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Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2021 Dec 9;141:105115. doi: 10.1016/j.compbiomed.2021.105115

Extinction and stationary distribution of a stochastic COVID-19 epidemic model with time-delay

Rukhsar Ikram a, Amir Khan b,c, Mostafa Zahri d, Anwar Saeed e, Mehmet Yavuz f,h,, Poom Kumam e,g
PMCID: PMC8654723  PMID: 34922174

Abstract

We reformulate a stochastic epidemic model consisting of four human classes. We show that there exists a unique positive solution to the proposed model. The stochastic basic reproduction number R0s is established. A stationary distribution (SD) under several conditions is obtained by incorporating stochastic Lyapunov function. The extinction for the proposed disease model is obtained by using the local martingale theorem. The first order stochastic Runge-Kutta method is taken into account to depict the numerical simulations.

Keywords: Stochastic SIVR model, Delay, Brownian motion, Extinction, Stationary distribution

1. Introduction

The outspread of infectious diseases like COVID-19 have been reported employing mathematical models such as stochastic and deterministic. Almost all models are the offshoots of a classical SIR model by Kermack Mckendrick [1]. SIR model is sub-divided in three groups such as susceptible S, infected I and recovered R population. The primary framework of the disease in a population is associated with the rate of incidence. It is therefore related with the mean of secondary cases evolved by an infected individual in the susceptible population. Many descendent models have been employed after Kermack McKendrick model [2,3]. The variations in our social and environmental differences in our daily life are the justifications of establishing stochastic integration in such models. Stochastic noise of a model reshapes the solution behavior of correlated deterministic system and also changes the threshold level of a system for an epidemic to occur. The noise induction affects the dynamics of the population [4]. An epidemiological infection with a source of noise with memory was employed with a dynamical model [5]. The epidemic dynamics model was analyzed by employing pulse noise model. Elsewhere threshold variation is described to examine the stochastic SIR model [6]. An increasing attention has been noticed for the analysis and control of COVID-19, also for vaccination and treatment policies. The association of vaccination or other treatment strategies and their relation with the transmission of a disease has been a hot topic for theoretical and applied analysis [[7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21]]. The disease transmission modeling in a population where vaccination is under effect, the main issue is the inefficiency of the vaccine in a given population. There is a possibility of low efficacy such as partial induction of immunization. Considering SIR-type disease such as COVID-19 during the vaccination program is in effect, the total population is divided into four classes i.e susceptible, infected, vaccinated and removed represented as S, I, V, and R respectively. (see Table 1 )

dSdt=μβSI(tτ)(μ+φ)S(t)+θV(t),dIdt=βS(t)I(tτ)+ρβV(t)I(t)(λ+μ)I(t),dVdt=φS(t)ρβV(t)I(t)(μ+θ)V(t),dRdt=λI(t)μR(t). (1)

Table 1.

List of parameters.

Test 1 Test 2 Test 3 Test 4 Test 5 Test 6
Β 0.038 9 0.043 0 0.953 7 0.953 7 0.509 0 0.255 9
Φ 0.918 5 0.823 9 0.004 8 0.004 8 0.484 9 0.280 3
Θ 0.866 3 0.882 4 0.944 4 0.944 4 0.731 9 0.363 8
Δ 0.032 7 0.666 7 0.128 1 0.128 1 0.285 1 0.666 2
Ρ 0.947 3 0.255 3 0.349 4 0.349 4 0.437 8 0.149 5
σ1 0.080 1 0.037 4 0.131 8 0.131 8 0.192 1 0.096 1
σ2 0.349 2 0.669 8 0.276 4 0.276 4 0.107 8 0.570 0
σ3 0.038 8 0.235 1 0.220 6 0.220 6 0.159 8 0.095 3
σ4 0.081 2 0.054 5 0.047 6 0.047 6 0.041 3 0.132 1
S0 0.240 9 0.801 9 0.740 6 0.740 6 0.456 7 0.434 3
V0 0.635 3 0.498 1 0.280 3 0.280 3 0.081 0 0.725 6
R0 0.831 1 0.814 3 0.818 1 0.818 1 0.441 5 0.276 6
Τ 50Δt 100Δt 200Δt 300Δt 500Δt 1000Δt

