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Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2022 Aug 29;204:302–336. doi: 10.1016/j.matcom.2022.08.012

Global asymptotic stability, extinction and ergodic stationary distribution in a stochastic model for dual variants of SARS-CoV-2

Andrew Omame a,b,, Mujahid Abbas c,d, Anwarud Din e
PMCID: PMC9422832  PMID: 36060108

Abstract

Several mathematical models have been developed to investigate the dynamics SARS-CoV-2 and its different variants. Most of the multi-strain SARS-CoV-2 models do not capture an important and more realistic feature of such models known as randomness. As the dynamical behavior of most epidemics, especially SARS-CoV-2, is unarguably influenced by several random factors, it is appropriate to consider a stochastic vaccination co-infection model for two strains of SARS-CoV-2. In this work, a new stochastic model for two variants of SARS-CoV-2 is presented. The conditions of existence and the uniqueness of a unique global solution of the stochastic model are derived. Constructing an appropriate Lyapunov function, the conditions for the stochastic system to fluctuate around endemic equilibrium of the deterministic system are derived. Stationary distribution and ergodicity for the new co-infection model are also studied. Numerical simulations are carried out to validate theoretical results. It is observed that when the white noise intensities are larger than certain thresholds and the associated stochastic reproduction numbers are less than unity, both strains die out and go into extinction with unit probability. More-over, it is observed that, for weak white noise intensities, the solution of the stochastic system fluctuates around the endemic equilibrium (EE) of the deterministic model. Frequency distributions are also studied to show random fluctuations due to stochastic white noise intensities. The results presented herein also reveal the impact of vaccination in reducing the co-circulation of SARS-CoV-2 variants within a given population.

Keywords: SARS-CoV-2, Variants, Stochastic model, Asymptotic behavior, Extinction, Stationary distribution

1. Introduction

The “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2), the cause of the Coronavirus Disease 2019 (COVID-19) was first reported in Wuhan, China. SARS-CoV-2 is a single-stranded-RNA virus with a genetic material which mutates in a very short time [24]. A large number of patterns have shown that only few mutations can lead to a more severe disease with higher transmissibility and infectivity [42]. Different variants of SARS-CoV-2 have been reported in the last two years, for example; the B.1.1.7 (alpha) variant detected in the UK, the “highly transmissible” and deadlier B.1.617.2 (delta) variant detected in India in December 2020 [24] and the recent B.1.1.529 (Omicron) variant first reported in South Africa. These variants have been categorized as “variants of concern (VOC)”, by the World Health Organization (WHO) and were detected in almost every country of the world [24]. The recently reported variants such as Delta and Omicron are linked with surge in COVID-19 cases where they are dominantly in circulation and “Detection and spread of the Omicron VOC in many more countries is expected. However, some medical experts have reported that the disease due to the Omicron VOC is less severe compared to other variants” [42]. Notwithstanding, out of several control measures against COVID-19, different vaccines have proven to be highly effective against severe illness with any of the variants. These include, but not limited to: the BNT162b2 Pfizer-BioNtech vaccine, the mRNA-1273 Moderna vaccine, Johnson and Johnson vaccine, and several others [16], [50]. These vaccines have high efficacy against different SARS-CoV-2 variants, including the Delta and Omicron variant [6]. We refer to [5], [35], [49] for epidemiological studies on the efficacy of available COVID-19 vaccines against VOCs.

Dual infection is a phenomenon where an individual is simultaneously infected with two or more strains of the same virus. It can affect host immune responses and results in an increase of the viral population. Reports strongly support the possibility of concurrent infection with dual variants of COVID-19 [1], [2], [47]. Scientists in Brazil identified two cases where people were simultaneously infected with two different variants of COVID-19 [1]. Both cases involved two young women who had typical mild-to-moderate flu-like symptoms and did not become severely ill or require hospitalization. In one case, the two variants identified had been circulating in Brazil since the beginning of the pandemic. In the other case, the person was simultaneously infected with both an older strain of the virus, and with the P.2 variant first identified in Rio de Janeiro. In addition, the case of an unvaccinated elderly woman in Belgium who was found to be infected with both the alpha and beta variants of COVID-19, has been confirmed [2]. She tested positive for the two variants on the same day and then developed rapidly worsening respiratory symptoms, which later led to her death. Furthermore, dual infections with both omicron and delta were found in immuno-competent and immuno-compromised patients living in different geographical areas [15], [46], [55]. In recent years, a number of cases when individuals were infected with more than one strain of HIV have been identified [20], [22], [53]. The findings on dual infections were reported for influenza viruses [33], the Epstein-Barr virus [56] and other viruses. Liu et al. [28] reported that a patient hospitalized in Iceland was infected by two SARS-CoV-2 subtypes simultaneously in early March 2020. One strain of the SARS-CoV-2 coronavirus was more aggressive, while the second strain was a mutation from the original version of the coronavirus that appeared in Wuhan, China. Hashim et al. [32] also reported double infection in all 19 analyzed samples, with most of the detected mutations genetically related. The authors discussed that co-infecting strains could compensate for the damaging effect of the truncated spike protein. However, the authors in [47] observed, when studying the different dynamics between two strains, that, one strain could replace the other after several days.

Most epidemic models are always influenced by environmental factors, such as precipitation, temperature, relative humidity, etc. [17], [36], [37], [41], [44]. For human disease associated epidemics, the nature of epidemic growth and spread is random due to the unpredictability in human-to-human contacts [48]. Thus, the variability and randomness of the environment is felt through the different states of the epidemic [51]. In epidemic dynamics, stochastic models may be more ideal in modeling epidemics in many circumstances [29]. For instance, stochastic models are able to incorporate randomness of infectious contacts occurring in the different infectious periods [13]. It has equally been shown that stochastic models can provide additional degree of realism as compared with their deterministic counterparts [54]. In particular, Allen et al. [8] showed that stochastic models best answer the question of disease extinction better than the deterministic counterpart. Herwaarden et al. [54] pointed out that an endemic equilibrium in a deterministic model could disappear in its corresponding stochastic system due to stochastic fluctuations. Furthermore, Nasell [34] revealed that stochastic models provide better approach to describe epidemics for a large range of realistic parameter values as compared with their deterministic equivalents.

Several mathematical models have investigated the dynamics of SARS-CoV-2 [7], [11], [25], [38], [39], [40] and its strains [10], [12], [21], [45]. Most of the multi-strain SARS-CoV-2 models do not capture randomness. As the dynamical behavior of most epidemics, especially SARS-CoV-2, is unarguably driven by random factors, it is thus very important to consider a stochastic vaccination co-infection model for two strains of SARS-CoV-2. In this paper, we highlight our contributions as follows:

  • (i)

    We have developed a mathematical model for SARS-CoV-2 strains with vaccination, incorporating incident co-infection with both strains.

  • (ii)

    The stochastic model is analyzed for existence and uniqueness of solution.

  • (iii)

    The stochastic model is used to examine conditions for the extinction of both strains and their co-infection.

  • (iv)

    The conditions, for which the stochastic system fluctuates around the endemic equilibrium of the deterministic system are investigated. This was done with the help of appropriately defined Lyapunov functions.

  • (v)

    The conditions under which a unique stationary distribution exist for the stochastic model are examined.

  • (vi)

    The deterministic and stochastic models are simulated to support the theoretical results.

The remaining part of the manuscript is organized as follows. The model which governs the dynamics of the disease is formulated in Section 2. Deterministic analyses are carried out in Section 3. The existence and uniqueness of non-negative solution in global sense, detailed analyses establishing the sufficient conditions for the extinction of both strains of the disease, asymptotic behavior of the stochastic model, as well as existence of a unique stationary distribution of the proposed model are all presented in Section 4. The numerical scheme and simulations to validate analytical results are shown in Section 5. At the end, in Section 6, the major outcomes of the study is summarized and further directions are given.

1.1. Preliminaries

In this section, we recall some basic concepts from stochastic calculus and some known theorems needed in the sequel. Throughout the paper, it is assumed that (Ω,F,{Ft}t0,P) is a complete probability space with filtration {Ft}t0. The following notations are introduced:

R+d={x=(x1,,xd)Rd;xi>0,1id},
R¯+d={x=(x1,,xd)Rd;xi0,1id}.

Now, consider the d-dimensional stochastic differential equation [31]:

dx(t)=f(x(t))dt+g(x(t))dW(t)fortt0, (1)

with the initial condition x(0)=x0Rd where, W(t) stands for a d-dimensional standard Brownian motion defined on the given probability space. Let C2(Rd;R+¯) denote the family of all non-negative functions V defined on Rd which are continuously twice differentiable in x. The differential operator L of system (1) is defined by [31]:

L=i=1dfi(x,t)xi+12i,j=1d[gT(x,t)g(x,t)]i,j2xixj.

If L acts on a function VC2(Rd;R+¯), then

LV=Vx(x)f(x)+12trace[gT(x)Vxx(x)g(x)],

where, Vx=Vx1,,Vxd,Vxx=2Vxixjd×d.

By Ito’s lemma [31], if xRd, we have

dV(x(t))=LV(x(t))dt+Vx(x(t))g(x(t))dW(t).

2. Model formulation

At any time t, the total population N(t) consists of the following epidemiological states: Susceptible individuals: S(t), individuals infected with SARS-CoV-2 strain 1: I1(t), individuals infected with SARS-CoV-2 strain 2: I2(t), individuals co-infected with both strains: I12(t), individuals who have recovered from either or both strains of SARS-CoV-2: R(t). From now onwards, strain 1 denotes the original strain of SARS-CoV-2, while strain 2 denotes other variants, such as delta and omicron variants, which are more transmissible than the original strain of SARS-CoV-2, and hence are the variants of concern (VoCs).

The model is formulated based on the following assumptions:

  • i.

    Individuals in the susceptible state can acquire SARS-CoV-2 strain 1 at the rate ξ1I1N or strain 2 at the rate ξ2I2N, where ξ1 and ξ2 stand for effective contact rates for incident infections.

  • ii.

    As clinical reports affirm simultaneous infection with different variants of SARS-CoV-2 [1], [2], [28], [32], it is assumed that susceptible individuals can get co-infected with both strains from infected persons at the rate ξ12I12N, where, ξ12 is the effective contact rate for the transmission of dual strains of SARS-CoV-2.

  • iii.

    Individuals already infected with SARS-CoV-2 strain 1 only can also acquire SARS-CoV-2 strain 2 at the rate ψ2I2N, while those infected with SARS-CoV-2 strain 2 only can acquire strain 1 at the rate ψ1I1N, with ψ1 and ψ2 denoting effective contact rates for infected individuals.

  • iv.

    Susceptible individuals are vaccinated at the rate η, and are assumed to have immunity against infection. However, due to the imperfect nature of the vaccine, this immunity is not life-long and can wane at the rate δ, upon which a vaccinated individual returns back to the susceptible class, where they can get infected with any of the SARS-CoV-2 variants.

  • v.

    Individuals in the susceptible group suffer natural death (just as those in other epidemiological states) at the rate γ.

  • vi.

    Disease induced death is assumed for singly-infected and co-infected individuals at the rates β2,α2 and θ2, respectively.

