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ORIGINAL RESEARCH article

Front. Phys., 18 January 2021 | https://doi.org/10.3389/fphy.2020.601459

Dynamical Analysis of a Mathematical Model of COVID-19 Spreading on Networks

www.frontiersin.orgWang Li1, www.frontiersin.orgXinjie Fu2, www.frontiersin.orgYongzheng Sun1 and www.frontiersin.orgMaoxing Liu2*
  • 1School of Mathematics, China University of Mining and Technology, Xuzhou, China
  • 2School of Science, North University of China, Taiyuan, China

In this article, an SEAIRS model of COVID-19 epidemic on networks is established and analyzed. Following the method of the next-generation matrix, we derive the basic reproduction number R0, and it shows that the asymptomatic infector plays an important role in disease spreading. We analytically show that the disease-free equilibrium E0 is asymptotically stable if R01; moreover, the effects of various quarantine strategies are investigated and compared by numerical simulations. The results obtained are informative for us to further understand the asymptomatic infector in COVID-19 propagation and get some effective strategies to control the disease.

1 Introduction

Coronaviruses are a group of enveloped viruses with a positive-sense, single-stranded RNA and viral particles resembling a crown from which the name derives. They belong to the order of Nidovirales, family of Coronaviridae, and subfamily of Orthocoronavirinae. A recent coronavirus outbreak has started since December 2019. So far, the new virus has infected more than 25 million people and killed at least 842,000 of them [13].

In order to better study the spread and control of infectious diseases, several classical mathematical models have been discussed to understand the transmission mechanism and dynamics of the disease, such as the SI model, SIR model, SEIR model, and SEIRS model [4, 5]. Different factors are considered in different models, and the purpose of these models is finding the transmission mechanism and dynamics of the diseases for controlling the diseases. This process needs a contact between them. It is found that the best pattern of contact is contact in the networks [611], and study epidemic model on networks has been a hot field in mathematical biology [620,35].

To find the transmission mechanism, we have to know who is the infector [27]. An infector is an individual who carries the virus and can export the virus. Sometimes, an individual with the infected state may not show any symptoms of disease, and the state can be defined as asymptomatically infected. An individual with the infected state who shows symptoms of disease can be defined as symptomatically infected. Exposed state and asymptomatically infected state are more dangerous than symptomatically infected state. When a susceptible individual contacts a symptomatic one, he(she) will usually do something possible to prevent the disease spreading.

In the disease spreading process, a symptomatic infector will be restricted by individual behavior or public behavior, but a symptomatic one has a higher efficiency than an asymptomatic one. A class of works studied the role of symptomatic infectors and asymptomatic infectors in diseases infections, such as dengue virus [21, 22], malaria [23], and Norovirus [2427]. The results of these works all show that the asymptomatic cases cannot be neglected. Recently, several mathematic models within asymptomatic infection have been studied, such as SAIR model [21], CI model [28], SEIADR model [29], and SEIIeQR model [30]. But mathematical models within asymptomatic infection on networks are still relatively rare. When the COVID-19 pandemic begin to outbreak, quarantining certain individuals may be the most efficient way to stop the outbreak of disease, but the choice of which is an important step in the control process, and thus we also discuss the effect of different quarantine strategies.

In this article, we consider an SEAIRS epidemic model on scale-free networks to study the spread of COVID-19. Further, we consider the effect of the asymptomatic state changing into the symptomatic state. By studying the dynamics of the model, we try to find what role the three infectors, E, A, and I, play in disease spreading, especially for the asymptomatic infectors, E and A. Next, in Section 2, we establish an SEAIRS COVID-19 model on network. In Section 3, we study the dynamics of the model. In Section 4, we study and compare the effects of various control strategies, and carry out numerical simulations to illustrate the theoretical results in Section 5. Finally, conclusions and some discussions are given in Section 6.