The basic reproduction number of this model is R0=βμ+λ. In this model, it is assumed that during a given time, a fraction of the susceptible class is vaccinated. The vaccination may or may not immunize the individual, so the model includes ρ factor which is 0 < ρ < 1, where ρ = 0 refers to the effectiveness of the vaccine and ρ = 1 refers to the non-effectiveness of the vaccine. We also assume that the effect of vaccine is lost at some rate of proportion θ. Therefore, since the immunity is long lasting hence a fraction λ of infective goes to the removed class. It is also supposed that birth rate of the population takes place at a constant rate m of death and the neonates move into susceptible class. Thus, the overall population is constant and variables are normalized. In this study, we observed as a case where the vaccine is effective (θ = 0). This model can be further modified according to the environment of the system. The stochastic version of the above model is presented as:

dS=[μβSI(tτ)(μ+φ)S(t)+θV(t)]dt+σ1SdW1(t),dI=[βS(t)I(tτ)+ρβV(t)I(t)(λ+μ)I(t)]dt+σ2IdW2(t),dV=[φS(t)ρβV(t)I(t)(μ+θ)V(t)]dt+σ3VdW3(t),dR=[λI(t)μR(t)]dt+σ4RdW4(t), (2)

where W 1(t), W 2(t), W 3(t) and W 4(t) stand for the independent Brownian motions. σ12, σ22,σ32 and σ42 are white noises, with ICs:

S(φ)=ζ1(φ),I(φ)=ζ2(φ),V(φ)=ζ3(φ),R(φ)=ζ4(φ),φ[τ,0],φi(φ)C,i=1,2,3,4. (3)

This paper is presented as follows: The existence and uniqueness have been carried out in Section 2. In Section 3, Extinction analysis of the underlying model is investigated. In Section 4, the existence of ergodic stationary distribution. Numerical simulations by using first order stochastic Runge-Kutta scheme is demonstrated in Section 5. In the last section i.e 6, concluding remarks are presented.

2. Existence and uniqueness

As the solution of SDE (2) has biological significance, it should be nonnegative [22]. Moreover, in order for a stochastic differential equation to have a unique global (i.e., no explosion in a finite time) solution for any given initial value, the coefficients of the equation are generally required to satisfy a linear growth condition and a local Lipschitz condition [23]. However, the coefficients of SDE (2) do not satisfy a linear growth condition, though they are locally Lipschitz continuous. In this section, we will use a method similar to the proof of [24,25], to prove that the solution of SDE (2) is nonnegative and global.

Theorem 1

System (2) has a unique positive solution (S(t), I(t), V(t), R(t)) on t ≥ − τ, and the solution will remain in R+4 for the given initial condition (3) with probability one.

Proof 1

We define a C 2 − function V:R+4R+ as follows:

V(S,I,V,R)=SkklnSk+(I1lnI)+(V1lnV)+(R1lnR)+tt+τkβI(sτ)ds,

where k > 0 will be determined later on. By Ito's formula, we can obtain

dV=LVdt+σ1(Sk)dW1(t)+σ2(I1)dW2(t)+σ3(V1)dW3(t)+σ4(R1)dW4(t),

where

LV=1kS(μβSI(tτ)(μ+φ)S(t)+θV(t))+11I(βS(t)I(tτ)+ρβV(t)I(t)(λ+μ)I(t))+11V(φS(t)ρβV(t)I(t)(μ+θ)V(t))+11R(λI(t)μR(t))+kσ12+σ22+σ32+σ422+kβI(t)kβI(tτ)
4μ+φ+λ+θμSρβV+[β(ρ+k)μ]μV+kσ12+σ22+σ32+σ422.