Parameters in the model are well described in Table 1 while the governing equations and flow charts describing transitions in the model are given in (2) and Fig. 1, respectively.

dS(t)dt=Λξ1I1(t)S(t)N(t)ξ2I2(t)S(t)N(t)ξ12I12(t)S(t)N(t)+δV(t)(η+γ)S(t),dI1(t)dt=ξ1I1(t)S(t)N(t)(β1+β2+γ)I1(t)ψ2I2(t)I1(t)N(t),dI2(t)dt=ξ2I2(t)S(t)N(t)(α1+α2+γ)I2(t)ψ1I1(t)I2(t)N(t),dI12(t)dt=ξ12I12(t)S(t)N(t)+ψ2I2(t)I1(t)N(t)+ψ1I1(t)I2(t)N(t)(θ1+θ2+γ)I12(t),dR(t)dt=β1I1(t)+α1I2(t)+θ1I12(t)γR(t),dV(t)dt=ηS(t)(δ+γ)V(t). (2)

Table 1.

Model parameters and variables.

Parameter Description Value Source
Λ Birth/recruitment rate 0.01138 [3]
γ Natural death rate 176×365 [3]
ξ1 Strain 1 contact rate 0.2944 [27]
ξ2 Strain 2 contact rate 0.45 Assumed
ξ12 Co-infection contact rate 0.42 Assumed
ψ1 Strain 1 contact rate for infected persons 0.2944 [27]
ψ2 Strain 2 contact rate for infected persons 0.45 Assumed
β1 Strain 1 recovery rate [130,13]/day [14]
β2 Strain 1 induced death rate 0.0214 [4]
α1 Strain 2 recovery rate [130,13]/day [14]
α2 Strain 2 induced death rate 0.0214 [4]
θ1 Co-infection recovery rate [130,13]/day [14]
θ2 Co-infection induced death rate 0.004 Assumed
η Vaccination rate of SARS-CoV-2 0.01 Assumed
δ Waning vaccine-induced immunity of SARS-CoV-2 0.01 Assumed

Fig. 1.

Fig. 1

The detailed flowcharts of SARS-CoV-2 transmission for systems (2), (3) respectively.

As, the dynamical behavior of most epidemics, such as SARS-CoV-2, is unarguably influenced by random factors, we have considered the corresponding stochastic two-strain co-infection epidemic model with vaccination described below:

dS(t)=(Λξ1I1(t)S(t)N(t)ξ2I2(t)S(t)N(t)ξ12I12(t)S(t)N(t)+δV(t)(η+γ)S(t))dt+ϖ1S(t)dW1(t),dI1(t)=(ξ1I1(t)S(t)N(t)(β1+β2+γ)I1(t)ψ2I2(t)I1(t)N(t))dt+ϖ2I1(t)dW2(t),dI2(t)=(ξ2I2(t)S(t)N(t)(α1+α2+γ)I2(t)ψ1I1(t)I2(t)N(t))dt+ϖ3I2(t)dW3(t),dI12(t)=(ξ12I12(t)S(t)N(t)+ψ2I2(t)I1(t)N(t)+ψ1I1(t)I2(t)N(t)(θ1+θ2+γ)I12(t))dt+ϖ4I12(t)dW4(t),dR(t)=(β1I1(t)+α1I2(t)+θ1I12(t)γR(t))dt+ϖ5R(t)dW5(t),dV(t)=(ηS(t)(δ+γ)V(t))dt+ϖ6V(t)dW6(t), (3)

where, ϖ1,ϖ2,ϖ3,ϖ4,ϖ5, and ϖ6 are the standard Gaussian white noise intensities, which represent the random/environmental factors that could influence the dynamics of the disease in each of the epidemiological states, while W1,W2,W3,W4,W5 and W6 denote independent standard Wiener processes, respectively.

3. Deterministic analysis

In this section, we analyze the deterministic system (2).

3.1. Deterministic basic reproduction number

The deterministic system’s disease free equilibrium (DFE) is given by

Q0=S0,I10,I20,I120,R0,V0=Λ(δ+γ)γ(η+δ+γ),0,0,0,0,ηΛγ(η+δ+γ)

The reproduction number of the model (2) is obtained by using the method in [52]. The transfer matrices are given by:

F=ξ1(δ+γ)(η+δ+γ)000ξ2(δ+γ)(η+δ+γ)000ξ12(δ+γ)(η+δ+γ),andV=β1+β2+γ000α1+α2+γ000θ1+θ2+γ. (4)

The basic reproduction number of the model (2) is given by

R0=ρ(FV1)=max{R01,R02,R012}, where R01, R02 and R012 are the associated reproduction numbers for SARS-CoV-2 strain 1, strain 2, and the co-infection of both strains, respectively and are given by:

R01=ξ1(δ+γ)(η+δ+γ)(β1+β2+γ),R02=ξ2(δ+γ)(η+δ+γ)(α1+α2+γ),R012=ξ12(δ+γ)(η+δ+γ)(θ1+θ2+γ).

3.2. Local asymptotic stability of the disease free equilibrium (DFE) of the model

Theorem 3.1

The DFE, Q0 , of the model (2) is locally asymptotically stable (LAS) if R0<1 , and unstable if R0>1 .

Proof

The local stability of the model (2) is analyzed by the Jacobian matrix of the system (2) evaluated at the disease-free equilibrium, Q0 and is given by:

J=(γ+η)ξ1(δ+γ)(η+δ+γ)ξ2(δ+γ)(η+δ+γ)ξ12(δ+γ)(η+δ+γ)0δ0ξ1(δ+γ)(η+δ+γ)(β1+β2+γ)000000ξ2(δ+γ)(η+δ+γ)(α1+α2+γ)000000ξ12(δ+γ)(η+δ+γ)(θ1+θ2+γ)000β1α1α1γ0η0000(δ+γ), (5)

where, |JλI|=0 yields the characteristic polynomial given by

(λ+γ)(λ+η+γ)(λ+δ+γ)λ+(β1+β2+γ)(1ξ1(δ+γ)(η+δ+γ)(β1+β2+γ))×λ+(α1+α2+γ)(1ξ2(δ+γ)(η+δ+γ)(α1+α2+γ))×λ+(θ1+θ2+γ)(1ξ12(δ+γ)(η+δ+γ)(θ1+θ2+γ))=0.

The eigenvalue are λ1=γ,λ2=(η+γ),λ3=(δ+γ), and the solutions of the equations:

λ+(β1+β2+γ)(1R01)=0,λ+(α1+α2+γ)(1R02)=0,λ+(θ1+θ2+γ)(1R012)=0. (6)

Applying the Routh–Hurwitz criterion, the equations in (6) will all have negative real parts if and only if R0=max{R01,R02,R012}<1.

3.3. Endemic equilibrium points of the deterministic model

3.3.1. Boundary equilibria

When the reproduction number R0=max{R01,R02,R012}>1, the system (2) has three boundary endemic equilibria Ea,Eb and Ec as follows:

  • 1.

    Strain 1 only: Ea=(Sa,I1a,0,0,Ra,Va)

  • 2.

    Strain 2 only: Eb=(Sb,0,I2b,0,Rb,Vb)

  • 3.

    Co-infection only: Ec=(Sc,0,0,I12c,Rc,Vc)

where:

Sa=Λ(δ+γ)(β1+γ)γ(β1+β2+γ)(η+δ+γ)(R011)+γ(β1+γ)(η+δ+γ),I1a=Λ(R011)(β1+β2+γ)(R011)+(β1+γ),Ra=β1Λ(R011)γ(β1+β2+γ)(R011)+γ(β1+γ),Va=ηΛ(β1+γ)γ(β1+β2+γ)(η+δ+γ)(R011)+γ(β1+γ)(η+δ+γ),Sb=Λ(δ+γ)(α1+γ)γ(α1+α2+γ)(η+δ+γ)(R021)+γ(α1+γ)(η+δ+γ),I1b=Λ(R021)(α1+α2+γ)(R021)+(α1+γ),Rb=α1Λ(R021)γ(α1+α2+γ)(R021)+γ(α1+γ),Vb=ηΛ(α1+γ)γ(α1+α2+γ)(η+δ+γ)(R021)+γ(α1+γ)(η+δ+γ)Sc=Λ(δ+γ)(θ1+γ)γ(θ1+θ2+γ)(η+δ+γ)(R0121)+γ(θ1+γ)(η+δ+γ),I1c=Λ(R0121)(θ1+θ2+γ)(R0121)+(θ1+γ),Rc=θ1Λ(R0121)γ(θ1+θ2+γ)(R0121)+γ(θ1+γ),Vc=ηΛ(θ1+γ)γ(θ1+θ2+γ)(η+δ+γ)(R0121)+γ(θ1+γ)(η+δ+γ). (7)

3.3.2. Co-existence of endemic equilibria

In this section, we shall study the conditions for the co-existence of endemic equilibria of the deterministic system (2), and then will investigate the same numerically through simulations. We now prove the following result:

Theorem 3.2

The deterministic system (2) has a family of co-existence endemic equilibria when R0=max{R01,R02,R012}>1 .

Proof

Let,

λ1=ξ1I1N,λ2=ξ2I2N,λ12=ξ12I12N,λ¯1=ψ1I1N,λ¯2=ψ2I2N,G1=β1+β2+γ,G2=α1+α2+γ,G3=θ1+θ2+γ,Δ=η+δ+γ. (8)

At endemic equilibrium (EE), the deterministic system (2) becomes,

Λ+δV=λ1S+λ2S+λ12S+(η+γ)Sλ1S=(β1+β2+γ+λ¯2)I1λ2S=(α1+α2+γ+λ¯1)I2λ12S+λ¯2I1+λ¯1I2=(θ1+θ2+γ)I12β1I1+α1I2+θ1I12=γRηS=(δ+γ)V (9)

The steady state solutions E=(S,I1,I2,I12,R,V) is given by:

S=Λ(δ+γ)[(δ+γ)(λ1+λ2+λ12)+γΔ],I1=Λ(δ+γ)λ1(G1+λ¯2)[(δ+γ)(λ1+λ2+λ12)+γΔ],I2=Λ(δ+γ)λ2(G2+λ¯1)[(δ+γ)(λ1+λ2+λ12)+γΔ],I12=λ12S+λ2I1+λ1I2G3=Λ(δ+γ)[(G1+λ¯2)(G2+λ¯1)λ12+(G1+G2+λ¯1+λ¯2)λ1λ2]G3[(δ+γ)(λ1+λ2+λ12)+γΔ](G1+λ¯2)(G2+λ¯1),R=β1I1+α1I2+θ1I12γ=Λ(δ+γ)[β1(G2+λ¯1)G3λ1+α1(G1+λ¯2)G3λ2+θ1{(G1+λ¯2)(G2+λ¯1)λ12+(G1+G2+λ¯1+λ¯2)λ1λ2}]γG3[(δ+γ)(λ1+λ2+λ12)+γΔ](G1+λ¯2)(G2+λ¯1),V=ηΛ[(δ+γ)(λ1+λ2+λ12)+γΔ] (10)

Adding all the classes at steady states (10), we have,

N=Λ[γ(δ+γ+η)(G1+λ¯2)(G2+λ¯1)G3+(β1+γ)(δ+γ)(G2+λ¯1)G3λ1+(α1+γ)(δ+γ)(G1+λ¯2)G3λ2+H]γG3[(δ+γ)(λ1+λ2+λ12)+γΔ](G1+λ¯2)(G2+λ¯1),

where

H=(θ1+γ)(δ+γ){(G1+λ¯2)(G2+λ¯1)λ12+(G1+G2+λ¯1+λ¯2)λ1λ2}.

