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. 2022 Oct 21;137(10):1169. doi: 10.1140/epjp/s13360-022-03302-5

Theoretical and numerical results of a stochastic model describing resistance and non-resistance strains of influenza

El Mehdi Farah 1, Saida Amine 1, Shabir Ahmad 2, Kamsing Nonlaopon 3,, Karam Allali 1
PMCID: PMC9589591  PMID: 36310610

Abstract

In this world, there are several acute viral infections. One of them is influenza, a respiratory disease caused by the influenza virus. Stochastic modelling of infectious diseases is now a popular topic in the current century. Several stochastic epidemiological models have been constructed in the research papers. In the present article, we offer a stochastic two-strain influenza epidemic model that includes both resistant and non-resistance strains. We demonstrate both the existence and uniqueness of the global positive solution using the stochastic Lyapunov function theory. The extinction of our research sickness results from favourable circumstances. Additionally, the infection’s persistence in the mean is demonstrated. Finally, to demonstrate how well our theoretical analysis performs, various noise disturbances are simulated numerically.

Introduction

The respiratory system, which includes the nose, throat, and lungs, is affected by viruses that cause influenza, sometimes known as the flu [1]. Flu is frequently characterized by acute symptoms and potentially fatal consequences. Viruses with the names influenza A, B, C, and D are four different varieties [2]. Seasonal diseases brought on by influenza types A and B occur nearly every winter. The disease brought on by type C influenza is often quite mild and frequently symptomless. Cattle are affected by type D influenza viruses, which are not known to cause any illnesses in people. All subtype of type A influenza viruses is split into strains, and each strain is additionally categorized into subcategories. Just viruses of type A have sparked pandemic. The various types of proteins found on the outside of the influenza virus envelope are designated by the letters H and N. the different influenza subtypes Hemagglutinin, also known as the HA protein, and neuraminidase, sometimes known as the NA protein, are two types of proteins that attach to the surface of viruses. The immune system of the body may produce antibodies that can identify these particular viral proteins (antigens) and hence can combat this particular influenza virus.

Scholars have identified 18 distinct HA protein forms and 11 distinct NA protein types that may co-occur in a wide range of combinations in influenza viruses that infect birds. According to reports, each of these mixtures represents a unique strain of influenza virus with a specific number of H(number) and N(number) proteins, such as H7N1, H9N2, H5N1, etc [3, 4]. Although they might be classified as strains, type B influenza viruses are not classified into sub-types. Rarely does vaccination offer protection against novel influenza viruses. This was evident during the 2009 H1N1 influenza pandemic. Antiviral medication is thus necessary to prevent the spread of the flu epidemic [5]. Resistance to the influenza virus is increasingly a problem. As an illustration, consider the H3N2 and H1N1 viruses’ resistance to aminoadamantanes and oseltamivir, respectively [810]. Future pandemics might be brought on through resistance, which is lethal. In comparison to the original strain, a new strain’s force of transmission is typically thought to be quite weak. According to references [1012], mutation reduces the viral strength, which is connected to this event.

In epidemiology, mathematical modelling is crucial for a deeper understanding of the numerous facets of many illnesses. Because there are several diseases in which more than one pathogen strain is noted due to the process of viral mutation, for example, influenza [32], human immunodeficiency virus [33], tuberculosis [34], and COVID-19 [35], multi-strain epidemics models have attracted the focus of many researchers. Recently, in [2628], the research of the two-strain epidemic model by fractional differential equation was also established, because the fractional-order differential equations can be helpful in modelling biological systems [2931]. In actuality, some unknown environmental perturbations invariably affect population dynamics and epidemic systems. As we all know, real life is filled with randomness and unpredictability. Stochastic models can better conform to the actual situation, because most epidemic models are influenced by environmental factors, such as percipitation, temperature, relative humidity. Thus, the variability of epidemic growth and spread is random due to the different infectious periods. It has equally been shown that stochastic models can provide additional degree of realism as compared with their deterministic study. Furthermore, several writers have extensively examined certain stochastic epidemics models, including [3640]. An epidemic model with a twofold hypothesis that combines two transmission mechanisms, SIS and SIR, with two distinct saturation incidence rates is addressed in [36] Boukanjime et al. Although there might be two epidemic illnesses in the current world, one brought on by virus A and the other by virus B, the authors of [37] explored an SIS model with the twin epidemic theory. With two distinct saturation incidence rates, Chang et al. [38] constructed a stochastic SIRS model and determined the thresholds that determine whether the disease will remain or go away. The existence of an ergodic stationary distribution of the nonnegative solutions to a stochastic SIS epidemic model with double illnesses and the Beddington-DeAngelis incidence was demonstrated by Liu and Jiang, who used [39] as their source. In [40], it was looked at how two different infectious diseases might spread vertically under a stochastic epidemic model.