Let k=μρββ, then we have

LV4μ+φ+λ+θ+kσ12+σ22+σ32+σ422M, (4)

where M>0. Hence,

dV(S,I,V,R)=Mdt+σ1(Sk)dW1(t)+σ2(I1)dW2(t)+σ3(V1)dW3(t)+σ4(R1)dW4(t). (5)

Integrating (6) from 0 to τnT~=min{τn,T~} leads us

WVS(τnT~),I(τnT~),V(τnT~),R(τnT~)WVS(0),I(0),V(0),R(0)+MT~. (6)

implies

VS(τnT~),I(τnT~),V(τnT~),R(τnT~)(n1lnn)1n1ln1n. (7)

According to (7), we get

GV(S(0),I(0),V(0),R(0))+MT~G[1Ωn(ω)VS(τn,ω),I(τn,ω),V(τn,ω),R(τn,ω)]ε(n1lnn)1n1ln1n, (8)

limiting case leads us

>GV(S(0),I(0),V(0),R(0))+MT~=, (9)

contradiction arises hence τ  = , a.s.

3. Extinction

In this section, we will show that if the noise is sufficiently large, the solution to the associated SDE (2) will become extinct with probability 1 [[26], [27], [28]].

Lemma 1

LetM={Mt}t0be a real-valued continuous local martingale vanishing at t = 0, andM,Mtbe the quadratic variation of M. Then

limtM,Mt=,a.s.limtMtM,Mt=0a.s.,

and also.

limtsupM,Mtt<a.s.limtMtt=0,a.s.,

Lemma 2

Let (S(t), I(t), V(t), R(t)) be the solution of (2) with any (S(0),I(0),V(0),R(0))R+4, then

limtS(t)t=0,limtI(t)t=0,limtV(t)t=0,limR(t)t=0,a.s.,

Furthermore, ifμ>σ12σ22σ32σ422, then.

limt0tS(s)dW1(s)t=0,limt0tI(s)dW2(s)t=0,limt0tV(s)dW3(s)t=0,

limt0tR(s)dW4(s)t=0, a.s.

Theorem 2

IfR0s<1andμ>σ12σ22σ32σ422,then (2) obeys:

limStsup1tln(λ(I+V)+(λ+μ)R)(β+λφ)Sdt12(λ)2λ2σ222λ2μ+θ+σ322λ+μ(1λμ)+σ322<0andlimtS=1,a.s.

Proof 2

Let U(t)=λ(I+V)+(λ+μ)R, and applying Ito's formula leads us,

dlnU(t)=1λ(I+V)+(λ+μ)R[λβSI(tτ)+λφSλ(μ+θ)Vμ(λ+μ)Rμ]λ2σ22I2+λ2σ32V2+(λ+μ)2σ42R22(λ(I+V)+(λ+μ)R)2dt+λ2σ2Iλ(I+V)+(λ+μ)RdW2
+λ2σ3Vλ(I+V)+(λ+μ)RdW3+σ4(λ+μ)Rλ(I+V)+(λ+μ)RdW4
(β+λφ)Sdt1λ(I+V)+(λ+μ)Rλ2σ222I2+λ2μ+θ+σ322V2+λ+μ(1λμ)+σ422R2dt+λ2σ2Iλ(I+V)+(λ+μ)RdW2+λ2σ3Vλ(I+V)+(λ+μ)RdW3+σ4(λ+μ)Rλ(I+V)+(λ+μ)RdW4
(β+λφ)Sdt12(λ)2λ2σ222λ2μ+θ+σ322λ+μ(1λμ)+σ322dt
+λ2σ2Iλ(I+V)+(λ+μ)RdW2+λ2σ3Vλ(I+V)+(λ+μ)RdW3
+σ4(λ+μ)Rλ(I+V)+(λ+μ)RdW4. (10)

From model (2), we have

d(S+I+V+R)=[μμ(S+I+V+R)]dt+σ1SdW1+σ2IdW2+σ3VdW3+σ4RdW4. (11)

Integration gives us

S+I+V+R=1+ψ1(t), (12)

where

ψ1=1μ1t(S(0)+I(0)+V(0)+R(0))1t(S(t)+I(t)+V(t)+R(t))+σ10tS(s)dW1t+σ20tI(s)dW2t+σ30tV(s)dW3t+σ40tR(s)dW4t. (13)