2 The Model

In the spread process, each node has five states: susceptible (S); exposed (E); asymptomatically infected (A), those who are infectious but have no symptoms; symptomatically infected (I), those who are infectious but have symptoms; and removed (R). The disease transmission flow is depicted in Figure 1. A susceptible individual can be infected by contact at rate β1 if there are infected individuals with A in its neighbors, or be infected by contact at rate β2 if there are symptomatically infected individuals I. The exposed individual will become A and I with rate pα and (1p)α, and A will become I individual at rate q. The infected A and I will become a recovered individual at rate μ1 and μ2 due to treatment, respectively. A recovered individual will become S at rate δ. All parameters are nonnegative.

FIGURE 1
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FIGURE 1. State-transition rules of the SEAIRS model of COVID-19.

In this article, we consider an SEAIRS epidemic model on scale-free networks as follows:

{dSk(t)dt=β1kSk(t)θ1(t)β2kSk(t)θ2(t)+δRk(t),dEk(t)dt=β1kSk(t)θ1(t)+β2kSk(t)θ2(t)αEk(t),dAk(t)dt=pαEk(t)qAk(t)μ1Ak(t),dIk(t)dt=(1p)αEk(t)+qAk(t)μ2Ik(t),dRk(t)dt=μ1Ak(t)+μ2Ik(t)δRk(t).(2.1)

Following [6], k=kkPk describes the average degree and Pk(k=1,2,,n) describes the degree distribution; the probability θi(i=1,2,3) is a link pointing to an exposed individual, asymptomatic infected individual, and symptomatic infected individual. Here, Nk is a constant that stands for the number of nodes with degree k. Then, Nk=Sk(t)+Ek(t)+Ak(t)+Ik(t)+Rk(t),(k=1,2,,n) and kNk=N. We have

θ1(t)=1kkkPkAk(t)Nk,(2.2)
θ2(t)=1kkkPkIk(t)Nk.(2.3)

For the practice, the initial condition for model (2.1) satisfies the following:

{0Sk(0),Ek(0),Ak(0),Ik(0),Rk(0)Nk,Sk(0)+Ek(0)+Ak(0)+Ik(0)+Rk(0)=Nk,(k=1,2,,n).(2.4)

3 Dynamical Behaviors of the Model

In this section, we study the stability of disease-free equilibrium of model (2.1). First, we derive the basic reproduction number of the model.

3.1 Equilibria and Basic Reproduction Number

Lemma 3.1. Suppose that Sk(t),Ek(t),Ak(t),Ik(t),Rk(t) is a solution of model (2.1) satisfying initial conditions of Eq. (2.4), then

Ω={(Sk,Ek,Ak,Ik,Rk)|0Sk,Ek,Ak,Ik,RkNk,k=1,2,,n}

is a positive invariant for model (2.1).The proof of this lemma is similar to that in [31]. We ignore it here. The stability analysis and numerical simulations are investigated in the positive invariant Ω.It is easy to find that model (2.1) has a disease-free equilibrium E0, it is the only susceptible state. E0=(S10,0,0,0,0,S20,0,0,0,0,,Sn0,0,0,0,0), where Sk0=Nk, k=1,2,,n. Following the method of the next-generation matrix [32], the basic reproduction number can be calculated by R0=ρ(FV1). Here, F is the matrix of the rate of generation of new infections, and V is the matrix of the rate of transfer of individuals out of the two compartments. F is given by

F=(A11A12A1nA21A22A2nAn1An2Ann)3n×3n

and

Aij=(0β1Si0PjkNjijβ2Si0PjkNjij000000).