In our case we will study two strains of an influenza epidemic model, after analyze the situation in which the two strains can coexist and the difference in their mode of transmission, we employ the use of mathematical modeling. Principal element in mathematical modeling is the incidence rate. Its significance in epidemiology can’t be over emphasized.

Recently, Baba et al. [41] constructed and studied a resistance and non-resistance strains of influenza.

dS(t)dt=Λ-αS(t)IN(t)-βS(t)IR(t)1+κIR(t)-dS(t),dIN(t)dt=αS(t)IN(t)-(d+μ)IN(t),dIR(t)dt=βS(t)IR(t)1+κIR(t)-(d+γ)IR(t),dR(t)dt=μIN(t)+γIR(t)-dR(t). 1.1

Here S(t) is the susceptibles, IR(t) is the infective resistant individuals, IN(t) is the infective non-resistant individuals and R(t) is the removed ones. The parameters in the model (1.1) are positive constants where : Λ is a recruitment into susceptible. 1d is natural mortality rate, The rate of infection by resistant strain is represented by α, the rate of infection by non-resistant strain is denoted by β, removal of individuals carrying the resistant strain from the population is 1γ, removal of individuals carrying the non-resistant strain is 1μ, and the mutation effect on the resistant strain is κ. Both illnesses are spread by interaction between people in the susceptible compartment and those in the IN and IR compartments, which have, respectively, bilinear and saturation incidence rates. We anticipate that the populations that reside in environments where random accidents are prevalent are mostly impacted by the contact rate, which will primarily present itself as changes in the saturated response rate, so that α turn into α+σNB˙(t) and β turn into β+σRB˙(t) where BN(t) and BR(t)) are standard Brownian motion with intensities σN>0 and σR>0. Now, the corresponding stochastic model of the system (1.1) is as follows:

dS(t)=(Λ-αS(t)IN(t)-βS(t)IR(t)1+κIR(t)-dS(t))dt-σNS(t)IN(t)dBN(t)-σRS(t)IR(t)1+κIR(t)dBR(t),dIN(t)=(αS(t)IN(t)-(d+μ)IN(t))dt+σNS(t)IN(t)dBN(t),dIR(t)=(βS(t)IR(t)1+κIR(t)-(d+γ)IR(t))dt+σRS(t)IR(t)1+κIR(t)dBR(t),dR(t)=(μIN(t)+γIR(t)-dR(t))dt. 1.2

Fig. 1.

Fig. 1

The detailed flowchart of system (1.2)

The remaining of this paper is arranged as: In the Sect. 2, we show the positivity and the boundedness of solutions of the stochastic system (1.2). The extinction of the non-resistance and resistance infectious diseases will be discussed in Sect. 3. In Sect. 4 we study the persistence in mean of the epidemic. In Sect. 5, the numerical simulations are carried out to confirm our theoretical results. Lastly, a brief discussion is given in the end to conclude this paper.

Existence and uniqueness of the global nonnegative solution

The notations, definitions, and lemmas we utilised to examine our primary outcomes are provided in this part.

Consider a filtration {Ft}t0 with a complete probability space Ω,F,Ftt0,P that fulfills the usual conditions with increasing and right continuous while F0 is the set of P-null sets. The function B(t) denotes a scalar Brownian motion which is defined on Ω.

We introduce the following notations:

R+d=x=x1,,xdRd:xi>0,1idandR¯+d=x=x1,,xdRd:xi0,1id.

In general, consider the d-dimensional stochastic differential equation

dX(t)=f(X(t))dt+g(X(t))dB(t)fortt0,

with initial value X(0)=X0Rd. B(t) denotes a d-dimensional standard Brownian motion defined on the complete probability space Ω,F,Ftt0,P. Denote by C2Rd;R¯+the family of all nonnegative functions V(X) defined on Rd such that they are continuously twice differentiable in X. The differential operator L of Eq. (1.5) is defined by [42]

L=i=1dfi(X)Xi+12i,j=1dgT(X)g(X)ij2XiXj.