Using Lemmas 1 and 2,

limtψ1(t)=0a.s.

limit of (13) gives us,

limtsupS+I+V+R=1,a.s. (14)

Integrating leads us

lnU(t)t(β+λφ)Sdt12(λ)2λ2σ222λ2μ+θ+σ322λ+μ(1λμ)+σ322dt+ψ2, (15)

where

ψ2(t)=lnU(0)t+λσ2t0tI(s)λ(I+V)+(λ+μ)RdW2+λσ3t0tV(s)λ(I+V)+(λ+μ)RdW3+(λ+μ)σ4t0tR(s)λ(I+V)+(λ+μ)RdW4.

Incorporating Lemmas 1 and 2.

limtψ2(t)=0,a.s.

Since R0s<1, limit of (15) leads us

limtsuplnU(t)t(β+λφ)Sdt12(λ)2λ2σ222λ2μ+θ+σ322λ+μ(1λμ)+σ322dt<0, (16)

implying limtI(t)=0,limtV(t)=0,limtR(t)=0 a.s.

From (14), we have limtS=1,a.s.

4. Stationary distribution

Herein, we construct a suitable stochastic Lyapunov function to study the existence of a unique ergodic stationary distribution [29,30] of the positive solutions to the system (2).

Consider

R0s=φρβμλ^θ^φ^μ^, (17)

where λ^=φρβμ(λ+μ+σ222),θ^=φρβμ(μ+θ+σ322),φ^=μ+φ+σ122 and μ^=μ+σ422.

Theorem 3

Assume thatR0s>1andμσ12σ22σ32σ422>0, then for value(S(0),E(0),I(0),Q(0))R+4, then (2) possess SD π(.).

Proof 3

To prove the theorem we take the help of two conditions in Lemma 1 of [24]. For this, we consider the diffusion matrix of model (2) as:

Λ=v12S20000v22I20000v32V20000v42R2.

It is easy to show that Λ is positive definite, hence the first condition of Lemma 1 in Ref. [24] is satisfied.

Furthermore, consider C2-function V:R+4R:

V(S,I,V,R)=QlnSc1lnIc2lnVc3lnR+βtt+τI(sτ)dslnS+βtt+τI(sτ)dslnVlnR+1ρ+1(S+I+V+R)ξ+1=NV1+V2+V3+V4+V5,

where c1=φρβμλ+μ+σ122,c2=φρβμμ+θ+σ322andc3=φρβμμ+σ422. Let

V~(S,I,V,R)=QlnSc1lnIc2lnVc3lnR+βtt+τI(sτ)dslnS+βtt+τI(sτ)dslnVlnR+1ρ+1(S+I+V+R)ρ+1V(S(0),I(0),V(0),R(0))NV1+V2+V3+V4+V5V(S(0),I(0),V(0),R(0)), (18)

where (S,I,V,R)(1n,n)×(1n,n)×(1n,n)×(1n,n) and n > 1.

V1=lnSc1lnIc2lnVc3lnR+βtt+τI(sτ)ds,

V2=lnS+βtt+τI(sτ)ds,

V3=lnV,V4=lnR,

V5=1ξ+1(S+I+V+R)ξ+1,

ξ > 1 is a constant satisfying

μξ2(σ12σ22σ32σ42)>0,

and N>0, obeying

Qη+R2, (19)

Where η=φρβμλ^θ^(μ+φ+σ122)c3(μ+σ422)>0,

R=sup(S,I,V,R)R+414μξ2(σ12σ22σ32σ42)Iξ+13μ+θ+φ+β(1+ρ)I+A+σ122+σ222+σ322, (20)

and

A=sup(S,I,V,R)R+4μ(S+I+V+R)ρ12μξ2(σ12σ22σ32σ42)×(S+I+V+R)ξ+1<. (21)

