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ORIGINAL RESEARCH article

Front. Phys., 10 January 2023
Sec. Social Physics
This article is part of the Research Topic Impacts of Heterogeneity on Biological Complex Systems View all 7 articles

Dynamic analysis and optimal control of worm propagation model with saturated incidence rate

Ruiling WangRuiling Wang1Yakui Xue
Yakui Xue1*Kailin XueKailin Xue2
  • 1School of Mathematics, North University of China, Taiyuan, China
  • 2Department of Mathematics, University of South Australia, Adelaide, Australia

In order to prevent the propagation of computer worms effectively, based on the latent character of worms, the exposed compartments of computer and USB device are introduced respectively, and a series of computer worm propagation models with saturation incidence rate are proposed. The qualitative behavior of the proposed model is studied. Firstly, the threshold R0 of the model is derived by using the next-generation matrix method, which completely characterized the stability of disease free equilibrium and endemic equilibrium. If R0 < 1, the disease free equilibrium is asymptotically stable, implying that the worm dies out eventually and its attack remains under control; if R0 > 1, the asymptotic stability of endemic equilibrium under certain conditions is proved, which means that the worm is always persistent and uncontrollable under such conditions. Secondly, the theoretical results are verified by numerical study, in which the relative importance of each parameter in worm prevalence is evaluated by sensitivity analysis. Finally, so as to minimize the number of computer and USB device carrying computer worms in short span of time, the worm propagation model is extended to incorporate three control strategies. The Pontryagin’s maximum principle is used to characterize the controls’ optimal levels. According to the control effect diagram, the combined strategy is effective in minimizing the transmission dynamics of worm virus in computer and USB devices populations respectively.

1 Introduction

As a storage medium, USB device is favored by many office workers because of its large storage capacity and portability. It is often used to copy data between different computers. In fact, the transmission of data via USB device may be accompanied by the spread of worms [1]. Computer worm is a common computer virus, which has the characteristics of wide spread and serious harm [2]. On 13 January 2021, the news of incaseformat worm flooded wechat circle of friends, and infection cases were found in many provinces, cities, and industries, with a trend of large-scale outbreak. After execution, the worm will automatically copy to the windows directory of the system disk and create a registry to start itself [3]. Once the user restarts the computer, this will cause the worm host to execute from the windows directory, and then the worm process will traverse all disks except the system disk and delete the files, causing irreparable losses to the user. Therefore, it has become an urgent problem in the field of network security to study the propagation rule of computer worm and effectively control its propagation.

A computer worm is a group of programmed code that can reproduce itself and affect the normal use of the computer [4]. A biological virus is a unique tiny living organism, which can make use of the nutrients of the host cell to copy its own essential constituent material DNA or RNA and proteins [57]. Computer worms and biological viruses are two concepts from different fields, but some of their properties have striking similarities [8]. Mainly in the following four aspects: firstly, computer worms and biological viruses are infectious. Computer worms can spread from an infected computer to an uninfected computer through network or other remavable devices. Biological viruses can also be transmitted by direct or indirect contact between living organisms. Then, computer worms and biological viruses are latent and generally not easy to find. Computer worms can integrate their own program fragments into the system programs, so that their most important code can be saved from the anti-virus software. Biological viruses can also integrate their genetic material into the host’s DNA or RNA, thereby escaping attack by the host’s immune system. In addition, computer worms and biological viruses will mutate in the process of spreading, making their species more and more diverse. Finally, both computer worms and biological viruses are destructive. Computer worms can damage the computer system and interfere with the normal operation of the computer. Biological viruses may damage the cells or organs of the host organism, which may pose a threat to the organism’s life. Because of the high similarity between computer worms and biological viruses, we used the method of studying the transmission of infectious diseases to explore the dynamic behavior of computer worms.

In epidemiology, dynamic model has been an important method in analysing the spread and control of infectious diseases qualitatively and quantitatively [911]. In 1991, Kephart and White first introduced the dynamic model of infectious disease into the study of the propagation of computer virus. Since then, the dynamic model has also become a vital tool for the study of various computer viruses [1216]. The research on computer worms have experienced a rapid growth, and a large number of models have been established, mathematically analyzed, which provides some useful and valid references for the characteristics of computer worms transmission [17]. In 2011, Song et al. [18] studied removable device as an independent carrier for the first time. They hypothesized that computer worms spread via both web-based scanning and removable devices, established SIR model of computer population and SI model of removable devices population, studied their dynamic behavior, and gave corresponding control strategy. In 2012, Zhu et al. [19] proposed a new dynamic model to describe the spread of computer virus by using the same method as in Ref. [18]. In addition, by qualitative analysis, it is concluded that controlling R0 below one is an effective means to extinguish virus, which provides a good start point for understanding the transmission of computer virus through such interactions. In 2015, Ma et al. [20] proposed SIBV model of fixed nodes and SI model of mobile nodes considering the influence of benign worms and mobile devices in the network environment, discussed the influences of removable devices on the interaction dynamics between malicious worms and benign worms. Through numerical analysis and simulation, it is proved that the anti-worm technology can effectively suppress the spread of malicious worms. In 2018, Zhu et al. [21] introduced two control strategies of disconnecting computers from removable devices and reorganizing computers on the basis of Ref. [19], and studied the optimal control of virus transmission between computers and removable devices. Different from previous studies, this paper does not use a fixed cost weight index in the objective function, but uses a state-based cost weight index. In 2020, Kim et al. [1] proposed and analyzed a scheme to control virus transmission through vaccination, that is, installing effective anti-virus software. The results showed that the higher the vaccination rate, the lower the number of infected computers.

Inspired by the models above, we establish a new worm transmission model. We adopt the saturation incidence rate [22, 23], which can present the inhibition effect of susceptible devices and the crowding effect of infectious devices and can also ensure the boundness of contact rate by choosing suitable parameters [24]. In addition, considering the latent character of computer worms, the exposed compartments of computer and USB are introduced [2528]. The rest of the article is organized as follows: in Section 2, qualitative analysis of the dynamical system is carried out, and sufficient conditions for the existence of equilibria and asymptotic stability are given; numerical findings and discussion are conducted in Section 3; in Section 4, optimal control strategy is proposed; and conclusion is presented in Section 5.

2 Dynamical model

The main purpose of this paper is to explore the dynamic behavior of computer worms transmission in the process of using USB devices to transmit data, so as to formulate effective strategies to control the spread of worms. This model is an improved version of Kim et al. [1]. In this model, the computer acts as the host and the USB device acts as a vector. Among them, the total computer population is divided into the following four subclasses, which are Sc(t), Ec(t), Ic(t), and Rc(t), representing the numbers of susceptible computers, exposed computers, infectious computers and recovered computers at time t. And similarly for USB devices population, which is classified into three vector population subclasses, namely Su(t), Eu(t), and Iu(t), represent the numbers of susceptible USB devices, exposed USB devices and infectious USB devices at time t, respectively. In addition, the following model assumptions are presented:

(H1) All newly launched computers and removable USB devices are susceptible.

