Skip to main content
Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2021 Jun 24;150:111202. doi: 10.1016/j.chaos.2021.111202

Self organizing maps for the parametric analysis of COVID-19 SEIRS delayed model

Zhenhua Yu a, Robia Arif b, Mohamed Abdelsabour Fahmy c,d, Ayesha Sohail b,
PMCID: PMC8221985  PMID: 34188365

Abstract

Since 2019, entire world is facing the accelerating threat of Corona Virus, with its third wave on its way, although accompanied with several vaccination strategies made by world health organization. The control on the transmission of the virus is highly desired, even though several key measures have already been made, including masks, sanitizing and disinfecting measures. The ongoing research, though devoted to this pandemic, has certain flaws, due to which no permanent solution has been discovered. Currently different data based studies have emerged but unfortunately, the pandemic fate is still unrevealed. During this research, we have focused on a compartmental model, where delay is taken into account from one compartment to another. The model depicts the dynamics of the disease relative to time and constant delays in time. A deep learning technique called “Self Organizing Map” is used to extract the parametric values from the data repository of COVID-19. The input we used for SOM are the attributes on which, the variables are dependent. Different grouping/clustering of patients were achieved with 2- dimensional visualization of the input data (https://creativecommons.org/licenses/by/2.0/). Extensive stability analysis and numerical results are presented in this manuscript which can help in designing control measures.

Keywords: Dynamical analysis, Numerical simulations, Delayed differential equations, Stability analysis, SARS-2

1. Introduction

The spread rate of SARS-2 infection is alarming currently due to its, mutated versions and the continuous waves [1], [2] in different parts of the world, especially Europe and America. The new variants of the disease are emerging with the passage of time, increasing the pressure on “designing accurate control measures”.

Coronavirus (SARS-CoV2) belongs to the beta-coronavirus genus. The transmission mechanism focuses on the viral S protein (spike protein) that binds the virus to a reaction catalyzed by some enzymes located on the surface of the host cell.

Different control measure studies, at different levels, have recently emerged in the literature [3], [4]. The daily based incidence data of the disease positive case-counts, was discussed by Clouston et’al. [3]. They examined the spread and severity of the infectious disease with the aid of statistical analysis, by keeping in view different variables, such as age, gender and race. As a major outcome, the importance of social distancing was concluded.

Computational frameworks have been reported in the literature, to address the compartmental transmission dynamics of this infection, see  [5], [6], [7] and the references therein. Some models were based on the data based studies, whereas others were evidence based studies. The work conducted by  [6] raised questions linked with the pandemic and addressed the questions in a technical manner. It was reported that the modeling results showed great variation with respect to time and number of individuals suffering from the pandemic. Perhaps there was not much information and evidence available for the statistical inference at the beginning to the the disease outbreak, especially before January 23 when Wuhan was quarantined and locked down, and that there was a lack of reliable data, except for the confirmed case data that could be used for model calibration.

It has been reported in the literature that delay played an important role in the dynamics of the disease transmission [8]. [9] reported the delayed dynamics due to the quarantine strategy. Recently the research conducted by [10] reported that the pandemic was delayed due to the control measures practiced by different countries in different ways, including extensive testing, contact tracking, and quarantining; thus the widespread measures, enforcing “social isolation” were successful but not ideal for long term practice due to the socioeconomic pressure.

Mathematical models can help to understand the nonlinear dynamics in a cost effective manner [11], [12], [13], [14], [15], [16]. In the field of computational biology, different methods have been used [17], [18]. During this research, we have presented a delayed nonlinear model with demographic effects. The model takes into account the delays between compartments, thus making it more realistic. Complete stability analysis is provided in the manuscript to make it more authentic. Numerical results, leading to some proposals to control the pandemics are reported at the end.

2. Materials and methods

2.1. Proposed model

The “SEIRS” model (as shown in schematic (Fig. 1 and Table 1)) utilized during this research is given as:

Fig. 1.

Fig. 1

Schematic description of the mathematical model.

Table 1.

Description of Compartments.

Symbols Description
V1(t) Susceptible nodes.
V2(t) Expose nodes.
V3(t) Infectious nodes.
V4(t) Recovered nodes.