Applying Itô’s formula to V1, we have

LV1=μS+βI+(μ+φ)θVSc1βSI(tτ)Ic1ρβI+c1(λ+μ)+c1σ222c2φSVc2ρβI+c2(μ+θ)+c2σ322c3λIR+c3μ+c3σ422
3φρβμc1c23+μ+φ+σ122+c1λ+μ+σ222+c2μ+θ+σ322c3μ+σ422+βI(t)+c2ρβI
φρβμμ^λ^θ^+μ+φ+σ122+c3μ+σ422+βI(t)+β(1+c2ρ)I=ψ+β(1+c2ρ)I. (22)

Similarly, we can get

LV2=μS+(μ+φ)θVS+βI+σ122, (23)
LV3=φφSV+ρβI+μ+θ+σ322, (24)
LV4=λIR+μ+σ422, (25)
LV5=(S+I+V+R)ρ[μμ(S+I+V+R)]+ξ2(S+I+V+R)ξ1×(σ12S2σ22I2σ32V2σ42R2)(S+I+V+R)ξ[μμ(S+I+V+R)]+ξ2(S+I+V+R)ξ+1(σ12σ22σ32σ42)μ(S+I+V+R)ξ(S+I+V+R)ξ+1μξ2ϖA12μξ2ϖ(S+I+V+R)ξ+1A12μξ2ϖ(Sξ+1+Iξ+1+Vξ+1+Rξ+1), (26)

where ϖ=(σ12σ22σ32σ42), Using (22), (23), (24), (25), (26), leads us

LV~Qψ+Qβ(1+c2ρ)I12μξ2ϖ(Sξ+1+Iξ+1+Vξ+1+Rξ+1)
+3μ+φ+θμS+σ122+σ322+σ422QVS+β(1+ρ)I+AQSVλIR
Qψ+Qβ(1+c2ρ)I14μξ2ϖ(Sξ+1+Iξ+1+Vξ+1+Rξ+1)
μS14μξ2ϖIξ+1+3μ+φ+θ+σ122
+σ322+σ422QVS+β(1+ρ)I+AQSVλIR.

Let

D=(S,I,V,R)R+4:εS1ε,εI1ε,ε2V1ε2,ε3R1ε3,

a bounded closed set and ε > 0. In the set R+4\D, consider

με+H1, (27)
Qψ+Qβ(1+c2ρ)ε+R1, (28)
14μξ2ϖ(εξ+1+ε2(ξ+1))+H1, (29)
14μξ2ϖ(ε2(ξ+1)+ε3(ξ+1))+H1, (30)
14μξ2ϖ1εξ+1+H1, (31)
14μξ2ϖ1ε2ξ+2+H1, (32)
14μξ2ϖ1ε3ξ+3+H1, (33)

where

H=sup(S,I,V,R)R+4Qβ(1+c2ρ)I14μξ2ϖIξ+1+3μ+φ+θ+β(1+ρ)I+A+σ222+σ122+σ422.

To complete the proof we required LV1 for any (S,I,V,R)R+4\D, and R+4\D=i=18Di, where

D1=(S,I,V,R)R+4;0<S<ε,D2=(S,I,V,R)R+4;0<I<ε,D3=(S,I,V,R)R+4;0<V<ε2,Iε,D4=(S,I,V,R)R+4;0<R<ε3,Vε2,D5=(S,I,V,R)R+4;S>1ε,D6=(S,I,V,R)R+4;I>1ε,D7=(S,I,V,R)R+4;V>1ε2,D8=(S,I,V,R)R+4;R>1ε3. (34)

Case 1. Let (S,I,V,R)D1, and utilizing (29). We obtain

LVμS+Qβ(1+c2ρ)I14μξ2ϖIξ+1+3μ+φ+θ
+β(1+ρ)I+A+σ122+v322+v422
μS+Hμε+H1,

which implies, LV1 for any (S,I,V,R)D1.

Case 2. Let (S,I,V,R)D2, and utilizing (30) and (24). We obtain

LVQψ+Qβ(1+c2ρ)I14μξ2ϖIξ+1
+β(1+ρ)I+A+σ122+3μ+φ+θ+v322+v422Qψ+Qβ(1+c2ρ)I+RQψ+Qβ(1+c2ρ)ε+R,

implies, LV1 for any (S,I,V,R)D2.