(H2) At time t, the infectious force of infected USB devices to susceptible computers is given by 1σνβ1ScIu1+α1Iu, while the infectibility of infected computers to susceptible USB devices is 1σνβ1SuIc1+α2Ic.

(H3) Infected computers will gain temporary immunity after recovery due to anti-virus software installed, but after a period of time will join again susceptible class because of the variability of computer worms.

(H4) Computer dysfunction is not only related to natural death, but also to worm invasion.

The improved model as follow:

dScdt=Λ11σνβ1ScIu1+α1Iuσν+μ1Sc+τRc,dEcdt=1σνβ1ScIu1+α1Iuη+ϵ+μ1Ec,dIcdt=ηEcγ+μ1+θIc,dRcdt=σνSc+ϵEc+γIcτ+μ1Rc,dSudt=Λ2β2SuIc1+α2Icμ2Su+ϕEu+pIu,dEudt=β2SuIc1+α2Icξ+ϕ+μ2Eu,dIudt=ξEup+μ2Iu.(1)

For the computer population in system (Eq. 1), Λ1 is the recruitment rate of computer population; σ is the efficiency coefficient of the anti-virus software; ν is installation coverage rate coefficient of anti-virus software; β1 is infection rate coefficient of susceptible computers by infectious USB devices; α1 is the degree coefficient of protection measures taken for susceptible computers in case of worms outbreak; μ1 is the natural elimination rate coefficient of computer population; θ is the elimination rate coefficient of computer population caused by worm invasion; τ, η, ϵ, γ are the transition rate coefficients among states in the computer population.

As for the USB population in system (Eq. 1), Λ2 is the recruitment rate of USB population; β2 is infection rate coefficient of susceptible USB devices by infectious computers; α2 is the degree coefficient of protection measures taken for susceptible USB devices in case of worms outbreak; μ2 is the natural elimination rate coefficient of USB population; ϕ, p, ξ are the transition rate coefficients among states in the USB population.

Suppose Nc and Nu are the total number of computer population and USB population at time t, respectively, satisfying Nc = Sc + Ec + Ic + Rc and Nu = Su + Eu + Iu. Add the equations in system (Eq. 1) to get dNcdt=Λ1μ1NcθIcΛ1μ1Nc and dNudt=Λ2μ2Nu. The operable region for system (Eq. 1) is given below:

Δ=Sc,Ec,Ic,Rc,Su,Eu,IuR+7|0NcΛ1μ1,0NuΛ2μ2.(2)

In this section, we firstly prove the existence of disease free equilibrium and endemic equilibrium of system (Eq. 1), and obtain the basic reproduction number R0 through calculation which determines the propagation dynamics of system (Eq. 1). Secondly, we provide the local and global stability of disease free equilibrium and endemic equilibrium under certain conditions, which establishes the theoretical foundation for the control strategies of worm attack.

2.1 Existence of basic reproduction number and equilibria

Our aim is to study the characteristics of disease free equilibrium and endemic equilibrium. Let the right-hand side of system (Eq. 1) equals zero, and the disease free equilibrium can be obtained:

P0=Sc0,Ec0,Ic0,Rc0,Su0,Eu0,Iu0=Λ1τ+μ1μ1σν+τ+μ1,0,0,Λ1σνμ1σν+τ+μ1,Λ2μ2,0,0.(3)

Next, we calculate the basic reproduction number R0, which is essentially the number of secondary infectious cases produced in a susceptible class by a single infectious node in its overall infectious duration. This is a decisive threshold in epidemiological systems that can be used to predict whether computers will be continuously attacked by worms [29]. According to the next-generation matrix method in literature [30], we have the following:

F=0001σνβ1Sc000000β2Su0000000,V=η+ϵ+μ1000ηγ+μ1+θ0000ξ+ϕ+μ2000ξp+μ2.

Thus, we obtain the basic reproduction number:

R0=1σνβ1β2ηξSc0Su0η+ϵ+μ1γ+μ1+θξ+ϕ+μ2p+μ2=1σνβ1β2ηξτ+μ1Λ1Λ2η+ϵ+μ1γ+μ1+θξ+ϕ+μ2p+μ2σν+τ+μ1μ1μ2.(4)

Theorem 1 When R0 > 1, system (Eq. 1) has a unique endemic equilibrium.

Proof: Make the right side of system (Eq. 1) equal to zero, and substitute the endemic equilibrium P*=(Sc*,Ec*,Ic*,Rc*,Su*,Eu*,Iu*) into the equation:

Ec=γ+μ1+θηIc,Rc=σνSc+ϵEc+γIcτ+μ1,Eu*=p+μ2ξIu*,
Sc=Λ1τ+μ1+τϵEc+γIcμ1σν+τ+μ1+1σνβ1Iu*τ+μ11+α1Iu*,Su*=Λ2+pIu*μ2+ξ+μ2ξ+ϕ+μ2β2Ic1+α2Ic,
Iu*=ξβ2Λ2Icξ+ϕ+μ2p+μ21+α2Icμ2+μ2β2p+ξ+μ2Ic.

We get the expression GIc*=aIc*+b for Ic*, where

a=α2μ2ξ+ϕ+μ2p+μ2+μ2β2p+ξ+μ2+ξβ2Λ2α1μ1η+ϵ+μ1γ+μ1+θσν+τ+μ1+ξβ2Λ2ηβ1μ1γ1σν+μ1+θ1σντ+μ1+ξβ2Λ2β1μ1γ+μ1+θ1σντ+μ1+ϵ>0,
b=μ1μ2η+ϵ+μ1γ+μ1+θσν+τ+μ1ξ+ϕ+μ2p+μ21R02.

When R0 > 1, b < 0, so Ic*=ba>0 and GIc*=0, that is, when R0 > 1, there is a unique positive equilibrium P*.

2.2 Stability of disease free equilibrium

In this subsection, we analyze the asymptotical stability of disease free equilibrium P0.

Theorem 2 The disease free equilibrium P0 of system (Eq. 1) is locally asymptotically stable if R0 < 1 and is unstable if R0 > 1.

