (2.4)

–Mλ + 2M(μ + δ)ε + E ≤ –1, (2.5)

–μ + δ

ε+ G ≤ –1, (2.6)

–ρ

41

εm+1 + H ≤ –1, (2.7)

–ρ

41

εm+1 + J ≤ –1, (2.8)

–ρ

41

ε2m+2 + N ≤ –1, (2.9)

where G, H , J , N will be determined later. Hence,

R3+ \ Dε = Dc

1 ∪ Dc2 ∪ Dc

3 ∪ Dc4 ∪ Dc

5 ∪ Dc6,

with

Dc1 =

{(S, I, D) ∈ Ω , 0 < S < ε

}, Dc

2 ={

(S, I, D) ∈ Ω , 0 < I < ε}

,

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 7 of 16

Dc3 =

{(S, I, D) ∈ Ω , 0 < D < ε, I ≥ ε

}, Dc

4 ={

(S, I, D) ∈ Ω , S >1ε

}

,

Dc5 =

{

(S, I, D) ∈ Ω , I ≥ 1ε

}

, Dc6 =

{

(S, I, D) ∈ Ω , D >1ε2

}

,

then we will prove that LV (S, I, D) ≤ –1 on R3+ \ Dε .

Case 1. If (S, I, D) ∈ Dc1, we achieve that

LV ≤ – Mλ + M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

–AS

+(

β1

α1+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F

–ρ

2(Sm+1 + Im+1 + Dm+1)

≤ –AS

+ G

≤ –Aε

+ G, (2.10)

where

G = sup(S,I,D)∈R3

+

{

M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F –

ρ

2(Sm+1 + Im+1 + Dm+1)

}

.

Making use of (2.4), we have that LV ≤ –1 for all (S, I, D) ∈ Dc1.

Case 2. If (S, I, D) ∈ Dc2, we obtain that

LV ≤ – Mλ + M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

–AS

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F

–ρ

2(Sm+1 + Im+1 + Dm+1)

≤ – Mλ + 2M(μ + δ)I + E

≤ – Mλ + 2M(μ + δ)ε + E. (2.11)

By inequality (2.5), we can achieve that LV ≤ –1 for all (S, I, D) ∈ Dc2.

Case 3. If (S, I, D) ∈ Dc3, we get that

LV ≤ – (μ + δ)ID

+ M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F –

ρ

2(Sm+1 + Im+1 + Dm+1)

≤ –μ + δ

ε+ G. (2.12)

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Wang and Jia Advances in Difference Equations (2019) 2019:433 Page 8 of 16

Applying (2.6), we have that LV ≤ –1 for all (S, I, D) ∈ Dc3.

Case 4. If (S, I, D) ∈ Dc4, we have that

LV ≤ –14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Sm+1 –14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Sm+1

–12

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)](Im+1 + Dm+1) + M +

α1MSρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ )

+σ 2

1 + σ 23

2+ F

≤ –ρ

4Sm+1 + H

≤ –ρ

41

εm+1 + H , (2.13)

where

H = sup(S,I,D)∈R3

+

{

–14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Sm+1

–12

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)](Im+1 + Dm+1)

+ M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F

}

.

Combining with (2.7), it can be obtained that LV ≤ –1 for all (S, I, D) ∈ Dc4.

Case 5. If (S, I, D) ∈ Dc5, we can see that

LV ≤ –14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Im+1 –14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Im+1

–12

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)](Sm+1 + Dm+1) + M +

α1MSρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ )

+σ 2

1 + σ 23

2+ F

≤ –ρ

4Im+1 + J

≤ –ρ

41

εm+1 + J , (2.14)

where

J = sup(S,I,D)∈R3

+

{

–14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Im+1

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–12

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)](Sm+1 + Dm+1)

+ M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F

}

.

According to inequality (2.8), it can be achieved that LV ≤ –1 for all (S, I, D) ∈ Dc5.