Substituting the steady state solutions into the force of infection λ1=ξ1I1N, and simplifying, we obtain the following:

(β1+γ)(δ+γ)(G2+λ¯1)G3λ1+{(α1+γ)(δ+γ)(G1+λ¯2)G3+γ(δ+γ+η)(G2+λ¯1)G3}λ2+H=γ(δ+γ+η)G1(G2+λ¯1)G3ξ1(δ+γ)(η+δ+γ)(β1+β2+γ)1=γ(δ+γ+η)G1(G2+λ¯1)G3R011. (11)

Also, substituting the steady state solutions into the force of infection λ2=ξ2I2N, and simplifying, we have:

{(β1+γ)(δ+γ)(G2+λ¯1)G3+γ(δ+γ+η)(G1+λ¯2)G3}λ1+(α1+γ)(δ+γ)(G1+λ¯2)G3λ2+H=γ(δ+γ+η)(G1+λ¯2)G2G3ξ2(δ+γ)(η+δ+γ)(α1+α2+γ)1=γ(δ+γ+η)(G1+λ¯2)G2G3R021. (12)

Finally, substituting the steady state solutions into the force of infection λ12=ξ12I12N, and simplifying, we obtain the following:

(β1+γ)(δ+γ)(G2+λ¯1)G3λ1λ12+(α1+γ)(δ+γ)(G1+λ¯2)G3λ2λ12+Hλ12=ξ12Λγ(δ+γ)(G1+G2+λ¯1+λ¯2)λ1λ2+γ(G1+λ¯2)(G2+λ¯1)(δ+γ+η)×G3ξ12(δ+γ)(η+δ+γ)(θ1+θ2+γ)1=ξ12Λγ(δ+γ)(G1+G2+λ¯1+λ¯2)λ1λ2+γ(G1+λ¯2)(G2+λ¯1)(δ+γ+η)G3R0121. (13)

Since all the model parameters are positive, the model (2) exhibit co-existence endemic equilibria when the associated reproduction numbers: R01>1,R02>1 and R012>1. The epidemiological implication of this result is that, when the associated basic reproduction numbers of the deterministic system are greater than unity, then both strains and their co-infection become endemic in the population.

4. Stochastic analysis

The existence and uniqueness of solution, the global asymptotic behavior, and conditions for extinction and ergodic stationary distribution of the stochastic system are examined in this section.

4.1. Existence of a unique solution

In order to study the dynamical behavior, the first important question is whether the global solution exist or not. Moreover, for a model describing the dynamics of population, the nature of the value of the solution is also a matter of great interest. In this section, we show that the solution of stochastic system (3) is global and non-negative. It is known that, for a stochastic differential equation to have a unique global solution (that is, no explosion in a finite time) for any given initial value, the coefficients of the equation are generally required to satisfy the linear growth condition and local Lipschitz condition [9], [31].

Theorem 4.1

Given any initial states X0=(S(0),I1(0),I2(0),I12(0),R(0),V(0))D , the random system (3) possesses a unique solution Xt=X(t)=(S(t),I1(t),I2(t),I12(t),R(t),V(t)) for t0 , which will remain in D with probability one, that is:

P{(S(t),I1(t),I2(t),I12(t),R(t),V(t))Dt0}=1.

Proof

For any given initial conditions X0=(S(0),I1(0),I2(0),I12(0),R(0),V(0))D, there is a unique local solution Xt=X(t)=(S(t),I1(t),I2(t),I12(t),R(t),V(t)) for t[0,τe), with τe denotes the explosion time [31]. Suppose that ϱ0>0 is such that S(0),I1(0),I2(0),I12(0),R(0),V(0) stay within [1ϱ0,ϱ0]. Then, each ϱϱ0, consider the stopping time:

τϱ=inf{t[0,τe):S(t)1ϱ,ϱorI1(t)1ϱ,ϱorI2(t)1ϱ,ϱorI12(t)1ϱ,ϱorR(t)1ϱ,ϱorV(t)1ϱ,ϱ} (14)

where infϕ=, where ϕ denotes the empty set. Note that, τϱ is increasing as ϱ. Thus, τ=limϱτϱ, so ττe almost surely (a.s.). We need to show that τ= a.s., so that τe= and (S(t),I1(t),I2(t),I12(t),R(t),V(t))D a.s for all t0.

Suppose that τ<, then there exist a pair of constants T>0 and ζ(0,1) such that P{τT}>ζ, so there exists an integer ϱ1ϱ0 with

P{τϱT}ζϱϱ1. (15)

Define C2 function V1:R+6R+ by

V1(S,I1,I2,I12,R,V)=(S1lnS)+(I11lnI1)+(I21lnI2)+(I121lnI12)+(R1lnR)+(V1lnV) (16)

Applying Ito’s lemma [31] on (16), we have

dV1=11SdS+121S2(dS)2+11I1dI1+121I12(dI1)2+11I2dI2+121I22(dI2)2
+11I12dI12+121I122(dI12)2
+11RdR+121R2(dR)2+11VdV+121V2(dV)2
=11S(Λξ1I1SNξ2I2SNξ12I12SN+δV(η+γ)S)dt
+11Sϖ1S(t)dW1(t)+12ϖ12dt
+11I1(ξ1I1SN(β1+β2+γ)I1ψ2I2I1N)dt+11I1ϖ2I1(t)dW2(t)+12ϖ22dt
+11I2(ξ2I2SN(α1+α2+γ)I2ψ1I1I2N)dt+11I2ϖ3I2(t)dW3(t)+12ϖ32dt
+11I12(ξ12I12SN+ψ2I2I1N+ψ1I1I2N(θ1+θ2+γ)I12)dt
+11I2ϖ3I2(t)dW4(t)+12ϖ42dt
+11R(β1I1+α1I2+θ1I12γR)dt+11Rϖ4R(t)dW5(t)+12ϖ52dt
+11V(ηS(δ+γ)V)dt+11Vϖ5V(t)dW6(t)+12ϖ62dt

On simplification, we have

dV1=(11S(Λξ1I1SNξ2I2SNξ12I12SN+δV(η+γ)S)+12ϖ12
+11I1(ξ1I1SN(β1+β2+γ)I1ψ2I2I1N)+12ϖ22
+11I2(ξ2I2SN(α1+α2+γ)I2ψ1I1I2N)+12ϖ32
+11I12(ξ12I12SN+ψ2I2I1N+ψ1I1I2N(θ1+θ2+γ)I12)+12ϖ42
+11R(β1I1+α1I2+θ1I12γR)+12ϖ52
+11V(ηS(δ+γ)V)+12ϖ62)dt
+(ϖ1(S1)dW1+ϖ2(I11)dW2+ϖ3(I21)dW3+ϖ4(I121)dW4
+ϖ5(R1)dW5+ϖ6(V1)dW6),

and hence we obtain that

dV1=LV1dt+(ϖ1(S1)dW1+ϖ2(I11)dW2+ϖ3(I21)dW3+ϖ4(I121)dW4+ϖ5(R1)dW5+ϖ6(V1)dW6)

where

LV1=11S(Λξ1I1SNξ2I2SNξ12I12SN+δV(η+γ)S)+12ϖ12
+11I1(ξ1I1SN(β1+β2+γ)I1ψ2I2I1N)+12ϖ22
+11I2(ξ2I2SN(α1+α2+γ)I2ψ1I1I2N)+12ϖ32
+11I12(ξ12I12SN+ψ2I2I1N+ψ1I1I2N(θ1+θ2+γ)I12)+12ϖ42
+11R(β1I1+α1I2+θ1I12γR)+12ϖ52
+11V(ηS(δ+γ)V)+12ϖ62
LV1=(ΛγSγI1γI2γI12γRγV)+[ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)]+[β2I1ξ1SN+(β1+β2+γ)+ψ2I2N]+[α2I2ξ2SN+(α1+α2+γ)+ψ1I1N]+[θ2I12ξ12SNψ2I2I1NI12ψ1I1I2NI12+(θ1+θ2+γ)]+[β1I1Rα1I2Rθ1I12R+γ]+[ηSV+(δ+γ)]
LV1ΛγN+(η+γ)+(β1+β2+γ)+(α1+α2+γ)+(θ1+θ2+γ)+(δ+γ)+ξ1I1N+ξ2I2N+ξ12I12N+ψ1I1N+ψ2I2N+12ϖ12+12ϖ22+12ϖ32+12ϖ42+12ϖ52+12ϖ62 (17)

Note that NΛγ,I1N1,I2N1,I12N1, and hence

LV1η+6γ+β1+β2+α1+α2+θ1+θ2+ξ1+ξ2+ξ12+ψ1+ψ2+12ϖ12+12ϖ22+12ϖ32+12ϖ42+12ϖ52+12ϖ62K

Thus, we have

dV1=Kdt+(ϖ1(S1)dW1+ϖ2(I11)dW2+ϖ3(I21)dW3+ϖ4(I121)dW4+ϖ5(R1)dW5+ϖ6(V1)dW6) (18)

Integrating both sides of (18) from 0 to τϱT, we obtain that

0τϱTdV1(S(r),I1(r),I2(r),I12(r),R(r),V(r))0τϱTKdr+0τϱT(ϖ1(S(r)1)dW1+ϖ2(I1(r)1)dW2+ϖ3(I2(r)1)dW3+ϖ4(I12(r)1)dW4+ϖ5(R(r)1)dW5+ϖ6(V(r)1)dW6) (19)

If we take expectation on the both sides, we have

EV1(S(τϱT),I1(τϱT),I2(τϱT),I12(τϱT),R(τϱT),V(τϱT))V1(S(0),I1(0),I2(0),I12(0),R(0),V(0))+E0τϱTKdr,
EV1(S(τϱT),I1(τϱT),I2(τϱT),I12(τϱT),R(τϱT),V(τϱT))V1(S(0),I1(0),I2(0),I12(0),R(0),V(0))+KT.

Let Ωϱ={τϱT}ϱϱ1. Then, by (15), we have P(Ωϱ)ζ. Note that, for every ωΩ, we have at least S(τϱ,ω) or I1(τϱ,ω) or I2(τϱ,ω) or I12(τϱ,ω) or R(τϱ,ω) or V(τϱ,ω) which is equivalent to ϱ or 1ϱ. Since

ϱ1lnϱor1ϱ1lnϱ=1ϱ1+lnϱ.

So,

S(τϱ,ω),I1(τϱ,ω),I2(τϱ,ω),I12(τϱ,ω),R(τϱ,ω),V(τϱ,ω)(ϱ1lnϱ)(1ϱ1+lnϱ).