If L acts on a function VC2Rd;R¯+, then

LV(X)=VX(X)f(X)+12tracegT(X)VXX(X)g(X),

where VX=VX1,,VXd,VXX=2VXiXjd×d.

In view of Itô’s formula [42], if X(t)Rd, then

dV(X(t))=LV(X(t))dt+VX(X(t))g(X(t))dB(t).

For arbitrary integrable function h on [0,+), define h(t)=0th(θ)dθt.

Let S(t)=(S(t),IN(t),IR(t),R(t)) and S0=(S(0),IN(0),IR(0),R(0)).

Definition 1

  1. The diseases IN(t) and IR(t) are said to go extinction if limt+IN(t)=0 and limt+IR(t)=0.

  2. The diseases IN(t) and IR(t) will be persist in mean if a1>0 and a2>0 such that lim inft+IN(t)a1 and lim inft+IR(t)a2.

Remark 2

Let the set

Γ=(S(t),IN(t),IR(t),R(t))R+4:S(t)+IN(t)+IR(t)+R(t)Λd.

The total population N(t)=S(t)+IN(t)+IR(t)+R(t) in systems (1.1) and (1.2) verifies, the equation

dN(t)dtΛ-dN(t),

which gives by integration

N(t)e-dtN(0)-Λd+ΛdmaxN(0),Λd.

If S0Γ, then N(t)Λd almost surely. Thus, the set Γ is almost surely positively invariant by the systems (1.1) and (1.2) respectively, throughout the rest, we assume that S0Γ.

Lemma 3

For the initial condition S0Γ, the model (1.2) has at most one solution and will belong to R+4 with probability one t0 almost surely.

Proof

As all the coefficients of the proposed stochastic model (1.2) are locally Lipschitz continuous, then for each initial condition S0R+4, exclusive local solution S(t) on t[0,τe), where τe denotes the explosion time.

It is obligatory to verify that the solution is global, one need only to prove that τe= almost surely.

For this, let us take m01 sufficiently large to get that S0[1m0,m0], integer m0m. Next, we express the stopping time by:

τm=inft[0,τe):S(t)1m,m,orIN(t)1m,m,orIR(t)1m,m,orR(t)1m,m, 2.1

where one can set inf=. Thus, τm increases as m tends to .

Let τ=limm+τm, and ττe almost surely. When τ= almost surely is true, then τe= almost surely and S(t)R+4 almost surely t0. To put it another way, we just need to demonstrate that τ= almost surely. Otherwise, there will be constants T>0 and 0<ε<1 with

ε<P{τT}. 2.2

So, m0m1 with

εP{Tτm},m1m. 2.3

Let us take a C2-function as

V(S,IN,IR,R)=χ(S)+χ(IN)+χ(IR)+χ(R), 2.4

where χ(x)=-1+x-logx, x]0,+[

Applying the Itô’s method on V, one get

dV(S,IN,IR,R)=LV(S,IN,IR,R)dt+σN(IN-S)dBN(t)+σR(IR-S)1+κIRdBR(t), 2.5

where LV:R+4R4 is defined by

LV=Λ+4d-ΛS-dS+αIN+βIR1+κIR+σN2IN22+σR2IR22(1+κIR)2 2.6
-dIN-αS+μ+σN2S22-dIR+σR2S22(1+κIR)2-βS1+kIR+γ-dR-μINR-γIRRΛ+4d+αIN+βκ+μ+γ+σN2IN22+σR22κ2+σN2S22+σR2S22(1+κIR)2Λ+4d+αΛd+βκ+μ+γ+σN2Λ22d2+σR22κ2+σN2Λ22d2+σR2Λ22κd2:=M. 2.7

Thus

dV(S,IN,IR,R)Mdt+σN(IN-S)dBN(t)+σR(IR-S)1+κIRdBR(t). 2.8

Integrating (2.8) from 0 to τmT=min{τm,T} and then using the notion of expectations, we have

EV(S(τmT),IN(τmT),IR(τmT),R(τmT))V(S0)+MT. 2.9

Let Ωm={τmT} for m1m. Using (2.3), one can acquire P(Ωm)ε. Notice that ϖΩm, S(τm,ϖ) or IN(τm,ϖ) or IR(τm,ϖ) or R(τm,ϖ) equals either m or 1m.