In addition, V=diag(B1,B2,,Bn), where

Bk=(α00pαq+μ10(1p)αqμ2),

and

Bk1=(1α00pq+μ11q+μ10q+(1p)μ1μ2(q+μ1)qμ2(q+μ1)1μ2),

so, V1=diag(B11,B21,,Bn1), and the basic reproduction number R0 can be obtained:

R0=ρ(FV1)=μ2pβ1+[q+(1p)μ1]β2μ2(q+μ1)k2k.(3.1)

Let J0 be the Jacobian matrix of the middle three equations of model (2.1), then J0=FV and s(J0)=max{Reλ: λ is an eigenvalue of J0}, R0<1s(J0)<0, R0>1s(J0)>0. [34]

Remark 3.1.Let R0,a=pβ1q+μ1k2k, R0,d=[q+(1p)μ1]β2μ2(q+μ1)k2k, then R0=R0,a+R0,d, if q=0, this result is corresponding to the result in [27].

Remark 3.2.If we do not consider the asymptomatic infected state, that is β1=0, μ1=μ2=μ, p=q=0, then R0=β2μk2k, which is corresponding to the result in [6, 33].

Lemma 3.2.If and only if R0>1, there is a unique endemic equilibrium E+.

Proof.We consider the right side of the model (2.1) to be equal to zero. Then, we obtain

{β1kSkθ1β2kSkθ2+δRk=0,β1kSkθ1+β2kSkθ2αEk=0,pαEkqAkμ1Ak=0,(1p)αEk+qAkμ2Ik=0,μ1Ak+μ2IkδRk=0.

Following the above equation, using θ=β1θ1*+β2θ2*, we can find

Ek*=kθαSk*,Ak*=pkθq+μ1Sk*,Ik*=[q+(1p)μ1]kθμ2(q+μ1)Sk*,Rk*=kθδSk*.(3.2)

According to the condition Nk*=Sk*+Ek*+Ak*+Ik*+Rk*, we can get

Sk*=μ2α(q+μ1)δNk*δμ2α(q+μ1)+{μ2α(q+μ1)+δμ2(q+μ1)+δμ2pα+δα[q+(1p)μ1]}kθ.(3.3)

Substituting Ek*, Ak*, and Ik* of Eq.(3.2) and Eq.(3.3) into θ, we can obtain θf(θ)=0, where

f(θ)=1A1kkk2PkA2+A3kθ,

and A1=δα{μ2pβ1+[q+(1p)μ1]β2}, A2=δμ2(q+μ1)α, A3=μ2(q+μ1)α+δ{μ2(q+μ1)+μ2pα+α[q+(1p)μ1]}. It is easy to find that θf(θ)=0 has a trivial solution with no condition, and model (2.1) has a disease-free equilibrium. In addition,

df(θ)dθ=A1A3kkk3Pk(A2+A3kθ)2>0,f(β1+β2)=1A1kkk2PkA2+A3k(β1+β2)>1A1kkk2P(k)A3k(β1+β2)=1A1A3(β1+β2)=1δα{μ2pβ1+[q+(1p)μ1]β2}μ2(q+μ1)α+δ{μ2(q+μ1)+μ2pα+α[q+(1p)μ1]}1β1+β2>1δα{μ2pβ1+[q+(1p)μ1]β2}μ2(q+μ1)α+δ{μ2(q+μ1)+μ2pα+α[q+(1p)μ1]}>0.

Thus, θf(θ)=0 has a nontrivial solution if and only if f(0)<0, that is if and only if R0>1, there is a unique endemic equilibrium.

3.2 Stability of Disease-free and Endemic Equilibrium

Theorem 3.1.If R01, E0 of model (2.1) is locally asymptotically stable; if R0>1, E0 is unstable, and there is a unique endemic equilibrium E+, and E+ is locally asymptotically stable.

Proof.From the results of Lemma 3.1, Lemma 3.2, and the basic reproduction number, we only need to prove the case of R0=1. We consider the following model:

{dSkdt=β1kSkθ1β2kSkθ2+δRk,dEkdt=β1kSkθ1+β2kSkθ2αEk,dAkdt=pαEkqAkμ1Ak,dIkdt=(1p)αEk+qAkμ2Ik.(3.4)

The Jacobian matrix of model (3.4) at disease-free equilibrium is given by

J=(J11J12J1nJ21J22J2nJn1Jn2Jnn)4n×4n

with

Jij=(δδβ1PjNikNjijδβ2PjNikNjijδ0αβ1PjNikNjijβ2PjNikNjij0pαqμ100(1p)αqμ2).