We have the following system of equations:

ddtV1(t)=nκκV1(t)ρV1(t)(V2(t)+V3(t))+ψV4(t),ddtV2(t)=ρV1(tτ1)(V2(tτ1)+V3(tτ1))κV2(t)σV2(t),ddtV3(t)=σV2(tτ2)ηV3(t)κV3(t),ddtV4(t)=ηV3(t)κV4(t)ψV4(t), (1)

with the initial conditions

V1(ϑ)=φ1(ϑ)0,V2(ϑ)=φ2(ϑ)0,V3(ϑ)=φ3(ϑ)0,V4(ϑ)=φ4(ϑ)0,ϑ[τ,0],τ=max[τ1,τ2]. (2)

Here, φi(ϑ) are the initial functions, where i= 1, 2, 3, 4. All the parameters are non negative. Each equation in the above system (1) is linked with the parameters. Parametric values and their definitions are listed in table (2 ). If time delay τ is negative all the nodes(population) will be negative which is not possible. The value of τ can never be negative, for that reason.

Table 2.

Parametric vales with the biological meanings

Symbols Description Value
κ birth & death rate. 0.1
n the total size of the population (assumed) [19]
ρ The infection rate. 0.09
σ Out break rate. 0.035
η Recovery rate. 0.1
ψ The restore rate. 0.3

2.2. Parametric analysis

Structure of SOM

The self organizing maps (SOM) are used to develop mapping for dimension reduction and for other multiple purposes in the fields of applied sciences. These maps are different from typical Artificial Neural Networks (ANN) in:

  • architecture,

  • algorithmic properties.

The algorithm of SOM is actually based on the competitive learning, whereas, the algorithm of ANN is based on the error correction learning. To preserve the topological properties of the given data, the SOM algorithm is linked with the neighborhood function.

There are two layers of the SOM-Kohonen Neural Networks. First layer is called the input layer, that is fully connected with the competitive layer of the processing neurons whereas the next layer is terms as the output layer.

For a network, we use an n× 1 input vector in general practice. The components of the vector are:

x=[x1x2xn]

The n-components of this input vector, are connected with each neurons in the array (the output layer of m×m processing neurons).

The input layer is connected to the Kohonen layer by weight, wj = (wj1, wj2, wjn), where wij is the weight value associated with ith component of input vector to the jth neurons.

2.3. Data source

In this analysis, we accessed the data repository: https://creativecommons.org/licenses/by/2.0/ (an open source data repository). The list of confirmed cases, reported cases and deaths, based on several countries regular counts. Data from 21 march 2020 can be accessed as time series. We have obtained and checked data from the COVID-19 database.

2.4. Basic consequences

The dynamical analysis of the mathematical models is of great significance in the field of biomathematics [20], [21], [22]. The positivity of solutions expresses existence of population, whereas the boundedness gives explanation of natural control of the growth because of restriction of the resources. We arrived at following Theorems.

Theorem 2.1

Each solution of a model(1)corresponding to the initial conditions(2)will remain a positive for all values of thet0, if initial-history function is positive.

Proof

As all parameters have positive values so in first equation nκ>0,

dV1(t)dtψV4(t)κV1(t)ρV1(t)(V2(t)+V3(t)).

Consequently, by the separating variables and then integrating

V1(t)V1(0)exp{(ρ(V1(t)+V2(t))κ)t}+exp{(ρ(V1(t)+V2(t))κ)t}0tψV4(t)×exp{(ρ(V1(t)+V2(t))+κ)t}dt. (3)

It shows that V1(t) will remain positive as the V1(0) is a positive and thus it is a property of positive invariant. □

To prove that V2(t) is positive we use (1) in the [0,τ], the second equation is

dV2(t)dtκV2(t)σV2(t),

since the parametric values are non negative. By separating and integrating both side it gives

V2(t)V2(0)exp{(κ+σ)t}. (4)

Similarly, from 3rd and 4th equations of model (1) and by using (2) we have;

dV3(t)dtηV3(t)κV3(t),
dV4(t)dtκV4(t)ψV4(t).