Proof: The Jacobian matrix of system (Eq. 1) at P0 is

J0=a1100τ001σνβ1Sc00a2200001σνβ1Sc00ηa330000σνϵγa4400000β2Su00μ2ϕp00β2Su000a66000000ξa77,(5)

where a11=σν+μ1,a22=η+ϵ+μ1,a33=γ+μ1+θ,a44=τ+μ1,a66=ξ+ϕ+μ2,a77=p+μ2. Obviously, one of the eigenvalues of J|0| is λ1 = −μ2. In order to obtain the rest eigenvalues, the following simplified matrix is considered:

J10=a1100τ01σνβ1Sc00a220001σνβ1Sc00ηa33000σνϵγa440000β2Su00a6600000ξa77.(6)

By elementary row operations, we get

J20=a1100τ01σνβ1Sc00a220001σνβ1Sc000b33001σνηβ1Sc0000b440b460000b551σνηβ1β2Sc0Su000000b66,(7)

where

b33=η+ϵ+μ1γ+μ1+θ,
b44=μ1τ+σν+μ1η+ϵ+μ12γ+μ1+θ,
b55=η+ϵ+μ1γ+μ1+θξ+ϕ+μ2,
b66=1σνξηβ1β2Sc0Su0η+ϵ+μ1γ+μ1+θξ+ϕ+μ2p+μ2,
b46=1σνηβ1Sc0γσν+μ1η+ϵ+μ1+ϵμ1σνη+μ11σνβ1Sc0η+ϵ+μ1γ+μ1+θ.

When (1σν)ξηβ1β2Sc0Su0(η+ϵ+μ1)(γ+μ1+θ)(ξ+ϕ+μ2)<(p+μ2), that is, when R0 < 1, the eigenvalues of J2|0| are all negative, and therefore the eigenvalues of J|0| are all negative. It shows that when R0 < 1, the disease free equilibrium P0 of system (Eq. 1) is locally asymptotically stable in Δ, whereas P0 is unstable in Δ if R0 > 1.

Theorem 3 The disease free equilibrium P0 of system (Eq. 1) is globally asymptotically stable in region Δ if R0 < 1 and is unstable if R0 > 1.

Proof: The Castillo-Chavez method in Refs. [31] is used to prove it. First, let χ1 = (Sc, Rc, Su), χ2 = (Ec, Ic, Eu, Iu) and define P0=(χ10,0), where

χ10=Λ1τ+μ1μ1σν+τ+μ1,Λ1σνμ1σν+τ+μ1,Λ2μ2.(8)

We decompose system (Eq. 1) into two subsystems,

dχ1dt=Gχ1,χ2,dχ2dt=Hχ1,χ2,(9)

where

Gχ1,χ2=Λ11σνβ1ScIu1+α1Iuσν+μ1Sc+τRcσνSc+Ec+γIcτ+μ1RcΛ2β2SuIc1+α2Icμ2Su+ϕEu+pIu,Hχ1,χ2=1σνβ1ScIu1+α1Iuη++μ1EcηEcγ+μ1+θIcβ2SuIc1+α2Icξ+ϕ+μ2EuξEup+μ2Iu.

Because Sc=Sc0, Rc=Rc0, Su=Su0, and Gχ1,0=0, we have

Gχ1,0=Λ1σν+μ1Sc0+τRc0σνSc0τ+μ1Rc0Λ2μ2Su0=0.(10)

According to (Eq. 10), when t, χ1χ10. Therefore, χ1=χ10 is globally asymptotically stable.

Moreover, it is obvious that

Hχ1,χ2=Bχ2H̄χ1,χ2=a22001σνβ1Sc0ηa33000β2Su0a66000ξa77EcIcEuIu1σνβ1Sc0Iu1σνβ1ScIu1+α1Iu0β2Su0Icβ2SuIc1+α2Ic0.(11)

The population limits of computer and USB device are Sc0,Su0, that is, ScSc0,SuSu0, so 1σνβ1Sc0Iu1σνβ1ScIu1+α1Iu,β2Su0Icβ2SuIc1+α2Ic, which means H̄χ1,χ20. Also from (Eq. 11), B is an M-matrix. Thus condition 1 and 2 are satisfied in section 4.1 of Refs. [32]. Therefore, Theorem 3 is proved.

2.3 Stability of endemic equilibrium

In this subsection, we analyze the asymptotical stability of endemic equilibrium P*.

Theorem 4 The endemic equilibrium P* of system Eq. 1 is locally asymptotically stable if maxϵ,γ<σν and 1<R0<1+α1Iu*1+α2Ic*τ+μ1Λ1Λ2σν+τ+μ1μ1μ2Sc*Su*.

Proof: The Jacobian matrix of system (Eq. 1) at P* is given by

J|*|=c1100τ001σνβ1Sc1+α1Iu21σνβ1Iu1+α1Iua2200001σνβ1Sc1+α1Iu20ηa330000σνϵγa4400000β2Su1+α2Ic20c55ϕp00β2Su1+α2Ic20β2Ic1+α2Ica66000000ξa77,(12)

where c11=σν+μ11σνβ1Iu*1+α1Iu*,c55=μ2β2Ic*1+α2Ic*.

After simplification we get

J1*=c1100τ001σνβ1Sc1+α1Iu20d2201σνβ1Iuτ1+α1Iu001σνβ1Scσν+μ11+α1Iu200d331σνβ1Iuητ1+α1Iu001σνβ1Scησν+μ11+α1Iu2000d4400d470000μ2ξ+μ2p00000d66d67000000d77,(13)

where

d22=a22c11,d33=a22a33c11,d44=μ1τ+σν+μ1a222a33c112+μ11σνβ1Iu1+α1Iua222a33c112+ημ1+θμ1a33τ1σνβ1Iu1+α1Iua22c112,d47=σνηθ+ϵσνμ1a33ημ1γσν1σνβ1Sc1+α1Iu2a22c112,d66=β2Ic1+α2Icξ+μ2+μ2a66a22a33c11d44,d67=β2Icp1+α2Ica22a33c11d44+μ1μ2ητ+σν+μ1×1σνβ1Sc1+α1Iu2β2Su1+α2Ic2a11a222a33c112+μ12μ2ητa33+μ1μ2ητϵa33+μ1μ2ηa11a22a33μ1μ2η2τμ1+θμ1μ2η2τγ1σνβ1Iu1+α1Iuβ2Su1+α2Ic21σνβ1Sc1+α1Iu2a22c112,d77=μ2p+ξ+μ2β2Ic1+α2Ica22a33c11d44+1σνβ1Iu1+α1Iuμ2a22a33a66a77d44+ξμ2ητσνηθ+ϵσνμ1a331σνβ1Iu1+α1Iuβ2Su1+α2Ic21σνβ1Sc1+α1Iu2a22c112+ξμ2ητημ1γσν1σνβ1Iu1+α1Iuβ2Su1+α2Ic21σνβ1Sc1+α1Iu2a22c112+a11a44d44R021σνβ1β2ηξΛ1Λ2μ1σν+τ+μ11σν+τ+μ1μ1μ2ScSuR02τ+μ1Λ1Λ21+α1Iu21+α2Ic2.+a11a44d44R021σνβ1β2ηξΛ1Λ2μ1σν+τ+μ11σν+τ+μ1μ1μ2ScSuR02τ+μ1Λ1Λ21+α1Iu21+α2Ic2.