Case 6. If (S, I, D) ∈ Dc6, we can see that

LV ≤ –14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Dm+1 –14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Dm+1

–12

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)](Sm+1 + Im+1) + M +

α1MSρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ )

+σ 2

1 + σ 23

2+ F

≤ –ρ

4Dm+1 + N

≤ –ρ

41

ε2m+2 + N , (2.15)

where

N = sup(S,I,D)∈R3

+

{

–14

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)]

Dm+1

–12

[

δ –m2

(σ 2

1 ∨ σ 22 ∨ σ 2

3)](Sm+1 + Im+1)

+ M +α1MS

ρ + μ + δ

(β1

α1+

β2

α2

)

+ 2M(μ + δ)I +MA

μ + q + σ 212

(β1

α1+

β2

α2

)

+(

β1

α1I+

β2

α2

)

+ (μ + q + γ ) +σ 2

1 + σ 23

2+ F

}

.

By inequality (2.9), it can be seen that LV ≤ –1 for all (S, I, D) ∈ Dc6.

Thus condition (H2) of Lemma 2.1 holds. By Lemma 2.1, we know that the solution ofsystem (1.3) is ergodic and system (1.3) has a unique stationary distribution π (·).

This completes the proof. �

Remark 1 Here, we construct a C2-function, and then we are going to do a step by stepcalculation of the function, to make the calculation process more logical. Then, the dis-cussion is divided into six cases. Finally, the ideal result is obtained.

3 ExtinctionIn this section, we give the sufficient conditions that lead to the extinction of the disease.For convenience, we introduce the following notation and lemma.

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If f (t) is an integral function on [0,∞), define 〈f (t)〉 = 1t∫ t

0 f (τ ) dτ .

Lemma 3.1 Let (S(t), I(t), D(t)) be the solution of system (1.3) with the initial value(S(0), I(0), D(0)) ∈ R3

+. Then S(t) + I(t) ≤ Aμ

, D(t) ≤ A(μ+δ)γμ

.

Proof Summing the first two equations of system (1.3), we can get

d(S(t) + I(t))dt

≤ A – μ(S(t) + I(t)

),

so we have

lim supt→∞

(S(t) + I(t)

) ≤ Aμ

.

In the same way, we have

lim supt→∞

D(t) ≤ A(μ + δ)γμ

.

Therefore, the positive invariant set of system (1.3) is

Ω ={

(S, I, D) ∈ R3+ : 0 ≤ S, I ≤ A

μ, 0 ≤ D ≤ A(μ + δ)

γμ

}

.

This completes the proof of Lemma 3.1. �

Lemma 3.2 Let (S(t), I(t), D(t)) be the solution of system (1.3) with the initial value(S(0), I(0), D(0)) ∈ Ω . Then

limt→∞

∫ t0 σ1S(τ ) dB1(τ )

t= 0, lim

t→∞

∫ t0 σ2I(τ ) dB2(τ )

t= 0.

Proof Let M1(t) =∫ t

0 σ1S(τ ) dB1(τ ), M1(t) is an integral and corresponds to the Brownianmotion and it is local continuous martingale. Also, if we replace the upper bound witht = 0 in M1(t), then we have M(0) = 0. Next, we can discover the quadratic variation andget the following limits:

lim supt→∞

〈M1, M1〉t

t≤ σ 2

1 A2

μ2 < ∞.

Applying the strong law of large numbers [9], we can deduce that

limt→∞

M1(t)t

= 0 a.s.

Let M2(t) =∫ t

0 σ2I(τ ) dB2(τ ). Similarly, we can get

lim supt→∞

〈M2, M2〉t

t≤ σ 2

2 A2

μ2 < ∞,

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then

limt→∞

M2(t)t

= 0 a.s.

This completes the proof of Lemma 3.2. �

Theorem 3.1 Let (S(t), I(t), D(t)) be the solution of system (1.3) with the initial value(S(0), I(0), D(0)) ∈ �3

+. If

�s0 :=

(β1 + β2)A

(μ + q)(ρ + μ + δ + σ 222 )

< 1,

then

lim supt→∞

ln I(t)t

≤(

ρ + μ + δ +σ 2

22

)(�s

0 – 1)

< 0 a.s.,

that is,

limt→∞ I(t) = 0 a.s.,

which means the disease dies out with probability one.Moreover,

limt→∞ S(t) =

Aμ + q

a.s., limt→∞ D(t) = 0 a.s.