By separating V3(t) and V4(t) receptively and integrating both sides; it gives

V3(t)V3(0)exp{(ηκ)t}, (5)
V4(t)V4(0)exp{(κψ)t}. (6)

From preceding analysis it is conclude that the positivity of V1(t), V2(t),V3(t) and V4(t) depends on the initial-history functions; V1(0), V2(0),V3(0) and V4(0) which are positive. Similarly, in the interval [τ,2τ] for equation 2nd 3rd and 4th equations respectively we have

V2(t)V2(τ)exp{t(κ+σ)}, (7)
V3(t)V3(τ)exp{(ηκ)t}, (8)
V4(t)V4(τ)exp{(κψ)t}. (9)

By this approach, the above method can be generalized to any finite interval [0,t] and this prove that V2(t), V3(t) and V4(t) will always positive t0.

Lemma 1

Given the 1st order differential inequality:

dXdt+αXβ,X(0)=X0, (10)

the solution of this inequality will satisfy that

X(t)βα(1eαt)+X0eαt (11)

and hence

lim supt+X(t)βα. (12)

Proof

Suppose we have 1st order differential equation;

dXdt+αX=β

there is an integration factor eαt. By multiplying both sides of the equation (10) with the integrating factor eαt gives an exact differential equation

ddt(Xeαt)βeαt,X(0)=X0,

Integrating over [0,t]

X(t)eαtX0βα(eαt1) (13)

after manipulation we obtain the required inequality. The final term of solution is obtained by taking the limt. □

Theorem 2.2

If the solution of a model(1)is positive invariant, then it follows that all solutions of the model(1)are ultimately bounded in the following domain

={(V1,V2,V3,V4):V1n,V2+V3nκm+κ,V3+V4κ}. (14)

Proof

By solving 1st equation of model (1)

dV1dt=nκκV1ρV1(V2+V3)+ψV4ρV1(V2+V3)

For that reason, the positivity of V1, V2 and V3 in the above equation implies that the maximum value that V1 can attain is n, since rate dV1dt<0 and which implies that

lim suptV1n. (15)

Again by adding the 2nd and 3rd equations of the model (1) we obtain

ddt(V2+V3)=ηV3κV3κV2σV2nκ(κ+m)(V2+V3)

Where m=max{η,σ}. According to the lemma (10) we obtain

lim supt(V2+V3)nκm+κ. (16)

Adding the 3rd and 4th equation

ddt(V3+V4)=ψV4(t)κV3κV4κ(V3+V4)

by applying lemma (10) we obtain

lim supt(V3+V4)κ. (17)

By combining (15), (16) and (17) it is established that its solution will ultimately be bounded in that domain . □

2.5. Mathematical analysis

The model (1) contain two equilibrium points. The infection free equilibrium point is

E0=(n,0,0,0). (18)

The endemic equilibrium point exist if ρ>κ, otherwise nodes (exposed, infectious and recovered) will become zero.

E*=(V1*,V2*,V3*,V4*), (19)

where

V1*=(η+κ)(κ+σ)ρ(η+κ+σ),V2*=A*(κ+ψ),V3*=A*σ(κ+ψ),V4*=A*ησ. (20)

The coefficient A* is as follows:

A*=(ρκ)(κ+σ)η(κρ+σ)ρ(η+κ+σ)(η(κ+σ+ψ)+(κ+σ)(κ+ψ)). (21)

2.5.1. Stability of E0

The characteristic equation of Jacobian matrix, at the equilibrium point E0 is as follows

(κλ)(κλψ)(eλτ22(nρeλτ1(η+2(κ+λ)+σ))eλτ2(eλτ1(ησ)+nρ)2+4nρσeλτ1)(eλτ2(eλτ1(ησ)+nρ)2+4nρσeλτ1+eλτ22(nρeλτ1(η+2(κ+λ)+σ))=0. (22)

Here we have two eigenvalues as λ1=κ and λ2=κψ that are the negative. the model is stable if following two equation gives us two negative real values

eλτ22(nρeλτ1(η+2(κ+λ)+σ))eλτ2(eλτ1(ησ)+nρ)2+4nρσeλτ1=0, (23)
eλτ2(eλτ1(ησ)+nρ)2+4nρσeλτ1+eλτ22(nρeλτ1(η+2(κ+λ)+σ))=0. (24)

The stability can be proved by the following theorem.