It is obvious that a22, a33, a66, c11, c55 < 0, and then, d22, d33, d44, d66 < 0 can be obtained according to the above expressions. Besides, when maxϵ,γ<σν and 1<R0<1+α1Iu1+α2Icτ+μ1Λ1Λ2σν+τ+μ1μ1μ2ScSu, we get d77 < 0. Just as we have shown that the real parts of all eigenvalues of J are negative, so the endemic equilibrium J is locally asymptotically stable under condition maxϵ,γ<σν and 1<R0<1+α1Iu1+α2Icτ+μ1Λ1Λ2σν+τ+μ1μ1μ2ScSu.

Next, the geometrical approach in Refs. [33] is used to determine the condition that system (Eq. 1) achieves global asymptotic stability at the endemic equilibrium.

Theorem 5 If maxϕScEcβ2Ic1+α2Ic,β2Ic1+α2IcEcSc<1σνβ1Iu1+α1Iu<β2Ic1+α2IcSuEu and R0 > 1, then system (Eq. 1) is globally asymptotically stable at endemic equilibrium P∗ and unstable otherwise.

Proof: We prove the global stability of endemic equilibrium P∗ under the above conditions by using geometrical approach [32, 34, 35], which is the generalization of Lyapunov theory in essence, by using the third additive compound matrix. Consider the subsystems of system (Eq. 1)

dScdt=Λ11σνβ1ScIu1+α1Iuσν+μ1Sc+τRc,dEcdt=1σνβ1ScIu1+α1Iuη+ϵ+μ1Ec,dSudt=Λ2β2SuIc1+α2Icμ2Su+ϕEu+pIu,dEudt=β2SuIc1+α2Icξ+ϕ+μ2Eu.(14)

Let J be the Jacobian matrix of system (Eq. 14) given by

J=σν+μ11σνβ1Iu1+α1Iu0001σνβ1Iu1+α1Iuη+ϵ+μ10000μ2β2Ic1+α2Icϕ00β2Ic1+α2Icξ+ϕ+μ2.(15)

Based on [35], the third additive compound matrix of J is denoted by

J3=A11ϕ00β2Ic1+α2IcA220000A330001σνβ1Iu1+α1IuA44,(16)

where

A11=σν+2μ1+μ2+η+ϵ1σνβ1Iu1+α1Iuβ2Ic1+α2Ic,A22=σν+2μ1+μ2+η+ϵ+ξ+ϕ1σνβ1Iu1+α1Iu,A33=σν+μ1+2μ2+ξ+ϕ1σνβ1Iu1+α1Iuβ2Ic1+α2Ic,A44=μ1+2μ2+η+ϵ+ξ+ϕβ2Ic1+α2Ic.

Now let us choose a function Pχ=PSc,Ec,Su,Eu so that Pχ=diagSc,Ec,Su,Eu, and accordingly, P1χ=diag1Sc,1Ec,1Su,1Eu. The time derivative of Pχ yields that Pfχ=diagṠc,Ėc,Ṡu,Ėu.

Therefore,

PfP1=diagṠcSc,ĖcEc,ṠuSu,ĖuEu,(17)

and

PJ3P1=A11ϕScEc00β2Ic1+α2IcEcScA220000A330001σνβ1Iu1+α1IuEuSuA44.(18)

So that B=PfP1+PJ3P1,

B=B11B1200B21B220000B33000B43B44,(19)

where

B11=ṠcScσν+2μ1+μ2+η+ϵ1σνβ1Iu1+α1Iuβ2Ic1+α2Ic,B12=ϕScEc,B22=ĖcEcσν+2μ1+μ2+η+ϵ+ξ+ϕ1σνβ1Iu1+α1Iu,B21=β2Ic1+α2IcEcSc,B33=ṠuSuσν+μ1+2μ2+ξ+ϕ1σνβ1Iu1+α1Iuβ2Ic1+α2Ic,B44=ĖuEuμ1+2μ2+η+ϵ+ξ+ϕβ2Ic1+α2Ic,B43=1σνβ1Iu1+α1IuEuSu.

Consequently, if 1σνβ1Iu1+α1Iu+β2Ic1+α2Ic>ϕScEc, then

h1t=B11+j=24B1j,h1t=ṠcScσν+2μ1+μ2+η+ϵ1σνβ1Iu1+α1Iuβ2Ic1+α2Ic+ϕScEc=ṠcScσν+2μ1+μ2+η+ϵ1σνβ1Iu1+α1Iu+β2Ic1+α2IcϕScEcṠcScσν+2μ1+μ2+η+ϵ.

and if 1σνβ1Iu1+α1Iu>β2Ic1+α2IcEcSc, then

h2t=B22+j=1j24B2j,h2t=ĖcEcσν+2μ1+μ2+η+ϵ+ξ+ϕ1σνβ1Iu1+α1Iu+β2Ic1+α2IcEcSc=ĖcEcσν+2μ1+μ2+η+ϵ+ξ+ϕ1σνβ1Iu1+α1Iuβ2Ic1+α2IcEcScĖcEcσν+2μ1+μ2+η+ϵ+ξ+ϕ.

Similarly,

h3t=B33+j=1j34B3j,h3t=ṠuSuσν+μ1+2μ2+ξ+ϕ1σνβ1Iu1+α1Iuβ2Ic1+α2Ic,ṠuSuσν+μ1+2μ2+ξ+ϕ.

and if β2Ic1+α2Ic>1σνβ1Iu1+α1IuEuSu, then

h4t=B44+j=13B4j,h4t=ĖuEuμ1+2μ2+η+ϵ+ξ+ϕβ2Ic1+α2Ic+1σνβ1Iu1+α1IuEuSu=ĖuEuμ1+2μ2+η+ϵ+ξ+ϕβ2Ic1+α2Ic1σνβ1Iu1+α1IuEuSuĖuEuμ1+2μ2+η+ϵ+ξ+ϕ.

If h1,h2,h3,h4R4 and we define the Lozinski measure μB as μB=hi,i=1,2,3,4 then integration of μB by taking limits as t the following equations follow:

limtsup1t0th1tdt1tlogSctSc0σν+2μ1+μ2+η+ϵ<σν+2μ1+μ2+η+ϵ,limtsup1t0th2tdt1tlogEctEc0σν+2μ1+μ2+η+ϵ+ξ+ϕ<σν+2μ1+μ2+η+ϵ+ξ+ϕ,limtsup1t0th3tdt1tlogSutSu0σν+μ1+2μ2+ξ+ϕ<σν+μ1+2μ2+ξ+ϕ,limtsup1t0th4tdt1tlogEutEu0μ1+2μ2+η+ϵ+ξ+ϕ<μ1+2μ2+η+ϵ+ξ+ϕ.