Proof Integrating system (1.3), we get

S(t) – S(0)t

+I(t) – I(0)

t= A – (μ + q)

⟨S(t)

⟩– (ρ + μ + δ)

⟨I(t)

+σ1

t

∫ t

0σ1S(τ ) dB1(τ ) +

σ2

t

∫ t

0σ2I(τ ) dB2(τ ), (3.1)

which means

⟨S(t)

⟩=

Aμ + q

–ρ + μ + δ

μ + q⟨I(t)

⟩+ Φ(t), (3.2)

where

Φ(t) =1

μ + q

[σ1

t

∫ t

0S(τ ) dB1(τ ) +

σ2

t

∫ t

0I(τ ) dB2(τ ) –

S(t) – S(0)t

–I(t) – I(0)

t

]

.

By Lemma 3.1 and Lemma 3.2 we can obtain

limt→∞Φ(t) = 0 a.s. (3.3)

Applying Itô’s formula to system (1.3), we get that

d ln I(t) =β1S(t)

1 + α1I(t)+

β2S(t)D(t)I(t)(1 + α2D(t))

– (ρ + μ + δ) –σ 2

22

+ σ2dB2(t). (3.4)

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Integrating both sides of (3.4) from 0 to t and division by t lead to the following equation:

ln I(t)t

= β1

⟨S(t)

1 + α1I(t)

+ β2

⟨S(t)D(t)

I(t)(1 + α2D(t))

– (ρ + μ + δ) –σ 2

22

+σ2B2(t)

t

≤ β1⟨S(t)

⟩+ β2

⟨S(t)

⟩– (ρ + μ + δ) –

σ 22

2+

σ2B2(t)t

= (β1 + β2)[

Aμ + q

–ρ + μ + δ

μ + q⟨I(t)

⟩+ Φ(t)

]

– (ρ + μ + δ) –σ 2

22

+σ2B2(t)

t

=(β1 + β2)A

μ + q–

(β1 + β2)(ρ + μ + δ)μ + q

⟨I(t)

⟩+ (β1 + β2)Φ(t)

– (ρ + μ + δ) –σ 2

22

+σ2B2(t)

t

=(

ρ + μ + δ +σ 2

22

)(�s

0 – 1)

–(β1 + β2)(ρ + μ + δ)

μ + q⟨I(t)

+ (β1 + β2)Φ(t) +σ2B2(t)

t

≤(

ρ + μ + δ +σ 2

22

)(�s

0 – 1)

+ (β1 + β2)Φ(t) +σ2B2(t)

t. (3.5)

From strong law of large numbers [9], we have

limt→∞

σ2B2(t)t

= 0 a.s. (3.6)

Combining (3.3) and (3.6), then taking the limit superior of both sides of (3.5), we have

lim supt→∞

ln I(t)t

≤(

ρ + μ + δ +σ 2

22

)(�s

0 – 1)

a.s.

This implies that if �s0 < 1, then

limt→∞ I(t) = 0 a.s.

According to system (1.3), the third equation with limiting system becomes

dD(t) = –γ D(t) dt,

thus, we obtain

limt→∞ D(t) = 0 a.s.

Similarly, according to the first equation of (1.3), we have

limt→∞ S(t) =

Aμ + q

a.s.

This completes the proof of Theorem 3.1. �

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Figure 1 Distributions of S(t), I(t), and D(t) of system (1.3) with σ1 = σ2 = σ3 = 0.1

Remark 2 Theorem 3.1 shows that the disease will become extinct if �s0 < 1. Note that

�s0 < 1 independent of σ1 and σ3, that is to say, when �s

0 < 1, even if the white noises σ1

and σ3 are zero, the disease is still extinct.