Theorem 2.3

If((ησ)+nρ)2+4nρσ>nρ(η+2κ+σ), then the equilibrium pointE0values of delayτi(i=1:2)is always the locally stable.

Proof

Consider the equilibrium point E0 is stable for τ1=τ2=0 its mean equation (23) as has all roots to be negative

λ<((ησ)+nρ)2+4nρσ(nρ(η+2κ+σ))<0 (25)

That implies ((ησ)+nρ)2+4nρσ>nρ(η+2κ+σ). Now, suppose that τi=0 varies continuously in a positive direction such that there is a τi* which give one imaginary eigenvalue pair by putting λ=+iϱ, ϱ>0, Hence substituting λ=iϱ in (23), after simplifying we obtain

((η+κ)2+ϱ2)((κ+σ)2+ϱ2)n2((η+κσ)2+ϱ2)=ρ2. (26)

 □

The equation (26) shows that ϱ2<0 if ((ησ)+nρ)2+4nρσ>nρ(η+2κ+σ).

For τ1=0 we have

((η+κ)(κ+σ)+nρ(ηκ)ϱ2)2+(ϱ(η2κσ)+nρϱ)2=(nρσ)2. (27)

This equation shows that ϱ2<0 if ((ησ)+nρ)2+4nρσ>nρ(η+2κ+σ).

Theorem 2.4

Ifη+2κnρ+σ>((ησ)+nρ)2+4nρσ, then equilibrium pointE0is stablevalues ofτi, wherei={1,2}.

2.6. Reproductive number and sensitivity analysis

For the model (1) the basic reproduction number R0 is as follows

R0=nρ(η+κ+σ)(η+κ)(κ+σ).

The sensitivity if the reproductive number is analyzed by taking the partial derivative with respect to the parameter.

R0dn=ρ(η+κ+σ)(η+κ)(κ+σ)>0,R0dρ=n(η+κ+σ)(η+κ)(κ+σ)>0,R0dη=nρσ(η+κ)2(κ+σ)<0,R0dκ=nρ(η2+η(2κ+σ)+(κ+σ)2)(η+κ)2(κ+σ)2<0,R0dσ=ηnρ(η+κ)(κ+σ)2<0.

Reproductive number is increased with increments in n and infection rate while decreases with inclusion or drop-out rate, the recovery rate and the outbreak rate.

Stability criteria

Theorem 2.5

The infection free equilibrium point E0 is stable asymptotically values of delay τ if R0<1 . The endemic equilibrium point E* exits if R0>1 .

Proof

It is obvious from definition and by Theorem (2.3) that if nρ(η+κ+σ)(η+κ)(κ+σ)<1, then all the conditions will remain suitable. Furthermore, nρ(η+κ+σ)(η+κ)(κ+σ)>1 is one of conditions for the existence of the positive equilibrium point. The remaining conditions for the existence from R0>1. □

2.7. Stability of E*

For the stability of endemic equilibrium point we will suppose that R0>1. The Jacobian matrix at endemic equilibrium point

JE*=(AκλBBψeλτ1ABeλτ1κλσeλτ1B00eλτ2σηκλ000eλτ3ηκλψ),

where as

A=(κ+ψ)((κ+σ)(nρκ)η(κnρ+σ))η(κ+σ+ψ)+(κ+σ)(κ+ψ),B=(η+κ)(κ+σ)η+κ+σ.