Thus, combining the above four inequalities, we get the following inequality:

q̄=limtsup1t0tμBdt<0.

This shows that the subsystem of system (Eq. 1) containing four non-linear differential equations is globally asymptotically stable around the equilibrium Sc,Ec,Su,Eu. The solutions to the rest of the equations of system (Eq. 1) are IcIc,RcRc,IuIu when t. Therefore, the endemic equilibrium P∗ is globally asymptotically stable.

3 Numerical simulation

In this section, we refer to the data of Refs. [3638] to analyze the performance and dynamic behavior of the studied model through numerical simulation, and demonstrate the feasibility of the theoretical results obtained.

3.1 Stability of equilibria

The stability of disease free equilibrium and endemic equilibrium of system (Eq. 1) is verified by numerical simulation. Figure 1 and Figure 2 show the stability simulation diagram of disease free equilibrium and endemic equilibrium. Initially the number of susceptible computers, exposed computers, infected computers, recovery computers, susceptible USB devices, exposed USB devices and infected USB devices are Sc(0) = 50,000, Ec (0) = 20,000, Ic(0) = 10,000, Rc (0) = 10,000, Su(0) = 5,000, Eu (0) = 3,000, and Iu(0) = 1,000, separately. We take the parameters Λ1 = 0.75, Λ2 = 0.1, σ = 0.6, ν = 0.1, β1 = 0.035, β2 = 0.035, α1 = 0.8, α2 = 0.3, μ1 = 0.1, μ2 = 0.1, τ = 0.1, η = 0.45, ϵ = 0.25, ϕ = 0.05, p = 0.003, ξ = 0.005, θ = 0.001, γ = 0.05, at which time, R0 ≈ 0.0039 < 1. It can be seen from Figure 1 that the number of exposed computers Ec, infected computers Ic, exposed USB devices Eu and infected USB devices Iu gradually approach zero, which shows the correctness of Theorem 2 and Theorem 3. When β1 = 0.053, μ1 = 0.01, ξ = 0.05, and other parameters remain unchanged, R0 ≈ 1.0670 > 1. Compared with Figure 1, the number of exposed computers Ec, infected computers Ic, exposed USB devices Eu and infected USB devices Iu in Figure 2 are not zero and reach a stable value, which is also consistent with Theorems 4 and 5.

FIGURE 1
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FIGURE 1. Time series plot of system (1) with Λ1 = 0.75, Λ2 = 0.1, σ = 0.6, ν = 0.1, β1 = 0.035, β2 = 0.035, α1 = 0.8, α2 = 0.3, μ1 = 0.1, μ2 = 0.1, τ = 0.1, η = 0.45, ϵ = 0.25, ϕ = 0.05, p = 0.003, ξ = 0.005, θ = 0.001, γ = 0.05. (A) the tendency of the worm propagation in a short period, (B) the tendency of the worm propagation in a later period.

FIGURE 2
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FIGURE 2. Time series plot of system (1) with Λ1 = 0.75, Λ2 = 0.1, σ = 0.6, ν = 0.1, β1 = 0.053, β2 = 0.035, α1 = 0.8, α2 = 0.3, μ1 = 0.01, μ2 = 0.1, τ = 0.1, η = 0.45, ϵ = 0.25, ϕ = 0.05, p = 0.003, ξ = 0.05, θ = 0.001, γ = 0.05. (A) the tendency of the worm propagation in a short period, (B) the tendency of the worm propagation in a later period.

3.2 Performance comparison of the SEIRSEI model with the SIRSI model

To evaluate the performance of the SEIRSEI model, numerical methods are used to compare it with the SIRSI model [1]. We simulate SEIRSEI and SIRSI models by Matlab. Both models share the same parameters as in Section 3.1. Figure 3 shows the number of infected computers and infected USB devices for both models. The results show that, compared with SIRSI model, the propagation speed of worms and the number of infected computers and USB devices in SEIRSEI model are significantly decreased. This implies that the SEIRSEI model takes much smaller time to combat the worm than the SIRSI model. Obviously, the results shown in Figure 3 verify that the proposed model is more effective in controlling computer worms attack than the previous model.

FIGURE 3
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FIGURE 3. Performance comparison of the SEIRSEI model with the SIRSI model. (A) graph of infectious number of computers, (B) graph of infectious number of USB devices.

3.3 Sensitivity analysis

Sensitivity analysis is used to determine which parameters have a significant effect on decreasing the spread of disease. Forward sensitivity analysis is considered an important component of epidemic modeling, although it is tedious to calculate for complex biological models. The ecologist and epidemiologist paid a lot of attention to the sensitivity study of R0.

Definition. The normalized forward sensitivity index of R0 that depends differentiability on a parameter ω is defined as

Sω=ωR0R0ω(20)

The following three methods are normally used to calculate the sensitivity indices, (i) by direct differentiation, (ii) by a Latin hypercube sampling method, (iii) by linearizing system (Eq. 1), and then solving the obtain set of linear algebraic equations. We will apply the direct differentiation method as it gives analytical expressions for the indices. The indices not only shows us the influence of various aspects associated with the spreading of infectious disease but also gives us important information regarding the comparative change between R0 and different parameters. Consequently, it helps in developing the control strategies.

Table 1 demonstrates that the parameters Λ1, Λ2, β1, β2, τ, η and ξ have a positive influence on the reproduction number R0, which describe that the growth or decay of these parameters say by 10% will increase or decrease the reproduction number by 10%, 10%, 10%, 10%, 1.1%, 4.3% and 9.6% respectively. But on the other hand, the index for parameters σ, ν, μ1, μ2, ϵ, ϕ, p, θ and γ illustrates that increasing their values by 10% will decrease the values of reproduction number R0 by 2.9%, 2.9%, 16.7%, 26.1%, 3.1%, 3.2%, 0.29%, 0.06%, and 3.3% respectively. α1 and α2 have no impact on the reproduction number R0. Figures 4A–H are plotted to demonstrate the variations in the basic reproductive number R0 with respect to the different model parameters.

TABLE 1
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TABLE 1. Sensitivity indices of the basic reproduction number R0 against mentioned parameters.

FIGURE 4
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FIGURE 4. Sensitivity analysis of different parameters. (A) R0 versus sensitive parameters p and ϕ, (B) R0 versus sensitive parameters γ and ϵ, (C) R0 versus sensitive parameters σ and η, (D) R0 versus sensitive parameters ν and η, (E) R0 versus sensitive parameters τ and μ1, (F) R0 versus sensitive parameters θ and μ1, (G) R0 versus sensitive parameters τ and η, (H) R0 versus sensitive parameters τ and γ.