4 Numerical simulationsIn this section, we use the Milstein method [20] and numerical simulations to verify theconclusions in this paper. The discrimination equations of system (1.3) are presented asfollows:

Si+1 = Si +(

A – Siβ1Ii

1 + α1Ii– Si

β2Di

1 + α2Di– μSi – qSi

)

�t

+ Si

(

σ1ξi√

�t +σ 2

12

(ξ 2

i – 1)�t

)

,

Ii+1 = Ii +(

Siβ1Ii

1 + α1Ii+ Si

β2Di

1 + α2Di– (ρ + μ + δ)Ii

)

�t

+ Ii

(

σ2ηi√

�t +σ 2

22

(η2

i – 1)�t

)

,

Di+1 = Di +((μ + δ)Ii – γ Di

)�t + Di

(

σ3ζi√

�t +σ 2

22

(ζ 2

i – 1)�t

)

,

where ξi, ηi, ζi (i = 1, 2, . . .) are independent N-distributed Gaussian random variables.

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Figure 2 Extinction: the stochastic trajectory and deterministic trajectory of S(t), I(t), D(t)

Example 4.1 We take the parameters in system (1.3) as follows: A = 5, α1 = 2, α2 = 2,β1 = 0.35, β2 = 0.45, μ = 0.06, δ = 0.3, ρ = 0.05, q = 0.7, γ = 0.5, σ1 = 0.1, σ2 = 0.1, σ3 = 0.1,and the initial value is (S(0), I(0), D(0)) = (0.7, 0.2, 0.1). We can obtain that

�s0 :=

β1

(μ + q + σ 212 )(ρ + μ + δ + σ 2

22 )

= 1.1024 > 1.

Theorem 2.2 implies that system (1.3) has a unique stationary distribution(Fig. 1). FromFig. 1, we can see that the numbers of susceptible group, infected group, and infectedcorpse group are normally distributed.

Example 4.2 We take the parameters as follows: A = 2, α1 = 2, α2 = 2, β1 = 0.05, β2 = 0.2,μ = 0.1, δ = 0.5, ρ = 0.1, q = 0.7, γ = 0.5, σ1 = 0.5, σ2 = 0.2, σ3 = 0.2, and the initial valueis (S(0), I(0), D(0)) = (0.7, 0.2, 0.1). We can easily calculate the basic reproduction number�0 = β1Aγ +β2A(μ+δ)

(μ+q)γ (ρ+μ+δ) = 1.036 > 1.

�s0 =

(β1 + β2)A

(μ + q)(ρ + μ + δ + σ 222 )

= 0.7576 < 1,

which satisfies the condition of Theorem 3.1. So, the disease will go to extinction, that is toshow that the white noise may lead to the extinction of disease. However, for deterministicmodels (1.2), the disease persists since �0 > 1. Thus, the numerical simulations validateour theoretical results (Fig. 2). Figure 2 shows the change curves of the numbers of sus-ceptible group, infected group, and infected corpse group over time. We can also see that

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the comparison of curves of the same variable makes the numerical simulation of model(1.3) closer to the reality.

5 ConclusionsIn this paper, a new SIRD epidemic model of Ebola with double saturated incidence ratesand vaccination is proposed and studied. Firstly, we construct suitable Lyapunov func-tions, we get that if �s

0 = β1

(μ+q+σ2

12 )(ρ+μ+δ+

σ222 )

> 1, then system (1.3) has a unique stationary

distribution. Next, we find that if �s0 = (β1+β2)A

(μ+q)(ρ+μ+δ+σ2

22 )

< 1, then the disease dies out with

probability one. Finally, numerical simulations are shown to verify our results.Some interesting topics deserve further consideration. On the one hand, one may pro-

pose some more realistic but complex models, such as considering the effects of impulsiveperturbations on system (1.3). On the other hand, in our model (1.2), we only introducethe white noise into it, one can also introduce the colored noise into model (1.2). More-over, our model is autonomous, it is interesting to investigate the nonautonomous system.We will leave these problems as our future work.

AcknowledgementsWe greatly appreciate the editor and the anonymous referees’ careful reading and valuable comments, their criticalcomments and helpful suggestions greatly improved the presentation of this paper.

FundingThis work is supported by the Natural Science Foundation of Shanxi province (201801D121011).

Competing interestsThe authors declare that they have no competing interests.

Authors’ contributionsAll authors contributed equally to the writing of this paper. The authors read and approved the final manuscript.

Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Received: 28 June 2019 Accepted: 25 September 2019

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