The characteristic equation for the equi point E* is

λ4+(a1λ3+a2λ2+a3λ+a4+eλτ1b1λ3+b2λ2+b3λ+b4)+eλτ1λτ2(c1λ3+c2λ2+c3λ+c4)=0, (28)

where the constants are defined as follows

a1=A+η+4κ+σ+ψ,a2=A(η+3κ+σ+ψ)+η(3κ+σ+ψ)+ψ(3κ+σ)+3κ(2κ+σ),a3=A(η(2κ+σ+ψ)+3κ2+2κ(σ+ψ)+σψ)+η(3κ2+2κ(σ+ψ)+σψ)+κ(κ2(σ+4)+3κ(σ+ψ)+2σψ),a4=A(η+κ)(κ+σ)(κ+ψ)+κ(η(κ+σ)(κ+ψ)+κ3+κψ(κ+σ)),b1=B,b2=B(η+3κ+ψ),b3=B(η(2κ+ψ)+κ(3κ+2ψ)),b4=Bκ(η+κ)(κ+ψ),c1=a,c2=Bσ,c3=Bσ(2κ+ψ),c4=Bκσ(κ+ψ).

Where a=0.

To gain insight regarding the endemic equilibrium point E* we will discuss stability of endemic equilibrium point and conditions of Hopf bifurcation of threshold parameters like τ1 and τ2 by considering the following cases.

Case 1. When τ1=0 and τ2=0 then equation (28) will become

λ4+λ3(a1+b1+c1)+λ2(a2+b2+c2)+λ(a3+b3+c3)+(a4+b4+c4)=0. (29)

Therefore, the endemic equilibrium point E* is asymptotically stable with following conditions if (R1) (a1+b1+c1)>0, (a4+b4+c4)>0 and (a1+b1+c1)(a2+b2+c2)(a3+b3+c3)(a3+b3+c3)2(a1+b1+c1)2(a4+b4+c4)>0 holds. Thus, according to the criteria of Routh-hurwitz all roots (29) have real negative values.

Case 2. When τ1=0 and τ2>0, (28) will become

λ4+λ3(a1+b1+c1eλτ2)+λ2(a2+b2+c2eλτ2)+λ(a3+b3+c3eλτ2)+(a4+b4+c4eλτ2)=0. (30)

By assuming that for some values of τ2>0, there exist a real ξ such that λ=iξ by putting λ=iξ after simplifying

ξ4ξ2(a2+b2)+(a4+b4)=c1ξ3sin(ξτ2)+c2ξ2cos(ξτ2)c3ξsin(ξτ2)c4cos(ξτ2),ξ(a3+b3)ξ3(a1+b1+c1)=c1ξ3cos(ξτ2)c2ξ2sin(ξτ2)c3ξcos(ξτ2)+c4sin(ξτ2), (31)

squaring and adding both equations in 32

υ4+e1υ3+e2υ2e3υ+e4=0,ξ2=υ. (32)

Where the constants are as follows

e1=(a1+b1)(a1+b1+2c1)2(a2+b2),e2=2(a3+b3)(a1+b1+c1)+(a2+b2)2+2(a4+b4)c22+2c1c3,e3=(a3+b3)22(a2+b2)(a4+b4)+c32+2c2c4,e4=(a4+b4)2c42.

By rule of signs of Descartes (32) has at least on real positive root if (D2) c1>0 and (a4+b4)2<c42 holds.

Eliminating sin(ξ0τ2) form the equations (31) we have

τ2,j=1ξ0cos1(E+ξ02(c2(a4+b4)c3(a3+b3)+c4(a2+b2))c4(a4+b4)c12ξ06+c22ξ042c1c3ξ04+c32ξ022c2c4ξ02+c42)+2jπξ0, (33)

where E=ξ06(c2c1(a1+b1+c1))+ξ04(c2((a2+b2))+c3(a1+b1)+c1(a3+b3+c3)c4) and j=0,1,2,...

By differentiate (32) with respect to the τ2, transversality will be obtain as τ2,j=τ2 and ξ=ξ0that is

Re(dλdτ2)1=a3+b3+b4+c3A1ξ02+A2ξ04+A3ξ06ξ02((ξ02((b2+c2))+b4+c4*)2ξ02(ξ02(b1+c1)+b3+c3)2), (34)

where:

A1=2(b4+c4*)(a2+b2+c2),A2=2(b2+c2)(a2+b2+c2)+3(b3+c3)(a1+b1+c1)),A3=3(b1+c1)(a1+b1+c1).