Finally, we have

V1(S(0),I1(0),I2(0),I12(0),R(0),V(0))+KTE1ΩϱV1(S(τϱT),I1(τϱT),I2(τϱT),I12(τϱT),R(τϱT),V(τϱT))=E1Ωϱ(ω)V1(S(τϱ,ω),I1(τϱ,ω),I2(τϱ,ω),I12(τϱ,ω)R(τϱ,ω),V(τϱ,ω)),E1Ωϱ(ω)(ϱ1lnϱ)1ϱ1+lnϱ=(ϱ1lnϱ)1ϱ1+lnϱE1Ωϱ(ω)ɛ(ϱ1lnϱ)1ϱ1+lnϱ, (20)

where, 1Ωϱ(ω) is the indicator function of Ωϱ(ω). If ϱ, then >V1(S(0),I1(0),I2(0),I12(0),R(0),V(0))+KT=, becomes a contradiction. Thus, the only possibility is that τ=, which completes the proof.

4.2. Extinction of the disease

In modeling the dynamics of any infectious disease, it is important to study conditions under which the disease will go into extinction or die out from the population. In this section, we will show that if the white noise is sufficiently large, then the solution of associated stochastic system (3) will become extinct with probability one.

To proceed, let us consider the following notation and results:

X(t)=1t0tX(s)ds.

Lemma 4.1 Strong Law of Large Numbers [31]

Let M={Mt}t0 be continuous and real valued local martingale vanishing at t=0 and M,Mt be its quadratic variation. Then

limtM,Mt=,a.s.limtMtM,Mt=0,a.s.and also,limtsupM,Mtt<0,a.s.limtMtt=0,a.s. (21)

Lemma 4.2

Let (S(t),I1(t),I1(t),I12(t),R(t),V(t)) be a solution of (3) subject to (S(0),I1(0),I2(0),I12(0),R(0),V(0))R+6 , then a.s.,

limtS(t)+I1(t)+I2(t)+I12(t)+R(t)+V(t)t=0. (22)

Moreover, if γ>(ϖ12ϖ22ϖ32ϖ42ϖ52ϖ62)2 , then

limt1t0tS(u)dW1(u)=0,limt1t0tI1(u)dW2(u)=0,limt1t0tI2(u)dW3(u)=0,limt1t0tI12(u)dW4(u)=0,limt1t0tR(u)dW5(u)=0,limt1t0tV(u)dW6(u)=0, (23)

This Lemma’s proof is omitted as we can draw conclusion following the arguments similar to those given in Lemmas (2.1) and (2.2) in [58].

The threshold quantity R0S for the stochastic system (3) can be written as

R0S=max{R01S,R02S,R012S}, (24)

where

R01S=ξ1(δ+γ)(η+δ+γ)(β1+β2+γ)ϖ222(β1+β2+γ)=R01ϖ222(β1+β2+γ),
R02S=ξ2(δ+γ)(η+δ+γ)(α1+α2+γ)ϖ322(α1+α2+γ)=R02ϖ322(α1+α2+γ),
R012S=ξ12(δ+γ)(η+δ+γ)(θ1+θ2+γ)ϖ422(θ1+θ2+γ)=R012ϖ422(θ1+θ2+γ).

The following theorem gives the necessary conditions for the extinction of infection.

Theorem 4.2

For any given initial value (S(0),I1(0),I2(0),I12(0),R(0),V(0))R6 the solution

(S(t),I1(t),I1(t),I12(t),S(t),V(t)) of system (3) has the following properties: If

  • (a)
    • (i)
      ϖ22>ξ12(δ+γ)22(η+δ+γ)2(β1+β2+γ) , then SARS-CoV-2 strain 1 goes into extinction almost surely (a.s).
    • (ii)
      ϖ32>ξ22(δ+γ)22(η+δ+γ)2(α1+α2+γ) , then SARS-CoV-2 strain 2 goes to extinction a.s.
    • (iii)
      ϖ42>ξ122(δ+γ)22(η+δ+γ)2(θ1+θ2+γ) , then the co-infection of both strains goes to extinction a.s.
  • (b)
    • (i)
      R01S<1 , then SARS-CoV-2 strain 1 dies out with probability 1.
    • (ii)
      R02S<1 , then SARS-CoV-2 strain 2 dies out with probability 1.
    • (iii)
      R012S<1 , then the co-infection of both strains die out with probability 1.

It means, if conditions (a) and (b) hold, then

limtlogI1(t)t<0,andlimtlogI2(t)t<0,andlimtlogI12(t)t<0,a.s.

That is, the disease goes into extinction with probability 1 .

Moreover,

limtS(t)=Λ(δ+γ)γ(η+δ+γ),limtI1(t)=0,limtI2(t)=0,limtI12(t)=0,limtR(t)=0,limtV(t)=ηΛγ(η+δ+γ), (25)

Proof

Integrating the model (3), we have,

S(t)S(0)t=Λξ1I1(t)S(t)N(t)ξ2I2(t)S(t)N(t)ξ12I12(t)S(t)N(t)+δV(t)(η+γ)S(t)+ϖ1t0tS(r)dW1(r),I1(t)I1(0)t=ξ1I1(t)S(t)N(t)(β1+β2+γ)I1(t)ψ2I2(t)I1(t)N(t)+ϖ2t0tI1dW2(r),I2(t)I2(0)t=ξ2I2(t)S(t)N(t)(α1+α2+γ)I2(t)ψ1I1(t)I2(t)N(t)+ϖ3t0tI2dW3(r),I12(t)I12(0)t=ξ12I12(t)S(t)N(t)+ψ2I2(t)I1(t)N(t)+ψ1I1(t)I2(t)N(t)(θ1+θ2+γ)I12(t)+ϖ4t0tI12dW4(r),R(t)R(0)t=β1I1(t)+α1I2(t)+θ1I12(t)γR(t)+ϖ5t0tR(r)dW5(r),V(t)V(0)t=ηS(t)(δ+γ)V(t)+ϖ6t0tV(r)dW6(r). (26)
  • (a)
    If Itoˆ formula is applied to second equation of (3), we have
    dlogI1(t)=[ξ1SI1N(β1+β2+γ)I1ψ2I2I1N]1I1dtϖ222dt+ϖ2dW2(t). (27)
    If we integrate Eq. (27) within [0,t], then we have
    logI1(t)=ξ1SN(β1+β2+γ)tψ2I2Nϖ222+ϖ2t0tdW2(r)+logI1(0),(ξ1(δ+γ)(η+δ+γ)(β1+β2+γ)tϖ222)+0tϖ2dW2(r)+logI1(0)
    This can be re-written as
    logI1(t)ϖ2220t(1ξ1(δ+γ)ϖ22(η+δ+γ))2dr(β1+β2+γ)t+0tξ12(δ+γ)22ϖ22(η+δ+γ)2dr+0tϖ2dW2(r)+logI1(0)((β1+β2+γ)ξ12(δ+γ)22ϖ22(η+δ+γ)2)t+0tϖ2dW2(r)+logI1(0)
    Division by t gives that
    logI1(t)t((β1+β2+γ)ξ12(δ+γ)22ϖ22(η+δ+γ)2)+1t0tϖ2dW2(r)+logI1(0)t, (28)
    By the Strong Law of Large number, limt1t0tϖ2dW2(r)=0.a.s. As ϖ22>ξ12(δ+γ)22(η+δ+γ)2(β1+β2+γ), by taking the limit superior on both sides of (28), we obtain
    limtsuplogI1(t)t((β1+β2+γ)ξ12(δ+γ)22ϖ22(η+δ+γ)2)<0.
    This implies, limtI1(0)=0. In a similar manner, it can be shown that
    limtsuplogI2(t)t((α1+α2+γ)ξ22(δ+γ)22ϖ22(η+δ+γ)2)<0,
    which implies that limtI2(0)=0. Note that,
    limtsuplogI12(t)t((θ1+θ2+γ)ξ122(δ+γ)22ϖ22(η+δ+γ)2)<0.
    which gives limtI12(0)=0.
  • (b)
    Again, if Eq. (27) is integrated within [0,t] and divided by t, then we have
    logI1(t)logI1(0)t=ξ1SN(β1+β2+γ)ψ2I2Nϖ222+ϖ2t0tdW2(r),ξ1(δ+γ)(η+δ+γ)(β1+β2+γ)ϖ222+ϖ2t0tdW2(r)=(β1+β2+γ)ξ1(δ+γ)(η+δ+γ)(β1+β2+γ)ϖ222(β1+β2+γ)1+ϖ2t0tdW2(r)=(β1+β2+γ)(R01S1)+ϖ2t0tdW2(r). (29)
    Moreover, M(t)=ϖ2t0tdW2(r) is continuous (locally) and M(0)=0. From Lemma 4.2 and t, we have
    limtsupM(t)t=0 (30)
    If R01S<1, then Eq. (29) becomes
    limtsuplogI1(t)t(β1+β2+γ)(R01S1)<0a.s. (31)
    Eq. (31) implies
    limtI1(t)=0a.s. (32)
    Likewise, if Itoˆ formula is applied to third equation of (3), then we obtain that
    logI2(t)logI2(0)t(α1+α2+γ)ξ2(δ+γ)(η+δ+γ)(α1+α2+γ)ϖ322(α1+α2+γ)1+ϖ3t0tdW3(r)=(α1+α2+γ)(R02S1)+ϖ3t0tdW3(r). (33)
    Note that M(t)=ϖ3t0tdW3(r), is also a locally “continuous martingale” and M(0)=0. By Lemma 4.2 and t, we have
    limtsupM(t)t=0. (34)
    If R02S<1, then Eq. (33) results in
    limtsuplogI2(t)t(α1+α2+γ)(R02S1)<0a.s. (35)
    Eq. (35) gives
    limtI2(t)=0a.s. (36)
    If Itoˆ formula is applied to fourth equation of (3), then we obtain that
    logI12(t)logI12(0)t(θ1+θ2+γ)ξ12(δ+γ)(η+δ+γ)(θ1+θ2+γ)ϖ422(θ1+θ2+γ)1+ϖ4t0tdW4(r)=(θ1+θ2+γ)(R012S1)+ϖ4t0tdW4(r). (37)
    Also, M(t)=ϖ4t0tdW4(r) is a “locally continuous martingale” and M(0)=0. With Lemma 4.2 and t, we have
    limtsupM(t)t=0 (38)
    If R012S<1 is satisfied, then Eq. (37) becomes
    limtsuplogI12(t)t(θ1+θ2+γ)(R012S1)<0a.s. (39)
    The Eq. (40) implies that
    limtI12(t)=0a.s. (40)
    Using 5th equation of (26), and by applying Eqs. (32), (36) and (40), as t, we have
    limtR(t)=0,a.s.
    From Eq. (26) and using Eqs. (32), (36) and (40), we obtain that
    S(t)S(0)+V(t)V(0)t=ΛγS(t)γV(t)+ϖ1t0tS(r)dW1(r)+ϖ6t0tV(r)dW6(r), (41)
    S(t)+V(t)=Λγ+ϕ(t). (42)
    Suppose the operator ϕ is given by
    ϕ(t)=1γ[S(t)S(0)t+V(t)V(0)tϖ1t0tS(r)dW1(r)ϖ5t0tV(r)dW6(r)].
    Obviously ϕ(t)0 as t. So we can get
    γS(t)+γV(t)=Λ. (43)
    Likewise, the last equation of (26) yields
    V(t)V(0)t=ηS(t)(δ+γ)V(t)+ϖ6t0tV(r)dW6(r)(δ+γ)V(t)ηS(t)=V(t)V(0)t+ϖ6t0tV(r)dW6(r). (44)
    then we obtain from Eq. (44), if t,
    (δ+γ)V(t)ηS(t)=0 (45)
    From Eqs. (43) and (45), we obtain
    limtS(t)=Λ(δ+γ)γ(η+δ+γ),a.s,
    and
    limtV(t)=ηΛγ(η+δ+γ),a.s.