Case 3. Let (S,I,V,R)D3, and utilizing (31) leads us,

LV14μξ2ϖ(Iξ+1+Vξ+1)+Qβ(1+c2ρ)I+3μ+β(1+ρ)I
14μξ2ϖIξ+1+φ+θ+A+σ122+v322+v422
14μξ2ϖ(Iξ+1+Vξ+1)+H14μξ2ϖ(εξ+1+ε2(ξ+1))+H1,

implies, LV1 for any (S,I,V,R)D3.

Case 4. Let (S,I,V,R)D4, and utilizing (32), we obtain

LV14μξ2ϖ(Vξ+1+Rξ+1)+Qβ(1+c2ρ)I+3μ+φ+β(1+ρ)I
14μξ2ϖIξ+1+θ+A+σ122+σ322+σ422
14μξ2ϖ(Vξ+1+Rξ+1)+H14μξ2ϖ(ε2(ξ+1)+ε3(ξ+1))+H1,

implies, LV1 for any (S,I,V,R)D4.

Case 5. Let (S,I,V,R)D5, and utilizing (33), we obtain

LV14μξ2ϖSξ+1+Qβ(1+c2ρ)I+3μ+φ+θ+σ122+β(1+ρ)I
14μξ2ϖIξ+1+σ322+σ422+β(1+ρ)I+A
14μξ2ϖSξ+1+H14μξ2ϖ1εξ+1+H1,

implies, LV1 for any (S,I,V,R)D5.

Case 6. Let (S,I,V,R)D6, and utilizing (34), we obtain

LV14μξ2ϖIξ+1+Qβ(1+c2ρ)I+θ+3μ+φ+σ122+β(1+ρ)I
14μξ2ϖIξ+1+σ322+σ422+β(1+ρ)I+A
14μξ2ϖIξ+1+H14μξ2ϖ1εξ+1+H1,

implies, LV1 for any (S,I,V,R)D6.

Case 7. Let (S,I,V,R)D7, and utilizing (35), we obtain

LV14μξ2ϖVξ+1+Qβ(1+c2ρ)I+θ+3μ+φ+σ122+β(1+ρ)I
14μξ2ϖIξ+1+σ322+σ422+β(1+ρ)I+A
14μξ2ϖVξ+1+H14μξ2ϖ1ε2ξ+2+H1,

implies, LV1 for any (S,I,V,R)D7.

Case 8. Let (S,I,V,R)D8, we obtain

LV14μξ2ϖRξ+1+Qβ(1+c2ρ)I+θ+3μ+φ+σ122+β(1+ρ)I

14μξ2ϖIξ+1+σ322+σ422+β(1+ρ)I+A

14μξ2ϖRξ+1+H14μξ2ϖ1ε3ξ+3+H1,

by taking into account (28). Hence, LV1 for any (S,I,V,R)D8.

5. Numerical simulation and discussion

In this section, we simulate six tests for the stochastic SIVR model (2). This stochastic coupled system is derived from the deterministic SIVR system (1). The numerical solution processes of the problem (2) is simulated using the first order stochastic Runge Kutta method. The derivation of stochastic Runge Kutta scheme for the system (2) is given as

Stn+1=Stn+[μβStnItn(tnτ)(μ+φ)Stn+θVtn]Δtn+σ1StnΔW1,tn+σ12Stn(ΔW1,tn)2Δtn2Δtn,Itn+1=Itn+[βStnI(tnτ)+ρβVtnItn(λ+μ)Itn]Δtn+σ2tnΔW2,tn+σ22Itn(ΔW2,tn)2Δtn2Δtn,Vtn+1=Vtn+[φStnρβVtnItn(μ+θ)Vtn]Δtb+σ3VtnΔW3,tn+σ32Vtn(ΔW3,tn)2Δtn2Δtn,Rtn+1=Rtn+[λItnμRtn]Δtn+σ4RtndW4,tn+σ42Rtn(ΔW4,tn)2Δtn2Δtn, (35)