The characteristic equation of the disease-free equilibrium is

(λ+μ2)n1(λ+q+μ1)n1(λ+δ)n(λ+α)n1(λ3+H2λ2+H1λ+H0)=0,

where

H2=α+q+μ1+μ2>0,H1=α(q+μ1)+αμ2+μ2(q+μ1)[pαβ1+(1p)αβ2]k2k,H0=μ2α(q+μ1)α{μ2pβ1+[q+(1p)μ1]β2}k2k,

when R0=1, H0=0, and

αμ2pβ1k2k<μ2α(q+μ1)αpβ1k2k<α(q+μ1),(1p)αμ1β2k2k<μ2α(q+μ1)(1p)αβ2k2k<μ2(α+q+μ1).

Then, we obtain H1>0, and the characteristic equation can be written as

λ(λ+μ2)n1(λ+q+μ1)n1(λ+δ)n(λ+α)n1(λ2+H2λ+H1)=0,

where the eigenvalues of J are all negative except zero eigenvalue when R0=1.

4 Quarantine Strategies

Quarantine is helpful in controlling diseases. In this section, we will discuss three different quarantine strategies for COVID-19 disease model on networks.

4.1 Proportional Quarantine

In this case, for fixed spreading rates β1 and β2, let ω(0<ω<1) is the density of quarantine nodes in the network. At the mean-field level, the presence of proportional quarantine will effectively reduce the spreading rate. Thus, we can approximately use β1(1ω) to substitute β1 and use β2(1ω) to substitute β2; thus, the system (2.1) becomes

{dSk(t)dt=β1(1ω)kSk(t)θ1(t)β2(1ω)kSk(t)θ2(t)+δRk(t)dEk(t)dt=β1(1ω)kSk(t)θ1(t)+β2(1ω)kSk(t)θ2(t)αEk(t)dAk(t)dt=pαEk(t)qAk(t)μ1Ak(t)dIk(t)dt=(1p)αEk(t)+qIk(t)μ2Ik(t)dRk(t)dt=μ1Ak(t)+μ2Ik(t)δRk(t)(4.1)

Using the same method in Section 3, we obtain a self-consistency equation as follows:

θ=δα(1ω)A1kkk2PkA2+A3kθθf˜(θ).

By arguments similar to those in Section 3, the epidemic threshold Rw˜ is determined by the following inequality:

df˜(θ)dθ|θ=0>1;

therefore, it can be shown that

Rw˜=μ2p(1ω)β1+[q+(1p)μ1](1ω)β2μ2(q+μ1)k2k,(4.2)

that is,

Rw˜=(1ω)R0.(4.3)

Note that in (4.3), when ω=0, that is, if no quarantine were done, then Rw˜=R0; when 0<ω<1, Rw˜<R0, that is, the quarantine scheme is effective; while as ω1, Rw˜0, that is, in the case of a full quarantine, it would be impossible for the epidemic to spread in the network.

4.2 Targeted Quarantine

While proportional quarantine schemes are effective, there may be more efficient schemes due to the heterogeneous nature of scale-free networks. We introduce an upper threshold κ such that all nodes with connectivity k>κ are immunized, that is, we define the quarantine rate ωk by

ωk={1,k>κ,c,k=κ,0,k<κ.

where 0<c<1 and kωkP(k)=ω¯, where ω¯ is the average quarantine rate. The epidemic dynamics model is

{dSk(t)dt=β1(1ωk)kSk(t)θ1(t)β2(1ωk)kSk(t)θ2(t)+δRk(t)dEk(t)dt=β1(1ωk)kSk(t)θ1(t)+β2(1ωk)kSk(t)θ2(t)αEk(t)dAk(t)dt=pαEk(t)qAk(t)μ1Ak(t)dIk(t)dt=(1p)αEk(t)+qIk(t)μ2Ik(t)dRk(t)dt=μ1Ak(t)+μ2Ik(t)δRk(t).(4.4)

This leads to

θ=δαA1kkk2Pk(1ωk)A2+A3kθθf˜(θ).