4.3. Stochastic asymptotic behavior of the perturbed model (3) around the endemic equilibrium (EE) of the deterministic system (2)

In this section, by constructing a suitable stochastic Lyapunov function, we study the asymptotic behavior of the stochastic system (3) around the endemic equilibrium (EE) of the deterministic system (3). Stochastic Lyapunov functions have been successfully constructed in several models to study the asymptotic behavior of the perturbed system around the endemic equilibrium of the deterministic systems [18], [30], [43]. In studying the dynamics of an epidemic system, when the disease will die out and when the disease will prevail in a population, are important questions to answer. If R0>1, then there is an endemic equilibrium for the deterministic system (2) but not for the stochastic system (3) as the stochastic system does not have the endemic equilibrium. Also, for R0>1, we have already shown the existence of endemic equilibria for the deterministic model (2). We shall now examine the conditions under which the solution of the perturbed system (3) fluctuates around the endemic equilibrium of the deterministic system (3) for a special case of the model. Due to strong non-linearity of the model, Lyapunov functions shall be constructed for a special case of the model when ψ1=ψ2=0.

Theorem 4.3

Let (S(t),I1(t),I2(t),I12(t),R(t),V(t)) be the solution of (3) with initial condition (S(0),I1(0),I2(0),I12(0),R(0),V(0))R+6 . Also, let the reproduction number of the deterministic system (2) , R0>1 (so that the endemic equilibrium exists). Then the solution of the stochastic system (3) has the asymptotic property:

limt1tE0tλ1(S(τ)S)2+λ2(I1(τ)I1)2+λ3(I2(τ)I2)2+λ4(I12(τ)I12)2+λ5(R(τ)R)2λ6(V(τ)V)2dτλ,

where,

λ1=η+2γδ2ϖ12γ,λ2=β1+2β2δ2ϖ22,λ3=α1+2α2δ2ϖ32,λ4=θ1+2θ2δϖ42,λ5=2γβ1α1θ12ϖ52λ6=2δ+2γη2ϖ62,λ=2ϖ12S2+2ϖ22I12+2ϖ32I22+2ϖ42I122+2ϖ52R2+2ϖ62V2+2(β1+β2+γ)(I1Λμ+I2+I12)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]+2(α1+α2+γ)(I2Λμ+I1+I12)+12ϖ32I2[2(η+γ)Λ+2(α1+α2+γ)Λμξ2]+2(θ1+θ2+γ)(I12Λμ+I1+I2)+12ϖ42I12[2(η+γ)Λ+2(θ1+θ2+γ)Λμξ12] (46)

Proof

For a special case of the model and when R0>1, the model has a co-existence endemic equilibria satisfying the following equations:

Λ=ξ1I1SN+ξ2I2SN+ξ12I12SN+δV+(η+γ)Sξ1I1SN=(β1+β2+γ)I1ξ2I2SN=(α1+α2+γ)I2ξ12I12SN=(θ1+θ2+γ)I12β1I1+α1I2+θ1I12=γRηS=(δ+γ)V (47)

Consider the stochastic Lyapunov function:

V2=V2a+V2b+V2c+V2d, (48)

where,

V2a=(SS+I1I1+I2I2+I12I12)2+(RR)2+(VV)2,
V2b=2(η+γ)Λ+2(β1+β2+γ)Λμξ1I1I1I1lnI1I1,
V2c=2(η+γ)Λ+2(α1+α2+γ)Λμξ2I2I2I2lnI2I2,
V2d=2(η+γ)Λ+2(θ1+θ2+γ)Λμξ12I12I12I12lnI12I12.

Applying the Ito’s lemma [31],

LV2a=(2(SS+I1I1+I2I2+I12I12)[Λξ1I1SNξ2I2SNξ12I12SN+δV(η+γ)S+ξ1I1SN(β1+β2+γ)I1+ξ2I2SN(α1+α2+γ)I2+ξ12I12SN(θ1+θ2+γ)I12]+2(RR)(β1I1+α1I2+θ1I12γR)+2(VV)(ηS(δ+γ)V)+ϖ12S2+ϖ22I12+ϖ32I22+ϖ42I122+ϖ52R2+ϖ62V2

which can be written as:

LV2a=2(SS+I1I1+I2I2+I12I12)[Λ+δV(η+γ)S(β1+β2+γ)I1(α1+α2+γ)I2(θ1+θ2+γ)I12]+2(RR)(β1I1+α1I2+θ1I12γR)+2(VV)(ηS(δ+γ)V)+ϖ12S2+ϖ22I12+ϖ32I22+ϖ42I122+ϖ52R2+ϖ62V2

substituting the expressions at steady state (47), we obtain that

LV2a=2(SS+I1I1+I2I2+I12I12)[ξ1I1SN+ξ2I2SN+ξ12I12SN+δ(VV)(η+γ)(SS)(β1+β2+γ)I1(α1+α2+γ)I2(θ1+θ2+γ)I12]+2(RR)(β1I1+α1I2+θ1I12γR)+2(VV)(ηS(δ+γ)V)+ϖ12S2+ϖ22I12+ϖ32I22+ϖ42I122+ϖ52R2+ϖ62V2

which can also be written as,

LV2a=2(η+γ)(SS)22(β1+β2+γ)(I1I1)22(α1+α2+γ)(I2I2)22(θ1+θ2+γ)(I12I12)22(β1+β2+γ)(SS)(I1I1)2(α1+α2+γ)(SS)(I2I2)2(θ1+θ2+γ)(SS)(I12I12)2(η+γ)(SS)(I1I1)2(η+γ)(SS)(I2I2)2(η+γ)(SS)(I12I12)2(α1+α2+γ)(I1I1)(I2I2)2(θ1+θ2+γ)(I1I1)(I12I12)2(β1+β2+γ)(I1I1)(I2I2)2(θ1+θ2+γ)(I2I2)(I12I12)2(β1+β2+γ)(I1I1)(I12I12)2(α1+α2+γ)(I2I2)(I12I12)+2δ(SS)(VV)+2δ(VV)(I1I1)+2δ(VV)(I2I2)+2δ(VV)(I12I12)+2(RR)[β1(I1I1)+α1(I2I2)+θ1(I12I12)γ(RR)]+2(VV)[η(SS)(δ+γ)(VV)]+ϖ12(SS+S)2+ϖ22(I1I1+I1)2+ϖ32(I2I2+I2)2+ϖ42(I12I12+I12)2+ϖ52(RR+R)2+ϖ62(VV+V)2 (49)

Applying the Young’s inequality [43]: xyxaa+ybb for x,y>0 and 1a+1b=1, and using the fact (x+y)22x2+2y2, we have

LV2a2(η+γ)(SS)22(β1+β2+γ)(I1I1)22(α1+α2+γ)(I2I2)22(θ1+θ2+γ)(I12I12)22γ(RR)22(δ+γ)(VV)22(β1+β2+γ)(SS)(I1I1)2(α1+α2+γ)(SS)(I2I2)2(θ1+θ2+γ)(SS)(I12I12)2(η+γ)(SS)(I1I1)2(η+γ)(SS)(I2I2)2(η+γ)(SS)(I12I12)2(α1+α2+γ)(I1I1)(I2I2)2(θ1+θ2+γ)(I1I1)(I12I12)2(β1+β2+γ)(I1I1)(I2I2)2(θ1+θ2+γ)(I2I2)(I12I12)2(β1+β2+γ)(I1I1)(I12I12)2(α1+α2+γ)(I2I2)(I12I12)+δ(SS)2+4δ(VV)2+δ(I1I1)2+δ(I2I2)2+δ(I12I12)2+β1(RR)2+β1(I1I1)2+α1(RR)2+α1(I2I2)2+θ1(RR)2+θ1(I12I12)2+η(SS)2+η(VV)2+2ϖ12(SS)2+2ϖ12S2+2ϖ22(I1I1)2+2ϖ22I12+2ϖ32(I2I2)2+2ϖ32I22+2ϖ42(I12I12)2+2ϖ42I122+2ϖ52(RR)2+2ϖ52R2+2ϖ62(VV)2+2ϖ62V2

Also, applying the Ito’s Lemma to V2b, we obtain that

LV2b=2(η+γ)Λ+2(β1+β2+γ)Λμξ1I1I1I1ξ1I1SN(β1+β2+γ)I1+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]=2(η+γ)Λ+2(β1+β2+γ)Λμξ1I1I1I1ξ1I1SNξ1SI1N+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]=2(η+γ)Λ+2(β1+β2+γ)ΛμSNSN(I1I1)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1][2(η+γ)+2(β1+β2+γ)](SS)(I1I1)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]=2(η+γ)(SS)(I1I1)+2(β1+β2+γ)(SS)(I1I1)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]=2(η+γ)(SS)(I1I1)+2(β1+β2+γ)(SS)(I1I1)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]+2(β1+β2+γ)(I1I1)(I2I2+I2)2(β1+β2+γ)(I1I1)I2+2(β1+β2+γ)(I1I1)(I12I12+I12)2(β1+β2+γ)(I1I1)I12

Using, 2(β1+β2+γ)I1I20,2(β1+β2+γ)I1I120 and I2,I12Λμ, we have

LV2b2(η+γ)(SS)(I1I1)+2(β1+β2+γ)(SS)(I1I1)+2(β1+β2+γ)(I1I1)(I2I2)+2(β1+β2+γ)(I1I1)(I12I12)+2(β1+β2+γ)(I1Λμ+I2+I12)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1] (50)

Similarly, we have

LV2c2(η+γ)(SS)(I2I2)+2(α1+α2+γ)(SS)(I2I2)+2(α1+α2+γ)(I1I1)(I2I2)+2(α1+α2+γ)(I2I2)(I12I12)+2(α1+α2+γ)(I2Λμ+I1+I12)+12ϖ32I2[2(η+γ)Λ+2(α1+α2+γ)Λμξ2]. (51)
LV2d2(η+γ)(SS)(I12I12)+2(θ1+θ2+γ)(SS)(I12I12)+2(θ1+θ2+γ)(I1I1)(I12I12)+2(θ1+θ2+γ)(I2I2)(I12I12)+2(θ1+θ2+γ)(I12Λμ+I1+I2)+12ϖ42I12[2(η+γ)Λ+2(θ1+θ2+γ)Λμξ12] (52)

Adding Eqs. (49), (50), (51), (52) give

LV22(η+γ)(SS)22(β1+β2+γ)(I1I1)22(α1+α2+γ)(I2I2)22(θ1+θ2+γ)(I12I12)22γ(RR)22(δ+γ)(VV)2+δ(SS)2+4δ(VV)2+δ(I1I1)2+δ(I2I2)2+δ(I12I12)2+β1(RR)2+β1(I1I1)2+α1(RR)2+α1(I2I2)2+θ1(RR)2+θ1(I12I12)2+η(SS)2+η(VV)2+2ϖ12(SS)2+2ϖ12S2+2ϖ22(I1I1)2+2ϖ22I12+2ϖ32(I2I2)2+2ϖ32I22+2ϖ42(I12I12)2+2ϖ42I122+2ϖ52(RR)2+2ϖ52R2+2ϖ62(VV)2+2ϖ62V2+2(β1+β2+γ)(I1Λμ+I2+I12)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]+2(α1+α2+γ)(I2Λμ+I1+I12)+12ϖ32I2[2(η+γ)Λ+2(α1+α2+γ)Λμξ2]+2(θ1+θ2+γ)(I12Λμ+I1+I2)+12ϖ42I12[2(η+γ)Λ+2(θ1+θ2+γ)Λμξ12] (53)