where Δt n = t n+1 − t n represents the non constant time increment and ΔWi,tn=Wi,tn+1Wi,tn refers the independent Gaussian Brownian motion increment, for i = 1, 2, 3, 4. In our case, we restrict ourselves to a constant time step Δt n = Δt. We subdivide the time interval into 1000 equidistant time steps. Where, the delay process I is taken into consideration separately and simulated using different memories τ = 50Δt, 100Δt, 200Δt, 300Δt, 500Δt, 1000Δt. We numerically solve the SIVR system (2) under various random initial conditions satisfying our theoretical results above. It should be stressed, that the delay condition means that the initial value I(0) can not be fixed. Therefore, It takes the end value of the process I starting from I(−τ). The starting values for the individuals S(0), V(0) and R(0) are generated randomly in the interval [0, 1]. Noted that, the system (2) is driven by four independent white noises ΔW i(t) for i = 1, 2, 3, 4. In order to ensure the first order of our numerical scheme, the multiple stochastic integrals are approximated using the Fourier series. The used parameters are summarized in Table (1) and 1000 realization have been taken for mean simulations. The values of the correlations coefficients σ i for i = 1, 2, 3, 4 are chosen randomly using the uniform random generator with values in (0, 1). We examine the following six tests:

In all Fig. 1, Fig. 2, Fig. 3, Fig. 4, Fig. 5, Fig. 6 , we present the numerical solution of the SIVR model (2). The two rows from the left show two solutions out of 1000 realizations for the Tests 1–6, while the third column represents the mean solution of the 1000 realizations. Using randomly chosen parameters, we performed short (50Δt and 100Δt) medium (200Δt and 300Δt) and long (500Δt and 1000Δt) memories. The stability of the asymptotic solution is justified for all tests, especially for the short and medium delays. However, for the long delay, we remarked different emerging of the solution. This happens in the transition phase [0, τ]. In addition, it should be stressed that convergence and stability are guaranteed for all tests even for fixed parameters. Finally, based on the simulation Tests 1–6, we remarked that all results satisfy the outcomes of Theorem (1). Namely, (S(t), I(t), V(t), R(t)) exits in R+4 for any on t ≥ − τ, Moreover, all tests show an accurate numerical stability of the SIVR system (2).

Fig. 1.

Fig. 1

Simulation of TEST 1.

Fig. 2.

Fig. 2

Simulation of TEST 2.

Fig. 3.

Fig. 3

Simulation of TEST 3.

Fig. 4.

Fig. 4

Simulation of TEST 4.

Fig. 5.

Fig. 5

Simulation of TEST 5.

Fig. 6.

Fig. 6

Simulation of TEST 6.

Given the deterministic SIVR model (1), if the basic reproduction number R0=βμ+λ<1, then the disease-free equilibrium point is globally asymptotically stable; whereas if R 0 > 1, the unique endemic equilibrium point is globally asymptotically stable. Repeated outbreaks of the infection can occur due to the time-delay in the transmission terms. In our stochastic SIVR model (2), if R0s=φρβμλ^θ^φ^μ^<1<R0 and μσ12σ22σ32σ422>0, the stochastic model (2) has disease extinction with probability one, and for R0s>1, the model has a unique ergodic stationary distribution.

6. Conclusion

We have reformulated a stochastic epidemic model consisting of four human classes. First of all, we have showed that there exists a unique positive solution to our proposed model. The stochastic basic reproduction number R0s has been established. The stationary distribution under several conditions has been obtained by incorporating stochastic Lyapunov function. The extinction for the proposed disease model has been obtained by using the local martingale theorem. The first order stochastic Runge-Kutta scheme is taken into account to depict the numerical simulations. It is derived from our results that the white noise plays a tremendous role in controlling COVID-19; a sufficient large white noise results in the extinction of COVID-19.

Declaration of competing interest

“The authors declare that they have no competing interests.”

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