Therefore,

V(S(τm,ϖ),IN(τm,ϖ),IR(τm,ϖ),R(τm,ϖ)))(m-1-logm)(1m-1+logm).

Then we attain

V(S0)+MTE(1ΩmV(S(τm,ϖ),IN(τm,ϖ),IR(τm,ϖ),R(τm,ϖ)))ε(m-1-logm)(1m-1+logm), 2.10

where 1Ωm(ϖ) is the indicator function of Ωm. For m, one reach

>V(S0)+MT=, 2.11

is a contradiction. Hence, τ=.

Lemma 4

[42] Let S(t) satisfies model (1.2) with S0Γ. Then

limt+1t0tσRS(ζ)1+κIR(ζ)dBR(ζ)=0,limt+1t0tσNS(ζ)dBN(ζ)=0,limt+1t0tσRS(ζ)dBR(ζ)=0. 2.12

Extinction

Here, we create the conditions that result in extinction of the non-resistance and resistance infectious strains motioned in the system (1.2).

Proposition 5

If

σN>α2(d+μ) 3.1

then the non-resistance strain of (1.2) go to the extinction almost surely.

Proof

Let S(t) satisfies the model(1.2) with S0Γ. Using the Itô’s method, one get

dlogIN(t)=(αS(t)-(d+μ)-σN2S2(t)2)dt+σNS(t)dBN(t)[-σN22(S(t)-ασN2)2+α22σN2-(d+μ)]dt+σNS(t)dBN(t) 3.2
[α22σN2-(d+μ)]dt+σNS(t)dBN(t). 3.3

Integrating (3.3) from 0 to t and doing some manipulation, we obtain

logIN(t)t-(d+μ-α22σN2)+MN(t)t+logIN(0)t, 3.4

where MN(t)=0tσNS(ζ)dBN(ζ) is the local continuous martingale satisfying MN(0)=0, and by the Lemma 4, we obtain

limt+MN(t)t=0. 3.5

Since σN>α2(d+μ). Applying superior limit of 3.4, we conclude

lim supt+logIN(t)t-(d+μ-α22σN2)<0, 3.6

which means that lim supt+IN(t)=0 almost surely. Hence the theorem.

Proposition 6

If

σR>β2(d+γ), 3.7

then the resistance strain of (1.2) go to the extinction almost surely.

Proof

Let S(t) satisfies the model (1.2) with S0Γ. Implementing the Itô’s technique on model (1.2) results in

dlogIR(t)=(βS(t)1+κIR(t)-(d+γ)-σR2S2(t)2(1+κIR(t))2)dt+σRS(t)1+κIR(t)dBR(t)[-σR22(βS(t)1+κIR(t)-βσR2)2+β22σR2-(d+γ)]dt+σRS(t)1+κIR(t)dBR(t) 3.8
[β22σR2-(d+γ)]dt+σRS(t)1+κIR(t)dBR(t). 3.9

Integrating Eq. (3.9), we reach

logIR(t)t-(d+γ-β22σR2)+MR(t)t+logIR(0)t, 3.10

where MR(t)=0tσRS(ζ)1+κIR(ζ)dBR(ζ) is the local continuous martingale satisfying MR(0)=0, and by the Lemma 4, one may reach

limt+MR(t)t=0. 3.11

Since σR>β2(d+γ). Applying superior limit to (3.10), we conclude

lim supt+logIR(t)t-(d+γ-β22σR2)<0, 3.12

which implies that lim supt+IR(t)=0 almost surely.

Remark 7

Proposition 5 and Proposition 6 shows that when σN>α2(d+μ) and σR>β2(d+γ) the non-resistance strain and resistance strain of system (1.2) die out almost surely, respectively. In other words, large white noise stochastic disturbance yield the two strains extinct. Hence, we presume that the white noise disturbance is not large in the rest of this manuscript.

Let

RNs=αΛd(d+μ)-σN2Λ22d2(d+μ),RRs=βΛd(d+γ)-σR2Λ22d2(d+γ).