On simplifying, we obtain that

LV2(η+2γδ2ϖ12γ)(SS)2(β1+2β2δ2ϖ22)(I1I1)2(α1+2α2δ2ϖ32)(I2I2)2(θ1+2θ2δϖ42)(I12I12)2(2γβ1α1θ12ϖ52)(RR)2(2δ+2γη2ϖ62)(VV)2+2ϖ12S2+2ϖ22I12+2ϖ32I22+2ϖ42I122+2ϖ52R2+2ϖ62V2+2(β1+β2+γ)(I1Λμ+I2+I12)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]+2(α1+α2+γ)(I2Λμ+I1+I12)+12ϖ32I2[2(η+γ)Λ+2(α1+α2+γ)Λμξ2]+2(θ1+θ2+γ)(I12Λμ+I1+I2)+12ϖ42I12[2(η+γ)Λ+2(θ1+θ2+γ)Λμξ12]. (54)

This can be simplified to obtain the following:

LV2λ1(S(τ)S)2λ2(I1(τ)I1)2λ3(I2(τ)I2)2λ4(I12(τ)I12)2λ5(R(τ)R)2λ6(V(τ)V)2+λ,

with,

λ1=η+2γδ2ϖ12γ,λ2=β1+2β2δ2ϖ22,λ3=α1+2α2δ2ϖ32,
λ4=θ1+2θ2δϖ42,λ5=2γβ1α1θ12ϖ52λ6=2δ+2γη2ϖ62,
λ=2ϖ12S2+2ϖ22I12+2ϖ32I22+2ϖ42I122+2ϖ52R2+2ϖ62V2+2(β1+β2+γ)(I1Λμ+I2+I12)+12ϖ22I1[2(η+γ)Λ+2(β1+β2+γ)Λμξ1]+2(α1+α2+γ)(I2Λμ+I1+I12)+12ϖ32I2[2(η+γ)Λ+2(α1+α2+γ)Λμξ2]+2(θ1+θ2+γ)(I12Λμ+I1+I2)+12ϖ42I12[2(η+γ)Λ+2(θ1+θ2+γ)Λμξ12].

On taking the expectation, we have

0EV2(t)V2(0)=E0tLV2dτE0t[λ1(S(τ)S)2λ2(I1(τ)I1)2λ3(I2(τ)I2)2λ4(I12(τ)I12)2λ5(R(τ)R)2λ6(V(τ)V)2]dτ+λt (55)

Dividing by t and taking limit as t give

limt1tE0tλ1(S(τ)S)2+λ2(I1(τ)I1)2+λ3(I2(τ)I2)2+λ4(I12(τ)I12)2+λ5(R(τ)R)2+λ6(V(τ)V)2dτλ.

The epidemiological implication of Theorem 4.3 is that the solution of the stochastic system (3) fluctuates around the positive endemic equilibrium of the deterministic system (2), as time t as long as the white noise intensities are very small, since the difference between the solution of the stochastic system (3) and the endemic equilibrium of the deterministic system (2) is small to indicate that the disease will persist in the population.

4.4. Existence of ergodic stationary distribution

In epidemiological modeling, it is important to determine under what conditions the disease will persist in the population. For the deterministic model (2), it was shown that the boundary and coexistence endemic equilibria exist when the associated deterministic reproduction number is above unity. In Section 4.3, we also discussed the conditions under which the solution of the perturbed system (3) will fluctuate around the endemic equilibrium (EE) of the deterministic system (2). By applying results from Khas’minskii [26], it is now shown that there exist an ergodic stationary distribution which reveals that the disease will persist in the population for a long time. The aim of this section is to examine the existence of the solution to the perturbed model (3) which is a stationary Markov process. The stationary solution implies that the disease can be persistent and cannot die out in the population. First, we present some definitions and known results about the stationary distribution. Let X(t) represent a time-homogeneous regular Markov process in R+6 described by the following SDE:

X(t)=f(X)dt+r=1khr(X)dWr(t). (56)

The corresponding diffusion matrix is defined as

A(x)=(aij(x)),aij(x)=r=1khri(x)hrj(x).

Lemma 4.3

The Markov process X(t) will have a unique ergodic stationary distribution π(.) whenever there exists a bounded open domain DR+6 having boundary Γ of regular type with the characteristics:

a. For every xR+6 , A(x) matrix is strictly positive-definite.

b. For xR+6D , the mean time τ is finite where τ is the time required for moving from x to D , and supxKExτ< for all compact subsets KR+6 . Then,

PxlimT1T0Tf(X)dt=R+6f(x)π(dx)=1,xR+6,

where f() represents a function integrable with respect to the measure π .

Theorem 4.4

Let us define the parameter

R¯0S=γξ1ξ2ξ12Λ(η+γ+ϖ122)(β1+β2+γ+ϖ222)(α1+α2+γ+ϖ322)(θ1+θ2+γ+ϖ422). (57)

Then the random model (3) possesses a unique stationary distribution π() having ergodicity whenever R¯0S>1 .

Proof

For (S(0),I1(0),I2(0),I12(0),R(0),V(0))R6, there exists a unique solution (S(t),I1(t),I1(t),I12(t),R(t),V(t))R6.

Moreover, the diffusion matrix of (3) is given as

B=ϖ12S2000000ϖ22I12000000ϖ32I22000000ϖ42I122000000ϖ52R2000000ϖ62V2(S(t),I1(t),I1(t),I12(t),R(t),V(t))R6

Suppose M=min(S(t),I1(t),I1(t),I12(t),R(t),V(t))D¯R+6{ϖ12S2,ϖ22I12,ϖ33I22,ϖ42I122,ϖ52R2,ϖ62V2}, then we have

i,j=16aij(S(t),I1(t),I1(t),I12(t),R(t),V(t))ϑi¯ϑj¯=ϖ12S2ϑ¯12+ϖ22I12ϑ¯22+ϖ32I22ϑ¯32+ϖ42I122ϑ¯42+ϖ52ϑ¯52R2+ϖ52ϑ¯52V2M|ϑ¯|2,(S,I1,I2,I12,R,V)D¯,

with, ϑ¯=(ϑ1¯,ϑ2¯,ϑ3¯,ϑ4¯,ϑ5¯,ϑ6¯)R+6.

Thus, condition (a) of Lemma 4.3 holds.

We now need to define a C2 function V:R+6R+.

Let

V3=S+I1+I2+I12+R+Vφ1lnSφ2lnI1φ3lnI2φ4lnI12,

where φ1,φ2,φ3 and φ4 are positive constants which we shall determine. Using Itoˆs lemma, we have the following:

L(S+I1+I2+I12+R+V)=Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12,L(lnS)=ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122L(lnI1)=ξ1SN+(β1+β2+γ)+ψ2I2N+ϖ222L(lnI2)=ξ2I2SN+(α1+α2+γ)+ψ1I1N+ϖ322L(lnI12)=ξ12SNψ2I2I1NI12ψ1I1I2NI12+(θ1+θ2+γ)+ϖ422L(lnR)=β1I1Rα1I2Rθ1I12R+γ+ϖ522,L(lnV)=ηSV+(δ+γ)+ϖ622. (58)

Therefore, we have

LV3=Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12+φ1(ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122)+φ2(ξ1SN+(β1+β2+γ)+ψ2I2N+ϖ222)+φ3(ξ2I2SN+(α1+α2+γ)+ψ1I1N+ϖ322)+φ4(ξ12SNψ2I2I1NI12ψ1I1I2NI12+(θ1+θ2+γ)+ϖ422),5[γ(S+I1+I2+I12+R+V)×φ1ΛS×φ2ξ1SN×φ3ξ2SN×φ4ξ12SN]15+Λ+φ1ξ1I1N+φ1ξ2I2N+φ1ξ12I12Nφ1δVS+φ1(η+γ)+φ1ϖ122+φ2(β1+β2+γ)+φ2ψ2I2N+φ2ϖ322+φ3(α1+α2+γ)+φ3ψ1I1N+φ3ϖ322+φ4(θ1+θ2+γ)+φ4ϖ422β2I1α2I2θ2I12,

which implies that

LV35[γφ1φ2φ3φ4Λξ1ξ2ξ3]15+Λ+φ1(η+γ+ϖ122)φ4ψ2I2I1NI12φ4ψ1I1I2NI12+φ2(β1+β2+γ+ϖ222)+φ3(α1+α2+γ+ϖ322)+φ4(θ1+θ2+γ+ϖ422)+φ1ξ1I1N+φ1ξ2I2N+φ1ξ12I12N+φ2ψ2I2N+φ3ψ1I1Nφ1δVSβ2I1α2I2θ2I12

Let

Λ=φ1(η+γ+ϖ122)=φ2(β1+β2+γ+ϖ222)=φ3(α1+α2+γ+ϖ322)=φ4(θ1+θ2+γ+ϖ422)

with

φ1=Λ(η+γ+ϖ122),φ2=Λ(β1+β2+γ+ϖ222),φ3=Λ(α1+α2+γ+ϖ322),φ4=Λ(θ1+θ2+γ+ϖ422). (59)

Consequently,

LV35(γξ1ξ1ξ3(Λ)5(η+γ+ϖ122)(β1+β2+γ+ξ2+ϖ222)(α1+α2+ξ1+γ+ϖ322)(θ1+θ2+γ+ϖ422))15Λ+φ1ξ1I1N+φ1ξ2I2N+φ1ξ12I12N+φ2ψ2I2N+φ3ψ1I1Nφ1δVSβ2I1α2I2θ2I12. (60)

It implies that,

LV35Λ(R¯0S)1/51+φ1ξ1I1N+φ1ξ2I2N+φ1ξ12I12N+φ2ψ2I2N+φ3ψ1I1Nφ1δVSβ2I1α2I2θ2I12φ4ψ2I2I1NI12φ4ψ1I1I2NI12.

Moreover, define

V4=φ5(S+I1+I2+I12+R+Vφ1lnSφ2lnI1φ3lnI2φ4lnI12)lnSlnR
lnV+S+I1+I2+I12+R+V=(φ5+1)(S+I1+I2+I12+V+R)(φ1φ5+1)lnS
φ2φ5lnI1φ3φ5lnI2φ4φ5lnI12lnVlnR,

where, φ5>0, shall be determined later. Note that

lim inf(S,I1,I2,I12,R,V)R+6UϱV4(S,I1,I2,I12,R,V)=+,asϱ, (61)

where Uϱ=(1ϱ,ϱ)×(1ϱ,ϱ)×(1ϱ,ϱ). We now show that V4(S,I1,I2,I12,R,V) possesses the least value V4(S(0),I1(0),I2(0),I12(0),R(0),V(0)), which is unique.