Therefore, the epidemic threshold

Rw^=μ2pβ1+[q+(1p)μ1]β2μ2(q+μ1)k2k2ωkk.(4.5)

Note that k2ωk=ω¯k2+σ, where σ=(ωkω¯)×[k2k2] is the covariance of ωk and k2. There may be κ (usually big enough) where σ<0, but for appropriately small κ, ωkω¯ and k2k2 have the same signs except for some k where ωkω¯ and/or k2k2 is zero; Therefore σ>0 for appropriate κ. Then,

Rw^<1ω¯1ωRw˜.

If we set ω¯=ω, then,

Rw^<Rw˜(0<ω<1),

which means the targeted quarantine scheme is more efficient than the uniform quarantine scheme for the same average quarantine rate.

4.3 High-Risk Quarantine

If a neighbor of a susceptible individual is infected, vaccinating this susceptible individual is called high-risk immunity [37]. We introduce the parameter σ, that is, the probability that a node is quarantined per unit time, and Γ=kPkkN, which denotes the probability that any given node is the neighbor of some specific nodes. The epidemic dynamics model is

{dSk(t)dt=β1(1σΓ)kSk(t)θ1(t)β2(1σΓ)kSk(t)θ2(t)+δRk(t)dEk(t)dt=β1(1σΓ)kSk(t)θ1(t)+β2(1σΓ)kSk(t)θ2(t)αEk(t)dAk(t)dt=pαEk(t)qAk(t)μ1Ak(t)dIk(t)dt=(1p)αEk(t)+qIk(t)μ2Ik(t)dRk(t)dt=μ1Ak(t)+μ2Ik(t)δRk(t)(4.6)

This leads to

θ=δαA1kkk2Pk(1σΓ)A2+A3kθθf¯(θ).

And the epidemic threshold

R¯0=μ2pβ1+[q+(1p)μ1]β2μ2(q+μ1)(k2kσk3Pkk2N)<R0.

This means that the implementation of high-risk quarantine is effective, and the longer the period of σk3Pk, the more effective it is.

5 Numerical Simulations

In this section, we present numerical simulations of model (2.1), (4.1) and (4.6) to illustrate the results in Section 3 and 4. Without loss of generality, we consider the dynamical process on scale-free networks with Pk=ckγ and k=1nPk=1, γ=3, n=200. The average infected number is A(t)+I(t)=k=1nAk(t)Pk+k=1nIk(t)Pk. The parameters of the model are estimated by MCMC using the number of cases in Wuhan (http://wjw.wuhan.gov.cn/ztzl_28/fk/yqtb/).

Figure 2 shows the asymptotical stability of model (2.1) with different values, and the parameter values are shown in Table 1. Figures 2A,B show the time series of the average infected number I(t) with different initial values, which is in accord with the asymptotical stability of the disease-free equilibrium.

FIGURE 2
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FIGURE 2. Asymptotical stability of the model.

TABLE 1
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TABLE 1. Parameters of Figure 2

TABLE 2
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TABLE 2. Parameters of Figure 4

The sensitivity analysis of the basic reproduction number R0 can be performed by model parameters. It is easy to obtain that

R0β1=pq+μ1k2k>0,R0β2=q+(1p)μ1(q+μ1)μ2k2k>0,R0μ1=β2pqβ1μ2pμ2(q+μ1)2k2k<0,R0μ2=β2[q+(1p)μ1]μ22(q+μ1)k2k<0,R0p=β1μ2β2μ1μ2(q+μ1)k2k,R0q=p(β2μ1β1μ2)μ2(q+μ1)2k2k.(5.1)