Theorem 8

Let S(t) satisfies the model (1.2) with S0Γ.

  1. If RNs<1 and σN2dαΛ then the non-resistant strain of system (1.2) exhibits extinction almost surely, i.e
    limt+IN(t)=0.
  2. If RRs<1 and σR2dβΛ then the resistant strain of system (1.2) exhibits extinction almost surely, i.e
    limt+IR(t)=0,
    Meanwhile, limt+S(t)=Λd, and limt+R(t)=0.

Proof

Firstly, taking integral of both sides of (3.2) and doing some manipulations gives

logIN(t)t=1t0t(αS(τ)-(d+μ)-σN2S2(τ)2)dτ+MN(t)t+logIN(0)t(αΛd-(d+μ)-σN2Λ22d2)+MN(t)t+logIN(0)t=(d+μ)(αΛd(d+μ)-σN2Λ22d2(d+μ)-1)+MN(t)t+logIN(0)t 3.13
=(d+μ)(RNs-1)+MN(t)t+logIN(0)t, 3.14

where MN(t)=0tσNS(ζ)dBN(ζ) is the local continuous martingale satisfying MN(0)=0, and by the Lemma 4, one have

limt+MN(t)t=0. 3.15

Using superior limit on Eq. (3.14), one get

lim supt+logIN(t)t(d+μ)(RNs-1)<0. 3.16

Consequently, limt+IN(t)=0, almost surely.

Secondly, for both sides of (3.8), integrating from 0 to t first and doing some manipulations gives

logIR(t)t=1t0t(βS(τ)1+κIR(τ)-(d+γ)-σR2S2(τ)2(1+κIR(τ))2)dτ+MR(t)t+logIR(0)t(βΛd-(d+γ)-σR2Λ22d2)+MR(t)t+logIR(0)t=(d+γ)(βΛd(d+γ)-σR2Λ22d2(d+γ)-1)+MR(t)t+logIR(0)t 3.17
=(d+γ)(RRs-1)+MR(t)t+logIR(0)t, 3.18

where MR(t)=0tσRS(ζ)1+κIR(ζ)dBR(ζ) is the local continuous martingale satisfying MR(0)=0, and by the Lemma 4, one have

limt+MR(t)t=0. 3.19

We achieve the following result by using superior limit

lim supt+logIR(t)t(d+γ)(RRs-1)<0, 3.20

Consequently, limt+IR(t)=0, almost surely.

Lastly, without loss of generality, one can suppose that 0<IN(t)<εN and 0<IR(t)<εR t0, from the first class of the model (1.2), one obtain

dS(t)dtΛ-(d+αεN+βεR+σNεN|B˙N|+σRεR|B˙R|)S(t), 3.21

As εN0 and εR0, thus

lim inft+S(t)Λd. 3.22

Also,

limt+S(t)Λd+εN+εR. 3.23

Let εN0 and εR0, one attain

lim supt+S(t)Λd. 3.24

From (3.24) and (3.22), one get

limt+S(t)=Λd. 3.25

Next, we prove the last conclusion. Using the third equation of (1.2), we obtain

dR(t)(μεN+γεR-dR(t))dt. 3.26

Its clear by comparison theorem we deduce

lim supt+R(t)=μεN+γεRd. 3.27

Extending εN and εR to 0, we have

limt+R(t)=0. 3.28

Remark 9

From Theorem 8 we show that the non-resistant and the resistant strains will die out if the white noise disturbances are large than certain values or RNs<1 and RRs<1, and the white noise disturbances are not so large.

Persistence in mean

In this section, our main concern to determine sufficient conditions for the persistence of the infectious disease.

Theorem 10

Let S(t) satisfies the model (1.2) with S0Γ,

  1. If RNs>1, RRs<1 and σR2dβΛ, then the resistance strain will go to extinct and the strain IN will persist, furthermore, IN satisfies

    lim inft+IN(t)dα(d+μ)(RNs-1).
  2. If RRs>1, RNs<1 and σN2dαΛ, then the non-resistance strain go to extinct and the strain IR will persist, furthermore, IR satisfies

    lim inft+IR(t)dβ+d(RRs-1).
  3. If RNs>1, RRs>1, then the two strains IN and IR are persistent in mean, furthermore, IN and IR satisfy

    lim inft+IN(t)+IR(t)1ϖmax(d+μ)(RNs-1)+(d+γ)(RRs-1),

where ϖmax=max{(α+β)d+μd,((α+β)d+1)(d+γ)}.