If we consider partial derivatives of V4(S,I1,I2,I12,R,V) with respect to each variable, we have

V4(S,I1,I2,I12,R,V)S=1+φ51+φ1φ5S,V4(S,I1,I2,I12,R,V)I1=1+φ5φ2φ5I1,
V4(S,I1,I2,I12,R,V)I2=1+φ5φ3φ5I2,V4(S,I1,I2,I12,R,V)I12=1+φ5φ4φ5I12.
V4(S,I1,I2,I12,R,V)R=1+φ51R.V4(S,I1,I2,I12,R,V)V=1+φ51V.

It can be observed that, at t=0 the function V4 have the unique stagnation point (S(0),I1(0),I2(0),I12(0),R(0),V(0))=(1+φ1φ51+φ5,φ2φ51+φ5,φ3φ51+φ5,φ4φ51+φ5,11+φ5,11+φ5). Furthermore, the Hessian matrix of the function V4(S,I1,I2,I12,R,V) at (S(0),I1(0),I2(0),I12(0),R(0),V(0)) is given by

B=1+φ1φ5S2(0)000000φ2φ5I12(0)000000φ3φ5I22(0)000000φ4φ5I122(0)0000001R2(0)0000001V2(0).

Note that B is positive-definite. Hence, V4(S,I1,I2,I12,R,V) has the least value.

Since V4 is continuous, by Eq. (61), we have V4(S,I1,I2,I12,R,V) possesses a unique least value V4(S(0),I1(0),I2(0),I12(0),R(0),V(0)) in R+6.

Now, consider a C2function V:R+6R+:

V(S,I1,I2,I12,R,V)=V4(S,I1,I2,I12,R,V)V4(S(0),I1(0),I2(0),I12(0),R(0),V(0)).

Applying Itos formula, we obtain that

LVφ5{5Λ(R¯0S)1/51+φ1ξ1I1N+φ1ξ2I2N+φ1ξ12I12Nφ1δVSβ2I1α2I2θ2I12φ4ψ2I2I1NI12φ4ψ1I1I2NI12}+Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12β1I1Rα1I2Rθ1I12R+γ+ϖ522ηSV+(δ+γ)+ϖ622ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122, (62)

which leads to the following assertion

LVφ5φ6+φ5φ1ξ1I1N+φ5φ1ξ2I2N+φ5φ1ξ12I12Nφ5φ1δVSφ5β2I1φ5α2I2φ5θ2I12φ5φ4ψ2I2I1NI12φ5φ4ψ1I1I2NI12+φ2ψ2I2N+φ3ψ1I1N+Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12β1I1Rα1I2Rθ1I12R+γ+ϖ522ηSV+(δ+γ)+ϖ622ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122, (63)

where

φ6=5Λ(R¯0S)1/51>0.

The next step is to define the set

D={ζ1<S<1ζ2,ζ1<I1<1ζ2,ζ1<I2<1ζ2,ζ1<I12<1ζ2,ζ1<R<1ζ2,ζ1<V<1ζ2},

with ζi>0 for i=1,2 being negligible constants, to be determined later. For convenience, let us divide the domain R+6D into sub-domains as follows:

D1={(S,I1,I2,I12,R,V)R+6,0<Sζ1},
D2={(S,I1,I2,I12,R,V)R+6,0<I1ζ1,S>ζ2},
D3={(S,I1,I2,I12,R,V)R+6,0<I2ζ1,I1>ζ2},
D4={(S,I1,I2,I12,R,V)R+6,0<I12ζ2,I2>ζ1},
D5={(S,I1,I2,I12,R,V)R+6,0<Rζ1,I12>ζ2},
D6={(S,I1,I2,I12,R,V)R+6,0<Vζ1,R>ζ2},
D7={(S,I1,I2,I12,R,V)R+6,S1ζ2},
D8={(S,I1,I2,I12,R,V)R+6,I11ζ2},
D9={(S,I1,I2,I12,R,V)R+6,I21ζ2},
D10={(S,I1,I2,I12,R,V)R+6,I121ζ2}.
D11={(S,I1,I2,I12,R,V)R+6,R1ζ2}.
D12={(S,I1,I2,I12,R,V)R+6,V1ζ2}.

Next, we show that LV<0 in all twelve regions which ultimately implies that LV(S,I1,I2,I12,R,V)<0 on R+6D.

Case1. Suppose (S,I1,I2,I12,R,V)D1, then using Eq. (63), we have

LVφ5φ6+φ5φ1ξ1I1N+φ5φ1ξ2I2N+φ5φ1ξ12I12Nφ5φ1δVSφ5β2I1φ5α2I2φ5θ2I12φ5φ4ψ2I2I1NI12φ5φ4ψ1I1I2NI12+φ2ψ2I2N+φ3ψ1I1N+Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12β1I1Rα1I2Rθ1I12R+γ+ϖ522ηSV+(δ+γ)+ϖ622ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122,φ5φ6+φ5φ1ξ1I1N+φ5φ1ξ2I2N+φ5φ1ξ12I12Nφ5φ1δVSφ5β2I1φ5α2I2φ5θ2I12φ5φ4ψ2I2I1NI12φ5φ4ψ1I1I2NI12+φ2ψ2I2N+φ3ψ1I1N+Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12β1I1Rα1I2Rθ1I12R+γ+ϖ522ηSV+(δ+γ)+ϖ622+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122Λζ1. (64)

If we choose a sufficiently small ζ1>0 so that the right hand side of the inequality in (64) is less than or equal to zero, then LV<0 for (S,I1,I2,I12,R,V)D1.

Just as in the proof above, we conclude that LV<0 for (S,I1,I2,I12,R,V)D2, (S,I1,I2,I12,R,V)D3, (S,I1,I2,I12,R,V)D4, (S,I1,I2,I12,R,V)D5, (S,I1,I2,I12,R,V)D6.

Case2. Consider (S,I1,I2,I12,R,V)D7, then by Eq. (63), we get

LVφ5φ6+φ5φ1ξ1I1N+φ5φ1ξ2I2N+φ5φ1ξ12I12Nφ5φ1δVSφ5β2I1φ5α2I2φ5θ2I12φ5φ4ψ2I2I1NI12φ5φ4ψ1I1I2NI12+φ2ψ2I2N+φ3ψ1I1N+Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12β1I1Rα1I2Rθ1I12R+γ+ϖ522ηSV+(δ+γ)+ϖ622ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122,φ5φ6+φ5φ1ξ1I1N+φ5φ1ξ2I2N+φ5φ1ξ12I12Nφ5β2I1φ5α2I2φ5θ2I12φ5φ4ψ2I2I1NI12φ5φ4ψ1I1I2NI12+φ2ψ2I2N+φ3ψ1I1N+Λγ(S+I1+I2+I12+R+V)β2I1α2I2θ2I12β1I1Rα1I2Rθ1I12R+γ+ϖ522ηSV+(δ+γ)+ϖ622ΛS+ξ1I1N+ξ2I2N+ξ12I12NδVS+(η+γ)+ϖ122φ5φ1δζ2ζ1. (65)

If we say, ζ1=ζ22, for a very large positive value of φ5 and the least value of ζ2>0 so that the right hand sides of the inequality in (65) is less than or equal to zero, then we have LV<0 for very (S,I1,I2,I12,R,V)D7.

Just as in Case 2, we can obtain that LV<0 for (S,I1,I2,I12,R,V)D8, (S,I1,I2,I12,R,V)D9,

(S,I1,I2,I12,R,V)D10, (S,I1,I2,I12,R,V)D11, (S,I1,I2,I12,R,V)D12.

Hence, there exist W>0 such that

LV(S,I1,I2,I12,R,V)<W<0for every(S,I1,I2,I12,R,V)R+6D.

Therefore,

dV(S,I1,I2,I12,R,V)<Wdt+[(φ5+1)S(φ1+1)ϖ1]dW1(t)+[(φ5+1)I1φ2φ5ϖ2]dW2(t)+[(φ5+1)I2φ3φ5ϖ3]dW3(t)+[(φ5+1)I12φ4φ5ϖ4]dW4(t)+[(φ5+1)Rϖ5]dW5(t)+[(φ5+1)Rϖ5]dW6(t). (66)

Let (S(0),I1(0),I2(0),I12(0),R(0),V(0))=(x1,x2,x3,x4,x5,x6)=xR+6D, and suppose that τx represents the time for a path to move from x to D

τn=inf{t:n=|X(t)|},andτ(n)(t)=min{τx,t,τn}.

Taking the integral on both sides of (66) within [0,τ(n)(t)], taking expectation and then applying the formula by Dynkin’s [19], we get

EV(S(τ(n)(t)),I1(τ(n)(t)),I2(τ(n)(t)),I12(τ(n)(t)),R(τ(n)(t)),V(τ(n)(t)))V(x)=E0τ(n)(t)LV(S(u),I1(u),I2(u),I12(u),R(u),V(u))duE0τ(n)(t)(W)du=WEτ(n)(t). (67)

Since the function V is not negative, therefore

Eτ(n)(t)1WV(x).

Following arguments similar to those given in the proof of Theorem 4.4, it can be easily seen that P{τe=}=1. Thus, the model (3) is regular. However, if we let n and t, then τ(n)(t)τx a.s. Hence, by using Fatou’s lemma [57], we have that

Eτ(n)(t)1WV(x)<.

Now, supxKEτx<, where K represents the subset of R+6 (which is compact); a direct fulfillment of condition b in Lemma 4.3. Thus, guaranteeing that the model (3) has unique stationary distribution.

5. Numerical scheme and simulations

The perturbed model (3) is simulated in this section. The numerical scheme used is based on the Milstein’s higher order method [23] and presented as follows:

Si+1=Si+[Λξ1SiI1,iN+ξ2SiI2,iNξ12SiI12,iN+δVi(η+γ)Si]t+ϖ1Sitς1,i+ϖ122Si(ς1,i21)t,I1,i+1=I1,i+[ξ1SiI1,iN(β1+β2+γ)I1,iψ2I2,iI1,iN]t+ϖ2I1,itς2,i+ϖ222I1,i(ς2,i21)t,I2,i+1=I2,i+[ξ2SiI2,iN+(α1+α2+γ)I2,iψ1I1,iI2,iN]t+ϖ3I2,itς3,i+ϖ322I2,i(ς3,i21)t,I12,i+1=I12,i+[ξ12SiI12,iN+ψ2I2,iI1,iN+ψ1I1,iI2,iN(θ1+θ1+γ)I12,i]t+ϖ4I2,itς4,i+ϖ422I2,i(ς4,i21)t,Ri+1=Ri+[β1I1,i+α1I2,i+θ1I12,iγRi]t+ϖ5Ritς5,i+ϖ522Ri(ς5,i21)t,Vi+1=Vi+[ηSi(δ+γ)Vi]t+ϖ6Vitς6,i+ϖ622Vi(ς6,i21)t. (68)

where, ςi,j(i=1,2,3,4,5,6), represent the independent Gaussian random variables, with normal distribution N(0,1), and Δt being step size. ϖi>0,(i=1,2,3,4,5,6) denote the white noise values.