Equation (5.1) shows R0 is linearly positively correlated with β1 and β2; R0 is negatively correlated with μ1 and μ2; the correlation between R0 and p or q is determined by β2μ1β1μ2. As can be seen from Figure 3 that the monotonicity of R0 increases or decreases with respect to p and q, respectively. In Figure 4, the parameters of the model are estimated by MCMC using the number of cases in Wuhan and the parameter values are shown in Table 2. Figure 4 shows the change of total infection density with time under different ω and σ. It can be seen that with the increase of ω and σ, the total infection density is becoming lower as ω and σ increase.

FIGURE 3
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FIGURE 3. Sensitivity of model parameters.

FIGURE 4
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FIGURE 4. Effectiveness of quarantine for different ω and σ respectively.

6 Conclusion and Discussion

In this article, we have generalized a traditional homogeneous epidemic model with asymptomatic infectors to a network case to study the spread of COVID-19. As one can see, homogeneous epidemic models can be considered as a special case of network epidemic models, and network epidemic models are more realistic and refined description of disease propagation in population. Considering two cases of infected state (show symptoms and show no symptoms), we investigated an SEAIRS model of COVID-19 on scale-free networks to approach the disease progress and calculated the basic reproduction number R0. By theoretical analysis, we obtained the asymptotical stability of the equilibria: if R01, E0 is asymptotically stable. Then, we analyzed the different quarantine strategies in the model. At last, numerical simulations illustrated the theoretical analysis. The results show that the asymptomatic infectors may infect health individuals as well as symptomatic infectors.

The SEAIRS model is an extension of the SEAIRS model, and it is a case of the SS model. The SS model, SI model, and SR model differ in terms of pathological mechanisms. It is difficult to say which one is better than others except introducing a special disease. Within SS models, formally, either the SIS model or SIRS model can be a special case of the SEIRS model. The parameters β1 and β2 denoted in the model are constant. In fact, many infectious diseases show seasonal phenomenon, such as measles, chickenpox, and mumps [36], and each individual has a periodic order; the parameters above should have some periodic property.

At the same time, we have also discussed proportional, targeted quarantine and high-risk quarantine schemes for network models. The result of Leung et al. [27] by illustration is suitable for Norovirus and measles. Different from their work, the formulaic result seems to be unsuitable for any kind of disease, for none of the parameters in the model is assigned to a specific value. In fact, for different disease, the parameters in the model may present special values. COVID-19 is now spreading faster abroad. Susceptible people will also be infected by asymptomatic patients. If not controlled, the epidemic will spread more widely and the number of infected people will be more difficult to control. The epidemic situation in China was obviously well controlled after the implementation of the strategy of lockdown, and other quarantine strategies. Therefore, the model and quarantine strategy in this article can also be applied to other countries. And, we hope that the results will be helpful to study and control the spread of COVID-19 disease.

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

ML and YS designed the study, and WL and ML carried out the analysis and contributed to writing the article. XF and YS performed numerical simulations.

Funding

Research Project Supported by Fund for Shanxi 1331KIRT and the outstanding youth fund of North University of China.

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.

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Keywords: COVID-19 epidemic, networks, asymptomatic, the basic reproduction number, quarantine

Citation: Li W, Fu X, Sun Y and Liu M (2021) Dynamical Analysis of a Mathematical Model of COVID-19 Spreading on Networks. Front. Phys. 8:601459. doi: 10.3389/fphy.2020.601459

Received: 01 September 2020; Accepted: 25 November 2020;
Published: 18 January 2021.

Edited by:

Chengyi Xia, Tianjin University of Technology, China

Reviewed by:

Chuansheng Shen, Anqing Normal University, China
Weigang Sun, Hangzhou Dianzi University, China

Copyright © 2021 Li, Fu, Sun and Liu. 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: Maoxing Liu, liumaoxing@126.com