Proof

  1. Let the function Θ(t) define by Θ(t)=S(t)+IN(t)+IR(t). Then the first three equation of model (1.2), implies
    Θ(t)-Θ(0)t=Λ-dS(t)-(d+μ)IN(t)-(d+γ)IR(t). 4.1
    Since RRs<1, and σR2dβΛ one can see from Proposition 6 that, lim supt+IR(t)=0 almost surely. Then we can choose for all t large enough εR small enough, such that 0<IR(t)<εR, therefore,
    S(t)Λ-(d+γ)εRd-d+μdIN(t)-Θ(t)d. 4.2
    Using the Itô’s formula to model (1.2), we obtain
    dlogIN(t)=(αS(t)-(d+μ)-σN2S2(t)2)dt+σNS(t)dBN(t). 4.3
    Hence,
    dlogIN(t)(αS(t)-(d+μ)-σN2Λ22d2)dt+σNS(t)dBN(t). 4.4
    Integration of (4.4) gives
    logIN(t)-logIN(0)tαS(t)-[d+μ+σN2Λ22d2]+MN(t)tα[Λ-(d+γ)εRd-d+μdIN(t)-Θ(t)d]-[d+μ+σN2Λ22d2]+MN(t)t=(d+μ)[α[Λ-(d+γ)εR]d(d+μ)-σN2Λ22d2(d+μ)-1]-α(d+μ)dIN(t)+MN(t)t-αΘ(t)d. 4.5
    So, we obtain
    logIN(t)t(d+μ)[α[Λ-(d+γ)εR]d(d+μ)-σN2Λ22d2(d+μ)-1]-α(d+μ)dIN(t)+MN(t)t-αΘ(t)d+logIN(0)t, 4.6
    where MN(t)=0tσNS(ζ)dBN(ζ) is the local continuous martingale satisfying MN(0)=0, and using Lemma 4, the result is:
    limt+MN(t)t=0. 4.7
    Since RNs>1, for all t large enough we can choose εR small enough, such that
    α[Λ-(d+γ)εR]d(d+μ)-σN2Λ22d2(d+μ)>1.
    By Lemmas 3 and 4, we get that
    lim inft+IN(t)dα(d+μ)(α[Λ-(d+γ)εR]d(d+μ)-σN2Λ22d2(d+μ)-1).
    Let εR0 yields
    lim inft+IN(t)dα(d+μ)(αΛd(d+μ)-σN2Λ22d2(d+μ)-1).
    Therefore,
    lim inft+IN(t)dα(d+μ)(RNs-1).
  2. Notice that
    S(t)Λd-(d+μ)dεN-(d+γ)dIR(t)-Θ(t)d. 4.8
    Applying the Itô’s formula leads to
    dlogIR(t)+IR(t)=βS(t)-(d+γ)-(d+γ)IR(t)-σR2S2(t)2(1+κIR(t))2dt+σRS(t)dBR(t)βS(t)-(d+γ)-(d+γ)IR(t)-σR2Λ22d2dt+σRS(t)dBR(t). 4.9
    Integration of (4.9) gives
    logIR(t)-logIR(0)t+IR(t)-IR(0)tβS(t)-(d+γ)-(d+γ)IR(t)-σR2Λ22d2+MR(t)tβΛ-(d+μ)εNd-(d+γ)-(d+γ)IR(t)-β(d+γ)dIR(t)-βΘ(t)d+MR(t)t=(d+γ)[β(Λ-(d+μ)εN)d(d+γ)-σR2Λ22d2(d+γ)-1]-[β(d+γ)d+(d+γ)]IR(t)-βΘ(t)d+MR(t)t. 4.10
    Hence, we have
    logIR(t)t(d+γ)[β(Λ-(d+μ)εN)d(d+γ)-σR2Λ22d2(d+γ)-1]-[β(d+γ)d+(d+γ)]IR(t)-βΘ(t)d+MR(t)t-IR(t)-IR(0)t+logIR(0)t, 4.11
    where MR(t)=0tσRS(ζ)1+κIR(ζ)dBR(ζ) is the local continuous martingale satisfying MR(0)=0, and using Lemma 4, one have
    limt+MR(t)t=0. 4.12
    Since RRs>1, for all t large enough we can choose εN small enough, such that
    β(Λ-(d+μ)εN)d(d+γ)-σR2Λ22d2(d+γ)>1,
    By Lemmas 3 and 4, we get that
    lim inft+IR(t)dβ+d(β(Λ-(d+μ)εN)d(d+γ)-σR2Λ22d2(d+γ)-1),
    Let εN0 yields
    lim inft+IR(t)dβ+d(βΛd(d+γ)-σR2Λ22d2(d+γ)-1).
    Therefore
    lim inft+IR(t)dβ+d(RRs-1).
  3. Notice that
    S(t)=Λd-(d+μ)dIN(t)-(d+γ)dIR(t)-Θ(t)d. 4.13
    Define
    ϑ(t)=log(IN(t))+log(IR(t))+IR(t). 4.14
    With the help of Itô’s formula, we reach:
    dϑ(t)=(αS(t)+βS(t)-(d+μ)-(d+γ)(1+IR(t))-σN22S2(t)-σR2S2(t)2(1+κIR(t))2)dt+σNS(t)dBN(t)+σRS(t)dBR(t). 4.15
    Therefore
    dϑ(t)(α+β)S(t)-(d+μ)-σN2Λ22d2+σNS(t)dBN(t)-(d+γ)(1+IR(t))-σR2Λ22d2+σRS(t)dBR(t). 4.16
    Integration of (4.16) gives
    ϑ(t)t-ϑ(0)t(α+β)S(t)-(d+μ)-(d+γ)-σN2Λ22d2+MN(t)t-(d+γ)IR(t)-σR2Λ22d2+MR(t)t=(α+β)Λd-(d+μ)-(d+γ)-σN2Λ22d2+MN(t)t-(α+β)d+μdIN(t)-(α+β)d+1(d+γ)IR(t)-σR2Λ22d2+MR(t)t-(α+β)Θ(t)d(α+β)Λd-(d+μ)-(d+γ)-σN2Λ22d2-σR2Λ22d2-ϖmax[IN(t)+IR(t)]-(α+β)Θ(t)d+MN(t)t+MR(t)t. 4.17
    Hence, the result becomes
    IN(t)+IR(t)1ϖmax[(α+β)Λd-(d+μ)-(d+γ)-σN2Λ22d2-σR2Λ22d2-(α+β)Θ(t)d+MN(t)t+MR(t)t-ϑ(t)t+ϑ(0)t], 4.18
    where MN(t)=0tσNS(ζ)dBN(ζ) and MR(t)=0tσRS(ζ)1+κIR(ζ)dBR(ζ) which are local continuous martingales satisfying MN(0)=0 and MR(0)=0, and by lemma 4, we have
    limt+MN(t)t=limt+MR(t)t=0. 4.19
    From Lemmas 3 and 4, we get that
    lim inft+IN(t)+IR(t)1ϖmax[(α+β)Λd-(d+μ)-(d+γ)-σN2Λ22d2-σR2Λ22d2].
    Hence
    lim inft+IN(t)+IR(t)1ϖmax[(d+μ)(RNs-1)+(d+γ)(RRs-1)]>0.
    This is completes the proofs.