If Re(dλdτ2)1>0 a Hopf bifurcation will occur for delay τ2 we reached following theorems.

Theorem 2.6

Suppose that(R1)and(D1)is hold with delayτ1=0and there exist aτ2>0such thatE*remain stable forτ2<τ2*and unstable forτ2>τ2*, whereτ2*=min{τ2,j}(33). Furthermore, model(1)undergoes the hopf bifurcation at pointE*whenτ2=τ2*.

Case 3. When τ2=0 and τ1>0 then equation (28) will be

λ4+a1λ3+a2λ2+a3λ+a4+eλτ1(λ3(b1+c1)+λ2(b2+c2)+λ(b3+c3)+b4+c4)=0. (35)

We suppose for some values of τ1 the λ=iξ we have two equations

ξ4a2ξ2+a4=ξ3(b1+c1)sin(ξτ1)+ξ2(b2+c2)cos(ξτ1ξ)(b3+c3)sin(ξτ1)(b4+c4)cos(ξτ1),a1ξ3+a3ξ=ξ3(b1+c1)cos(ξτ1)+ξ2(b2+c2)sin(ξτ1ξ)(b3+c3)cos(ξτ1)+(b4+c4)sin(ξτ1). (36)

Squaring and adding both equations

υ4+f1υ3+f2υ2+f3υ+f4=0,ξ2=υ. (37)

Where the coefficients are:

f1=a122a2(b1+c1)2,f2=a222a1a3+2a4(b2+c2)2+2(b1+c1)(b3+c3),f3=a32+2a2a4(b3+c3)2,f4=a42(b4+c4)2.

Similarly to previous case, we arrived at the following theorem.

Theorem 2.7

Suppose that(R1)and(D2)is holds with delayτ2=0and there exists aτ1>0such thatE*is locally asymptotically stable forτ1<τ1*and unstable forτ1>τ1*, whereτ1*=min{τ1,j}. Furthermore, model(1)undergoes the hopf bifurcation which occur at pointE*whenτ1=τ1*.

τ1,j=1ξ1arccos[B1(a2ξ12+a4+ξ14)(ξ2(b2+c2)+b4+c4)ξ14((b2+c2)2)+ξ12(ξ2(b1+c1)(b3+c3))2+(b4+c4)2]+2πjξ1. (38)

Where B1=a3ξ12(ξ12(b1+c1)b3c3)+a1ξ14(ξ12((b1+c1))+b3+c3) and j=0,1,2,....

Case 4. When τ1>0 and τ2>0 the equation (28) will be

λ4+λ3(a1+b1eλτ1+c2eλτ1λτ2)+λ2(a2+b2eλτ1+c2eλτ1λτ2)+λ(a3+b3eλτ1+c3eλτ1λτ2)+(a4+b4eλτ1+c4eλτ1λτ2)=0. (39)

We suppose for some values of τ1 and τ2 there is a real number ξ we have two equations of real and imaginary values at λ=iξ.

a2ξ2+a4+ξ4=(b1ξ3b3ξ)sin(ξτ1)(b4b2ξ2)cos(ξτ1)+(c1ξ3c3ξ)sin(ξ(τ1+τ2))(c4*c2ξ2)cos(ξ(τ1+τ2)),a3ξa1ξ3=((b3ξb1ξ3))cos(ξτ1)+(b4b2ξ2)sin(ξτ1)(c3ξc1ξ3)cos(ξ(τ1+τ2))+(c4*c2ξ2)sin(ξ(τ1+τ2)). (40)

By squaring and adding both equations in 41. Applying Rouche’s Theorem we have

υ4+g1υ3+g2υ2+g3υ+g4=0,ξ2=υ. (41)

Where the coefficients are:

g1=a122a22b1c1cos(ξτ2)b12c12,g2=a222a1a3+2a4+2b3(Ac1+b1)2b2c2cos(ξτ2)+2c3(b1cos(ξτ2)+c1)b22c22,g3=a322a2a4+2b4(c2cos(ξτ2)+b2)2b3c3cos(ξτ2)+2c4(b2cos(ξτ2)+c2)b32c32,g4=a422b4c4cos(ξτ2)b42c42.