Numerical simulations are carried out in this section, to validate theoretical results discussed earlier. The initial conditions used for the simulations are assumed as follows: S(0)=100,I1(0)=50,I2(0)=30,I12(0)=40,R(0)=10,V(0)=100. Unless, otherwise stated, the values of parameters used are given in Table 1. In Fig. 2, simulations of the deterministic system (2) and perturbed system (3) are presented, when the contact rates and the stochastic white noise terms are respectively given by ξ1=0.1,ξ2=0.15,ξ12=0.12, ϖ1=0.038,ϖ2=0.224;ϖ3=0.224,ϖ4=0.224,ϖ5=0.038,ϖ6=0.122, so that ϖ22=0.05>ξ22(δ+γ)22(η+δ+γ)2(α1+α2+γ)=0.0282, ϖ32=0.05>ξ12(δ+γ)22(η+δ+γ)2(β1+β2+γ)=0.0125, ϖ42=0.05>ξ122(δ+γ)22(η+δ+γ)2(θ1+θ2+γ)=0.0181 and the associated stochastic reproduction numbers are given by R0S=max{R01S,R02S,R012S}=max{0.2508,0.5012,0.3510}=0.5012<1. The figure reveals that both strains and their co-infection go into extinction exponentially with unit probability. This also confirms the conclusions of Theorem 4.2. The biological implication is that this results in the elimination of both strains and their co-infection with unit probability. Both deterministic and stochastic models show agreement, as they converge to the DFE.

Fig. 2.

Fig. 2

Simulations of (S(t),I1(t),I2(t),I12(t),R(t),V(t)) for the deterministic and stochastic models when the associated stochastic reproduction numbers are less than one. Parameter values used are: Λ=20;ξ1=0.1,ξ2=0.15,ξ12=0.12,ψ1=0.051,ψ2=0.051;β1=0.05;β2=0.05;α1=0.05;α2=0.05;θ1=0.05;θ2=0.05;δ=0.01;η=0.01 so that, R0S=max{R01S,R02S,R012S}=max{0.2508,0.5012,0.3510}=0.5012<1.

From Theorem 4.4, we have established that, the random model (3) possesses a stationary distribution, which is unique. For the simulations using the contact rates and stochastic white noise terms: ξ1=0.5,ξ2=0.45,ξ12=0.42, ϖ1=0.038,ϖ2=0.03,ϖ3=ϖ4=ϖ5=0.038,ϖ6=0.03, so that R0S=max{R01S,R02S,R012S}=max{2.4851,2.2366,2.0875}=2.4851>1, it is observed that, for weak white noise intensities, the epidemic will remain and persist within the population. This is depicted in Fig. 3, where both strains and their co-infection will persist in average, thereby satisfying the results of Theorem 4.4. This also satisfies the conclusions of Theorem 4.3, that for small or negligible white noise disturbances, the solution of the perturbed system fluctuates around the endemic equilibrium of the deterministic system (2). Hence, the stochastic system (3) has a unique ergodic stationary distribution. The probability distribution histograms for the various epidemiological states of the model under this scenario are depicted in Fig. 4.

Fig. 3.

Fig. 3

Simulations of (S(t),I1(t),I2(t),I12(t),R(t),V(t)) for the deterministic and stochastic models. Parameter values used are: Λ=20;ξ1=0.5,ξ2=0.45,ξ12=0.42,ψ1=0.051,ψ2=0.051;β1=0.05;β2=0.05;α1=0.05;α2=0.05;θ1=0.05;θ2=0.05;δ=0.01;η=0.01, so that R0S=max{R01S,R02S,R012S}=max{2.4851,2.2366,2.0875}=2.4851>1.

Fig. 4.

Fig. 4

The probability distribution histogram of S(t),I1(t),I2(t)I12(t),R(t) and V(t) for the stochastic model (3), when the associated reproduction numbers are greater than one. Parameter values used are: Λ=20;ξ1=0.5,ξ2=0.45,ξ12=0.42,ψ1=0.051,ψ2=0.051;β1=0.05;β2=0.05;α1=0.05;α2=0.05;θ1=0.05;θ2=0.05;δ=0.01;η=0.01, so that R0S=max{R01S,R02S,R012S}=max{2.4851,2.2366,2.0875}=2.4851>1.

The simulations of the deterministic and perturbed systems for the case when the associated reproduction number is R0S=max{R01S,R02S,R012S}=max{2.4962,2.1958,2.2959}=2.4962>1, are depicted in Fig. 5. The results reveal that both strains and their co-infection co-exist and persist within the population. This confirms the conclusions of Theorem 3.2, for the deterministic model (2). It is also observed that the random model (3) fluctuates around the co-existence endemic equilibrium when the associated stochastic model reproduction numbers for single infection and co-infection are greater than unity. Thus, in order to control the spread of different strains and their co-infection within the population, policies must ensure serious preventive efforts against the different variants.

Fig. 5.

Fig. 5

Simulations of (I1(t),I2(t),I12) for the deterministic and stochastic models, to numerically explore the coexistence of both strains and their co-infection. Parameter values used are: Λ=20;ξ1=0.50,ξ2=0.44,ξ12=0.46;,ψ1=0.051,ψ2=0.051;β1=0.05;β2=0.05;α1=0.05;α2=0.05;θ1=0.05;θ2=0.05;δ=0.01;η=0.01, so that, R0S=max{R01S,R02S,R012S}=max{2.4962,2.1958,2.2959}=2.4962>1.

5.0.1. Impact of white noise and vaccination

Simulations of the perturbed model (3) to assess the impact of stochastic white noise intensities are presented in Figs. 6(a), 6(b) and 6(c). It can be observed that increasing the white noise intensities, ϖ1,ϖ2,,ϖ6 hastens progression to extinction, for single and co-infected compartments. This simulation agrees with the conclusions of Theorem 4.3, confirming that for small white noise intensities, the solutions of the stochastic system fluctuates around the endemic equilibrium. However, for larger values of the white noise terms, the solution does not fluctuate around the EEP. This shows that sustained efforts in increasing stochastic disturbances through mass vaccination of susceptible individuals, adequate care and treatment for infected individuals could greatly reduce the spread and circulation of SARS-CoV-2 variants and their co-infection within the population. Simulations of the perturbed model (3) to assess the impact of vaccination are presented in Figs. 7(a), 7(b) and 7(c). It can be observed that increasing the vaccination rates have very high positive impact on the classes of individuals with single or dual strains of SARS-CoV-2. This shows that sustained efforts in vaccinating susceptible individuals could greatly reduce the spread and circulation of both variants and their co-infection within the population.

Fig. 6.

Fig. 6

Simulations of (I1(t),I2(t),I12) for the deterministic and stochastic models, to show the impact of stochastic white noise terms on the infected compartments, when Λ=20,ξ1=0.50,ξ2=0.44,ξ12=0.46;,ψ1=0.051,ψ2=0.051;β1=0.05;β2=0.05;α1=0.05;α2=0.05;θ1=0.05;θ2=0.05;δ=0.01;η=0.01, so that, R0S=max{R01S,R02S,R012S}=max{2.4962,2.1958,2.2959}=2.4962>1.

Fig. 7.

Fig. 7

Simulations of (I1(t),I2(t),I12) for the deterministic and stochastic models, to show the impact of vaccination on the infected components, when Λ=20,ξ1=0.50,ξ2=0.44,ξ12=0.46;,ψ1=0.051,ψ2=0.051;β1=0.05;β2=0.05;α1=0.05;α2=0.05;θ1=0.05;θ2=0.05, so that, R0S=max{R01S,R02S,R012S}=max{2.4962,2.1958,2.2959}=2.4962>1.

6. Conclusion

In this work, we have presented a new stochastic model for two variants of SARS-CoV-2. The existence and the uniqueness of unique global solution of the stochastic model was shown. Using appropriately constructed Lyapunov functions, the conditions under which the solution of the perturbed system will fluctuate around the endemic equilibrium of the deterministic model were also derived. Stationary distribution and ergodicity for the new co-infection model were also established. Numerical simulations were carried out to validate theoretical results on extinction and persistence of SARS-CoV-2 variants within the population. We investigated the situations when both deterministic and stochastic associated reproduction numbers are below one and also when they are greater than one. Frequency distributions to show random fluctuations due to stochastic white noises were also presented. The simulation results also investigated the impact of vaccination on the dynamics of SARS-CoV-2 variants within the population.

Highlights of the simulations are as follows:

  • (i)

    for the scenarios when the stochastic white noise terms, ϖ2,ϖ3,ϖ4 are larger than certain thresholds, that is: ϖ22=0.05>ξ22(δ+γ)22(η+δ+γ)2(α1+α2+γ)=0.0282, ϖ32=0.05>ξ12(δ+γ)22(η+δ+γ)2(β1+β2+γ)=0.0125, ϖ42=0.05>ξ122(δ+γ)22(η+δ+γ)2(θ1+θ2+γ)=0.0181 and the associated stochastic reproduction numbers are given by R0S=max{R01S,R02S,R012S}=max{0.2508,0.5012,0.3510}=0.5012<1, both strains and their co-infection go into extinction exponentially with unit probability. This is presented in Fig. 2.

  • (ii)

    it was observed that, for weak white noise intensities, the solution of the stochastic system fluctuates around the endemic equilibrium (EE) of the deterministic model. More-over, it was shown that the random model (3) possesses a unique stationary distribution. For instance, when contact rates and stochastic white noise terms are: ξ1=0.5,ξ2=0.45,ξ12=0.42, ϖ1=0.038,ϖ2=0.03,ϖ3=ϖ4=ϖ5=0.038,ϖ6=0.03, so that R0S=max{R01S,R02S,R012S}=max{2.4851,2.2366,2.0875}=2.4851>1, both strains and their co-infection remain and persist within the population. This is depicted in Fig. 3, where both strains and their co-infection persist in average, thereby satisfying the results of Theorem 4.3, Theorem 4.4.

  • (iii)

    increasing the vaccination rates resulted in high positive population level impact on the classes of individuals with single or dual strains of SARS-CoV-2. Thus, enhancing efforts in vaccinating susceptible individuals could greatly reduce the spread and circulation of SARS-CoV-2 variants within the population. This is shown in Fig. 7

The stochastic model proposed in this research is based on the dynamics of different variants of SARS-CoV-2 with vaccination. The model did not capture cross-immunity between the variants. This could be an extension on the model, with more realistic assumptions on the emerging variants of concern. More-over, the emergence of different variants of SARS-CoV-2 warrants further studies on their co-infections with other diseases, such as Hepatitis B virus, tuberculosis, influenza, Malaria and other diseases. We could therefore, consider a robust stochastic model for variants of SARS-CoV-2 and co-infection with other diseases. This direction of research is still open to be explored. Also, due to insufficient information and reliable data about emerging variants of concern, we could not fit our model to real SARS-CoV-2 data. We hope to do this with more realistic and reliable information about the dynamics of different variants of concern.

CRediT authorship contribution statement

Andrew Omame: Conceptualization, Formal analysis, Methodology, Writing – original draft, Software. Mujahid Abbas: Conceptualization, Writing – review & editing, Supervision. Anwarud Din: Validation, Visualization, Formal analysis, Methodology, Writing – original draft, Writing – review & editing.

Acknowledgments

Authors are grateful to the handling editor and reviewers for their constructive comments and remarks which helped to improve the quality of the manuscript. The third author (A. Din) was sponsored by the Fundamental Research Funds for the Central Universities , Sun Yat-sen University (Grant No. 2022qntd21).

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