Remark 11

Proposition 5 and Proposition 6 shows that the non-resistance and the resistance infections diseases can be extinct if the white noise disturbances are larger than certain values. Theorem 8 and 10 show that the non-resistant (resistant) infection diseases can prevail if the white noise disturbances are small enough such that RNs>1 ( RRs>1 ) respectively. This implies that the stochastic disturbance may cause epidemic diseases to die out.

Graphical analysis

In this section, we implement the Milstein procedure which is given in [43] to test numerically the persistence and the extinction of the disease. The discretization of system 1.2 is given by

Sj+1=Sj+[Λ-αSjINj-βSjIRj1+κIRj-dSj]Δt-σNSjINjΔtξj-σRSjIRj1+κIRjΔtξj+σN22Sj2INj2(ξj2-1)Δt+σR22(βSjIRj1+κIRj)2(ξj2-1)Δt,INj+1=INj+(αSjINj-(d+μ)INj)Δt+σNSjINjΔtξj+σN22Sj2INj2(ξj2-1)Δt,IRj+1=IRj+(βSjIRj1+κIRj-(d+γ)IRj)Δt+σRSjIRj1+κIRjΔtξj+σR22(βSjIRj1+κIRj)2(ξj2-1)Δt,Rj+1=Rj+(μINj+γIRj-dRj)Δt, 5.1

where ξk, (j=1,2,...,n) are the Guassian random variables which Obey Gaussian distribution N(0;1).