4 Optimal control strategy formulation

In order to explore how to effectively control the propagation of computer worms, system (Eq. 1) is improved in this section. Three control variables uiti=1,2,3 are introduced into system (Eq. 1), which denote the effectiveness of the corresponding control strategy to inhibit worm propagation. u1t0u1t1 represents the effectiveness of improving the installation coverage rate of anti-virus software, u2t0u2t1 and u3t0u3t1 represent the effectiveness of disinfecting computers and USB devices, respectively. Establish the optimal control system:

dScdt=Λ11u1β1ScIu1+α1Iuu1+μ1Sc+τRc,dEcdt=1u1β1ScIu1+α1Iuη+u2+μ1Ec,dIcdt=ηEcu2+μ1+θIc,dRcdt=u1Sc+u2Ec+u2Icτ+μ1Rc,dSudt=Λ2β2SuIc1+α2Icμ2Su+u3Eu+u3Iu,dEudt=β2SuIc1+α2Icξ+u3+μ2Eu,dIudt=ξEuu3+μ2Iu.(21)

Defining the objective function

Ju1,u2,u3=0TA1Ec+A2Ic+A3Eu+A4Iu+ 12B1u12+B2u22+B3u32dt,(22)

where A1, A2, A3 and A4 are positive weight constants of Ec, Ic, Eu and Iu respectively, and T is the final time to implement the control strategies.

The control set is defined as U=u1t,u2t,u3tuiti=1,2,3, which is a Lebesgue measurable control quantity satisfying uit0,1 and t0,T. The purpose of this paper is to find the optimal control u1,u2,u3 so that

Ju1t,u2t,u3t=minJu1t,u2t,u3tu1t,u2t,u3tU.

Based on the boundedness of the right end of system (Eq. 21) and the convexity of the integrand of (Eq. 22), the existence of the optimal control u1,u2,u3 can be obtained [39, 40].

To find the optimal solution of the optimal control problem (Eqs 21, 22), the Hamilton function is defined as follows

H=A1Ec+A2Ic+A3Eu+A4Iu+12B1u12+B2u22+B3u32+ λScdScdt+λEcdEcdt+λIcdIcdt+λRcdRcdt+λSudSudt+λEudEudt+λIudIudt,(23)

where λSc,λEc,λIc,λRc,λSu,λEu,λIu are the adjoint variables. According to Pontryagin’s maximum principle [41], the following theorem is obtained.

Theorem 6 Let u1t,u2t,u3t be optimal controls and Sc,Ec,Ic,Rc,Su,Eu,Iu be optimal state solutions of the optimal control problem (Eqs 21, 22), and then there exists adjoint variables λSc,λEc,λIc,λRc,λSu, λEu,λIu, satisfying,

dλidt=Hi,(24)

where i = Sc, Ec, Ic, Rc, Su, Eu, Iu. In addition, the corresponding optimal control variables u1t,u2t,u3t are

u1=max0,minβ1ScIu1+α1IuλEcλScScλRcλScB1,1,u2=max0,minEcλRcλEcIcλRcλIcB2,1,u3=max0,minEuλEuλSuIuλIuλSuB3,1.(25)

Proof: To prove the theorem, the differential of (Eq. 23), namely the Hamiltonian function H, with respect to the state variables Sc, Ec, Ic, Rc, Su, Eu, Iu are obtained, and the corresponding adjoint system is as follows:

dλScdt     =     HSc=1u1β1Iu1+α1IuλEcλScu1λRcλSc+μ1λSc,dλEcdt     =     HEc=A1ηλIcλEcu2λRcλEc+μ1λEc,dλIcdt     =     HIc=A2β2Su1+α2Ic2λEuλSuu2λRcλIc+μ1+θλIc,dλRcdt     =     HRc=τλRcλSc+μ1λRc,dλSudt     =     HSu=β2Ic1+α2IcλEuλSu+μ2λSu,dλEudt     =     HEu=A3+u3λEuλSuξλIuλEu+μ2λEu,dλIudt     =     HIu=A41u1β1Sc1+α1Iu2λEcλSc+u3λIuλEu+μ2λIu,(26)

and with transversality conditions λScT=0, λEcT=0, λIcT=0, λRcT=0, λSuT=0, λEuT=0, λIuT=0. Also, the optimal controls u1,u2 and u3 satisfy Hui=0, i = 1, 2, 3. Therefore, the optimal controls are characterized by

u1=max0,minβ1ScIu1+α1IuλEcλScScλRcλScB1,1,u2=max0,minEcλRcλEcIcλRcλIcB2,1,u3=max0,minEuλEuλSuIuλIuλSuB3,1.

For sufficiently small final time T, the uniqueness of the optimal control of the system has been achieved owing to the boundedness of the state variables and adjoint variables together with the Lipschitz property of systems (Eq. 21) and (Eq. 26).

In order to show the rationality and effectiveness of the control strategy mentioned in Section 4, numerical simulation is carried out. Figure 5 shows a substantial decrease in the population of exposed computers, infected computers, exposed USB devices and infected USB devices respectively relative to the case of no control, when the combined strategy is implemented, including the installation coverage rate of anti-virus software and the disinfection of computer and USB device. Parameter Λ1 = 0.75, Λ2 = 0.1, σ = 0.6, ν = 0.1, β1 = 0.035, β2 = 0.035, α1 = 0.8, α2 = 0.3, μ1 = 0.1, μ2 = 0.1, τ = 0.1, η = 0.45, ϵ = 0.25, ϕ = 0.05, p = 0.003, ξ = 0.005, θ = 0.001, γ = 0.05. We draw the conclusion that the spread of worm virus can be effectively controlled by strengthening users’ computer security education, improving their understanding of anti-virus software, and calling on users to disinfect computers and USB devices regularly.

FIGURE 5
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FIGURE 5. Plots of different classes showing the difference between with control and without control, respectively: (A) exposed computers, (B) infected computers, (C) exposed USB devices, (D) infected USB devices.

5 Conclusion and discussion

This paper mainly considers the dynamic behavior of computer worms in the process of using USB to transmit data. The novel ideas of our paper are as follows: (a) the exposed compartments of computer and USB are introduced because of the latent nature of worms; (b) infected computers will gain temporary immunity after recovery due to anti-virus software installed, but after a period of time will join again susceptible class because of the variability of computer worms; (c) the elimination rate of computers is not only related to natural mortality, but also to worm attacks; (d) the saturation incidence is used thanks to the inhibition effect of susceptible equipments and the crowding effect of infectious equipments.