By rule of signs of Descartes equation (41) has at least one positive real root if (D3) a122a2>2b1c1cos(ξτ)2+b12+c12 and a422b4c4cos(ξτ)2<b42+c42 hold. By eliminating sin(ξ0τ1) we have

τ1,j=1ξ0cos1(G2(a1ξ03a3ξ0)+G1(a2ξ02+a4+ξ04)G3G1G22)+2πjξ0,j=0,1,2,.... (42)

Where

G1=ξ0(c3sin(ξ0τ2)ξ0(c2cos(ξ0τ2)+b2+c1sin(ξ0τ2)ξ0))+c4cos(ξ0τ2)+b4,G2=ξ0(ξ0(c1ξ0cos(ξ0τ2)+b1ξ0c2sin(ξ0τ2))c3cos(ξ0τ2)b3)+c4sin(ξ0τ2),G3=(c4c2ξ02)cos(ξ0τ2)+b2ξ02b4+Bξ0(c3c1ξ02)sin(ξ0τ2).

To study Hopf bifurcation we would fix τ2 in the stable interval and take derivative with respect to τ1 of equation (40) while using substitutions of ξ=ξ0 τ1=τ1,0

P1(dRe(λ)dτ1|τ1=τ1,0)+P2(dξdτ1|τ1=τ1,0)=P3,P2(dξdτ1|τ1=τ1,0)+P1(dRe(λ)dτ1|τ1=τ1,0)=P4. (43)

Where

C1=cos(ξ0τ1,0),C2=cos(ξ0τ2),S1=sin(ξ0τ1,0),S2=sin(ξ0τ2),P1=2a2ξ0+C1(3b2ξ02+C2τ2(c1ξ03c3ξ0)C2(2c2ξ0)+S2τ2(c4c2ξ02)+S2(3c1ξ02c3))+S1(3b1ξ02b3+C2τ2(c4c2ξ02)+C2(3c1ξ02c3)S2τ2(c1ξ03c3ξ0)S2(2c2ξ0))4ξ03,P2=3a1ξ02a3+C1(3b1ξ02b3+C2τ2(c4c2ξ02)C2(c33c1ξ02)+S2τ2(c3ξ0c1ξ03)S2(2c2ξ0))+S1(2b2ξ0+C2τ2(c3ξ0c1ξ03)C2(2c2ξ0)S2τ2(c4c2ξ02)+S2(c33c1ξ02)),P3=ξ0S1(b1ξ03b3ξ0C2(c3ξ0c1ξ03)+S2(c4c2ξ02))C1ξ0(b2(ξ02)+b4+C2(c4c2ξ02)+S2(c3ξ0c1ξ03)),P4=ξ0S1(b2ξ02b4C2(c4c2ξ02)+S2(c1ξ03c3ξ0))C1ξ0(b1ξ03b3ξ0+C2(c1ξ03c3ξ0)+S2(c4c2ξ02)).

We obtain

dRe(λ)dτ1=P2P3P1P4P22P12. (44)

Hopf bifurcation will occur for τi=τ1,0 if dR(λ)dτ1>0.

Theorem 2.8

IfE*is existent, such that(R1)and(D3)hold, withτ3=0andτ1(0,τ1*), there is an existent positive parameterτ2such that endemic equilibrium point is locally stable forτ2<τ2and unstable forτ2>τ2, whereτ2=min{τ2,j}as in(42). Moreover, model(1)will undergoes hopf bifurcation at pointE*whenτ2=τ2.

Note: Similarly, For τ2(0,τ2*), there is exists threshold parameter τ1 such that endemic equi point is locally asymptotically a stable for τ1<τ1 and unstable if τ1>τ1. Moreover, hopf bifurcation occur for model (1) as τ1=τ1, where τ1=min{τ1,j} that is

τ2,j=1ξ2cos1(α2(c2ξ22c4)+α1ξ2(c1ξ2c3)ξ22(c1ξ22c3)2+(c2ξ22c4)2)+2jπξ2,j=0,1,2.... (45)

Where

α1=ξ2(a3cos(ξ2τ1)b1ξ22+b3)a1ξ23cos(ξ2τ1)+(a4+ξ24)sin(ξ2τ1)a2ξ22sin(ξ2τ1),α2=b4ξ2(a3s+b2ξ2)+(a4+ξ24)cos(ξ2τ1)a2ξ22cos(ξ2τ1)+a1ξ23sin(ξ2τ1).