Indeed, Fig. 2 shows the dynamics of the non-resistance and resistance strains of influenza for the chosen values of the parameters Λ=10, α=0.08, β=0.09, d=0.5, μ=0.5, κ=0.04, γ=0.5, σN=0.01 and σR=0.01. We clearly see that the all the model variables stay at a strictly positive level. Within this parameters, we have RNs=1.58>1 and RRs=1.78>1, then the two infectious diseases IN and IR will persist. This result is consistent with the theoretical result given in Theorem 10.

Fig. 2.

Fig. 2

Dynamic describing the persistence of the non-resistance and resistance diseases

Next, we take the parameters values for the stochastic model 1.2 as: Λ=10, α=0.03, β=0.09, d=0.3, μ=0.7, κ=0.4, σN=0.01 and σR=0.01. Within this parameters we get RNs=0.9444<1 and RRs=2.9306>1, σN=10-42dαΛ=0.0018. Thus, non-resistance strain IN goes to the extinction, and resistance strain IR will persist (see Fig. 3). This result is consistent with the theoretical result given in Theorem 10.

Fig. 3.

Fig. 3

Dynamic describing the persistence of the non-resistance strain and the extinction of resistance strain

In Fig. 4, we take the parameters values for the model 1.2 as: Λ=10, α=0.09, β=0.03, d=0.3, μ=0.7,γ=0.9, κ=0.4, σN=0.01 and σR=0.01. Within this parameters we get RNs=2.9444>1, RRs=0.9537<1 and σR=10-42dβΛ=0.0018. Thus, non-resistance strain IN is persistent, and resistance strain IR go to extinction.

Fig. 4.

Fig. 4

Dynamics of the infection describing the persistence of the non-resistance strain and the extinction of resistance strain

In Fig. 5, we take the parameters values for the model 1.2 as: Λ=10, α=0.03, β=0.03, d=0.3, μ=0.7, γ=0.9, κ=0.4, σN=0.01 and σR=0.01. Within this parameters we get RNs=0.9444<1, RRs=0.9537<1 and both conditions σN=0.012dαΛ=0.1341 and σR=0.012dβΛ=0.1341. Thus, both of them go to the extinction which is consistent with the theoretical result given in Sect. 3.

Fig. 5.

Fig. 5

Dynamics of the infection describing the persistence of the non-resistance strain and the extinction of resistance strain

Conclusion and discussion

The novelty of this study is that we analyzed the dynamics of two-strain SIR epidemic model including non-resistance and resistance sub-strain of influenza, by considering different incidence rates for these strains. This is due to the fact that the mutated strain will have a minimal effect. We have assumed saturated and bilinear incidence rates for the resistant and non-resistant strains respectively. Saturated incidence rate grasps the negotiating alteration and swarming impact of the infected people and hinders the unboundedness of the interconnection rate by fitting parameters, which was reused in several epidemic issue . Indeed, a stochastic two-strain epidemic model describing resistance and non-resistance strains of influenza was suggested and studied. The existence and uniqueness of the positive solution to the stochastic model (1.2) are proved. The extinction of our studied disease was derived with sufficient conditions. The persistence in the mean of the infection was also established. Different numerical simulations for different noises disturbance were performed to illustrate the efficiency of our theoretical study.

Some interesting topics deserve further investigation. On the one hand, one may propose some more realistic models, such as considering the effects of impulsive perturbations on system (1.2). On the other hand, it is interesting to introduce the telegraph noise, such as continuous-time Markov chain, into system (1.2). Also it is interesting to consider more complex influenza virus models, for example, multi-group model. These problems will be the subject of future work.

Data Availability

No data associated in the manuscript.

Contributor Information

Shabir Ahmad, Email: shabirahmad2232@gmail.com.

Kamsing Nonlaopon, Email: nkamsi@kku.ac.th.

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