Firstly, through theoretical analysis, the existence of disease free equilibrium and endemic equilibrium is studied, and the sufficient conditions for their asymptotic stability are given. The global stability of disease free equilibrium is carried out using the Castillo-Chavez method, whereas, the global stability of the unique endemic equilibrium is also investigated via using geometrical approach. It can be seen that when R0 < 1, worm transmission is effectively controlled and verified by numerical simulation. Therefore, one effective means to extinguish worm is to keep R0 below 1. Furthermore, the sensitivity analysis is complemented by numerical simulation to explore the influence of some parameter changes on the basic reproduction number R0. It is seen that Λ1, Λ2, β1, β2, τ, η and ξ are positively correlated with R0, while σ, ν, μ1, μ2, ϵ, ϕ, p, θ and γ are negatively correlated with R0. Finally, we establish a optimal control system by taking the installation coverage rate of anti-virus software and the disinfection of computer and USB device as control variables. The numerical simulation results show that compared with the situation without control measures, the total number of computers and USB devices in the exposed state and infected state is significantly reduced after control measures are taken, that is to say, adding control could effectively reduce the spread of computer worms.

In this paper, the mathematical model is used to describe the propagation process of computer worms, which is helpful to analyze the propagation characteristics of worms, and then propose more effective defense measures and control strategies. In addition, the research of this subject is beneficial to predict the propagation trend of worms, test the effect of various defensive measures, and provide theoretical guidance for the defense and control of computer worms.

Data availability statement

The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author.

Author contributions

RW, YX, and KX conceived the study. RW developed the mathematical model, computations, simulation coding, manuscript writing and data interpretation. YX contributed to supervision and validation. KX performed literature survey and computations. All authors contributed to the article and approved the submitted version.

Funding

This work was supported by the National Natural Science Foundation of China (grant number 11971278); the Shanxi Scholarship Council of China (grant number 2022-150) and Natural Science Foundation of Shanxi Province (grant number 202203021211086).

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

1. Kim KS, Ibrahim MM, Jung IH, Kim S. Mathematical analysis of the effectiveness of control strategies to prevent the autorun virus transmission propagation. Appl Maths Comput (2020) 371:124955. doi:10.1016/j.amc.2019.124955

CrossRef Full Text | Google Scholar

2. Deng Y, Pei Y, Li C. Parameter estimation of a susceptible–infected–recovered–dead computer worm model. SIMULATION (2022) 98:209–20. doi:10.1177/00375497211009576

CrossRef Full Text | Google Scholar

3. Piqueira JRC, Cabrera MA, Batistela CM. Malware propagation in clustered computer networks. Physica A: Stat Mech its Appl (2021) 573:125958. doi:10.1016/j.physa.2021.125958

CrossRef Full Text | Google Scholar

4. Xiao X, Fu P, Dou C, Li Q, Hu G, Xia S. Design and analysis of seiqr worm propagation model in mobile internet. Commun nonlinear Sci Numer simulation (2017) 43:341–50. doi:10.1016/j.cnsns.2016.07.012

CrossRef Full Text | Google Scholar

5. Zheng W, Wang T, Liu C, Yan Q, Zhan S, Li G, et al. Liver transcriptomics reveals microrna features of the host response in a mouse model of dengue virus infection. Comput Biol Med (2022) 106057:106057. doi:10.1016/j.compbiomed.2022.106057

PubMed Abstract | CrossRef Full Text | Google Scholar

6. Carrillo M, Góngora PA, Rosenblueth DA. An overview of existing modeling tools making use of model checking in the analysis of biochemical networks. Front Plant Sci (2012) 3:155. doi:10.3389/fpls.2012.00155

PubMed Abstract | CrossRef Full Text | Google Scholar

7. Yang G, Gómez Tejeda Zañudo J, Albert R. Target control in logical models using the domain of influence of nodes. Front Physiol (2018) 454:454. doi:10.3389/fphys.2018.00454

PubMed Abstract | CrossRef Full Text | Google Scholar

8. Ren J, Xu Y. A compartmental model for computer virus propagation with kill signals. Physica A: Stat Mech its Appl (2017) 486:446–54. doi:10.1016/j.physa.2017.05.038

CrossRef Full Text | Google Scholar

9. Razzaq OA, Khan NA, Faizan M, Ara A, Ullah S. Behavioral response of population on transmissibility and saturation incidence of deadly pandemic through fractional order dynamical system. Results Phys (2021) 26:104438. doi:10.1016/j.rinp.2021.104438

PubMed Abstract | CrossRef Full Text | Google Scholar

10. Paul AK, Kuddus MA. Mathematical analysis of a Covid-19 model with double dose vaccination in Bangladesh. Results Phys (2022) 35:105392. doi:10.1016/j.rinp.2022.105392

PubMed Abstract | CrossRef Full Text | Google Scholar

11. Tiwari V, Deyal N, Bisht NS. Mathematical modeling based study and prediction of Covid-19 epidemic dissemination under the impact of lockdown in India. Front Phys (2020) 8:586899. doi:10.3389/fphy.2020.586899

CrossRef Full Text | Google Scholar

12. Toutonji O, Yoo S-M. Passive benign worm propagation modeling with dynamic quarantine defense. KSII Trans Internet Inf Syst (Tiis) (2009) 3:96–107. doi:10.3837/tiis.2009.01.005

CrossRef Full Text | Google Scholar

13. Wang F, Zhang Y, Wang C, Ma J, Moon S. Stability analysis of a seiqv epidemic model for rapid spreading worms. Comput Security (2010) 29:410–8. doi:10.1016/j.cose.2009.10.002

CrossRef Full Text | Google Scholar

14. Yao Y, Xie X-w., Guo H, Yu G, Gao F-X, Tong X-j. Hopf bifurcation in an internet worm propagation model with time delay in quarantine. Math Comput Model (2013) 57:2635–46. doi:10.1016/j.mcm.2011.06.044

CrossRef Full Text | Google Scholar

15. Zhou P, Gu X, Nepal S, Zhou J. Modeling social worm propagation for advanced persistent threats. Comput Security (2021) 108:102321. doi:10.1016/j.cose.2021.102321

CrossRef Full Text | Google Scholar

16. Yang L-X, Yang X. The impact of nonlinear infection rate on the spread of computer virus. Nonlinear Dyn (2015) 82:85–95. doi:10.1007/s11071-015-2140-z

CrossRef Full Text | Google Scholar

17. Zhang Z, Zou J, Upadhyay RK, ur Rahman G. An epidemic model with multiple delays for the propagation of worms in wireless sensor networks. Results Phys (2020) 19:103424. doi:10.1016/j.rinp.2020.103424

CrossRef Full Text | Google Scholar

18. Song L-P, Jin Z, Sun G-Q, Zhang J, Han X. Influence of removable devices on computer worms: Dynamic analysis and control strategies. Comput Maths Appl (2011) 61:1823–9. doi:10.1016/j.camwa.2011.02.010

CrossRef Full Text | Google Scholar

19. Zhu Q, Yang X, Ren J. Modeling and analysis of the spread of computer virus. Commun Nonlinear Sci Numer Simulation (2012) 17:5117–24. doi:10.1016/j.cnsns.2012.05.030

CrossRef Full Text | Google Scholar

20. Ma J, Chen Z, Wu W, Zheng R, Liu J. Influences of removable devices on the anti-threat model: Dynamic analysis and control strategies. Information (2015) 6:536–49. doi:10.3390/info6030536

CrossRef Full Text | Google Scholar

21. Zhu Q, Loke SW, Zhang Y. State-based switching for optimal control of computer virus propagation with external device blocking. Security and Communication Networks (2018). doi:10.1155/2018/4982523

CrossRef Full Text | Google Scholar

22. Upadhyay RK, Kumari S. Detecting malicious chaotic signals in wireless sensor network. Physica A: Stat Mech its Appl (2018) 492:1129–52. doi:10.1016/j.physa.2017.11.043

CrossRef Full Text | Google Scholar

23. Gao Q, Zhuang J. Stability analysis and control strategies for worm attack in mobile networks via a veiqs propagation model. Appl Maths Comput (2020) 368:124584. doi:10.1016/j.amc.2019.124584

CrossRef Full Text | Google Scholar

24. Hu R, Gao Q, Wang B. Dynamics and control of worm epidemic based on mobile networks by seiqr-type model with saturated incidence rate. Discrete Dyn Nat Soc (2021) 2021:1–22. doi:10.1155/2021/6637263

CrossRef Full Text | Google Scholar

25. Madhusudanan V, Srinivas M, Nwokoye CH, Murthy BN, Sridhar S. Hopf-bifurcation analysis of delayed computer virus model with holling type iii incidence function and treatment. Scientific Afr (2022) 15:e01125. doi:10.1016/j.sciaf.2022.e01125

CrossRef Full Text | Google Scholar

26. Mishra BK, Pandey SK. Dynamic model of worm propagation in computer network. Appl Math Model (2014) 38:2173–9. doi:10.1016/j.apm.2013.10.046

CrossRef Full Text | Google Scholar

27. Mishra BK, Pandey SK. Dynamic model of worms with vertical transmission in computer network. Appl Math Comput (2011) 217:8438–46. doi:10.1016/j.amc.2011.03.041

CrossRef Full Text | Google Scholar

28. Guillén JH, Del Rey AM, Encinas LH. Study of the stability of a seirs model for computer worm propagation. Physica A: Stat Mech its Appl (2017) 479:411–21. doi:10.1016/j.physa.2017.03.023

CrossRef Full Text | Google Scholar

29. Upadhyay RK, Singh P. Modeling and control of computer virus attack on a targeted network. Physica A: Stat Mech its Appl (2020) 538:122617. doi:10.1016/j.physa.2019.122617

CrossRef Full Text | Google Scholar

30. Van den Driessche P, Watmough J. Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission. Math biosciences (2002) 180:29–48. doi:10.1016/S0025-5564(02)00108-6

PubMed Abstract | CrossRef Full Text | Google Scholar

31. Castillo-Chavez C, Blower S, Van den Driessche P, Kirschner D, Yakubu A-A. Mathematical approaches for emerging and reemerging infectious diseases: Models, methods, and theory, 126. Springer Science & Business Media (2002).

Google Scholar

32. Khan A, Zarin R, Inc M, Zaman G, Almohsen B. Stability analysis of leishmania epidemic model with harmonic mean type incidence rate. The Eur Phys J Plus (2020) 135:528–0. doi:10.1140/epjp/s13360-020-00535-0

PubMed Abstract | CrossRef Full Text | Google Scholar

33. Li MY, Muldowney JS. A geometric approach to global-stability problems. SIAM J Math Anal (1996) 27:1070–83. doi:10.1137/S0036141094266449

CrossRef Full Text | Google Scholar

34. Khan K, Zarin R, Khan A, Yusuf A, Al-Shomrani M, Ullah A. Stability analysis of five-grade leishmania epidemic model with harmonic mean-type incidence rate. Adv Difference Equations (2021) 2021:86–27. doi:10.1186/s13662-021-03249-4

CrossRef Full Text | Google Scholar

35. Khan A, Zarin R, Ahmed I, Yusuf A, Humphries UW. Numerical and theoretical analysis of rabies model under the harmonic mean type incidence rate. Results Phys (2021) 29:104652. doi:10.1016/j.rinp.2021.104652

CrossRef Full Text | Google Scholar

36. Yang F, Zhang Z, Zeb A. Hopf bifurcation of a veiqs worm propagation model in mobile networks with two delays. Alexandria Eng J (2021) 60:5105–14. doi:10.1016/j.aej.2021.03.055

CrossRef Full Text | Google Scholar

37. Haldar K, Mishra BK. A mathematical model for a distributed attack on targeted resources in a computer network. Commun Nonlinear Sci Numer Simulation (2014) 19:3149–60. doi:10.1016/j.cnsns.2014.01.028

CrossRef Full Text | Google Scholar

38. Khanh NH, Huy NB. Stability analysis of a computer virus propagation model with antidote in vulnerable system. Acta Mathematica Scientia (2016) 36:49–61. doi:10.1016/S0252-9602(15)30077-1

CrossRef Full Text | Google Scholar

39. Alexander ME, Moghadas SM, Röst G, Wu J. A delay differential model for pandemic influenza with antiviral treatment. Bull Math Biol (2008) 70:382–97. doi:10.1007/s11538-007-9257-2

PubMed Abstract | CrossRef Full Text | Google Scholar

40. Lukes DL. Differential equations: Classical to controlled (1982).

Google Scholar

41. Pontryagin LS. Mathematical theory of optimal processes. New York, NY: CRC Press (1987).

Google Scholar

Keywords: computer worms, saturation incidence rate, stability analysis, sensitivity analysis, optimal control, numerical simulation

Citation: Wang R, Xue Y and Xue K (2023) Dynamic analysis and optimal control of worm propagation model with saturated incidence rate. Front. Phys. 10:1098040. doi: 10.3389/fphy.2022.1098040

Received: 14 November 2022; Accepted: 09 December 2022;
Published: 10 January 2023.

Edited by:

Xiaoming Zheng, Central Michigan University, United States

Reviewed by:

Zizhen Zhang, Anhui University of Finance and Economics, China
Xue Ren, Harbin Engineering University, China

Copyright © 2023 Wang, Xue and Xue. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Yakui Xue, eHlrNTE1MkAxNjMuY29t

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.