3. Results and discussion

Dynamics without delay

Lower “Exposed to Infected” Rate

Fig. 2 presents the dynamics for σ=0.3, when the transmission from the exposed to the infected compartment is less.

Fig. 2.

Fig. 2

Left column η>0.5, right column η<0.5, delay τ1=0, τ2=0. Dynamics for σ = 0.3.

From Fig. 2, we can see that the impact of different transmission rates on the pandemic are noteworthy. For example, for the higher values of ψ, the rates at which the recovered individuals again become susceptible, is higher. This leads to higher infection rates (blue line).

On the other hand, the lower value of ψ corresponds to better recovery rate, with less probability of getting infected again, and thus leads to lower infection rates.

Next, from Fig. 3 , we can see that the best dynamics for the better control strategies of the pandemic are β0.09 and ψ0.035.

Fig. 3.

Fig. 3

Left column η>0.5, right column η<0.5, delay τ1=0, τ2=0. Dynamics for σ = 0.6.

Higher “Exposed to Infected” Rate

Fig. 3 presents the dynamics for σ=0.6, when the transmission from the exposed to the infected compartment, is higher.

We thus emphasize on the fact that it is not only important to control the interaction of infected people with the susceptible, but it is really necessary to discover a drug, which will reduce the probability of cyclic outbreak of the disease, where the recovered individuals will have fewer chances of becoming infectious again.

Dynamics with delay

Next, we have run the numerical experiments, based on the stability analysis. We can see from Figs. 4 and 5 that, different dynamics were revealed relative to different combinations of the delays.

Fig. 4.

Fig. 4

For equal and unequal delays.

Fig. 5.

Fig. 5

For different recovered to susceptible rates, for τ1<τ2

For lower and equal delays in different compartments, there was less delay in the onset of infection, whereas, for higher values of delay, there were higher intervals of delay in the onset of infection.

4. Conclusions

Over the past year, different mathematical models have been proposed in literature to highlight the importance of social distancing, as a precautionary tool, to control the spread of the novel corona virus. In this manuscript, important agent based (each individual was treated as an agent), strategy is adopted and the machine learning tool of self organizing maps is used to explore the parameters of the resulting mathematical model.

In this research, we conclude that it is not only important to emphasize on the isolation of susceptible individuals in a population, it is also necessary to control the interaction among the infected, recovered and asymptomatic individuals. We have verified this hypothesis with the aid of numerical simulations.

The outcome of isolation and lockdown, can delay and reduce the disease transmission, but it is not the permanent solution to the problem, since the social distancing, isolation and lockdown have a great influence on the world’s economy and is becoming a cause of the socioeconomic crisis, of the third world countries.

CRediT authorship contribution statement

Zhenhua Yu: Conceptualization, Data curation. Robia Arif: Formal analysis. Mohamed Abdelsabour Fahmy: Conceptualization. Ayesha Sohail: Conceptualization, Supervision.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Footnotes

Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.chaos.2021.111202.

Appendix A. Supplementary materials

Supplementary Data S1

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

Download video file (182.1KB, mp4)

References

  • 1.Dan J.M., Mateus J., Kato Y., Hastie K.M., Yu E.D., Faliti C.E., Grifoni A., Ramirez S.I., Haupt S., Frazier A., et al. Immunological memory to SARS-cov-2 assessed for up to 8 months after infection. Science. 2021 doi: 10.1126/science.abf4063. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Ozono S., Zhang Y., Ode H., Sano K., Tan T.S., Imai K., Miyoshi K., Kishigami S., Ueno T., Iwatani Y., et al. Sars-cov-2 d614g spike mutation increases entry efficiency with enhanced ace2-binding affinity. Nature Commun. 2021;12(1):1–9. doi: 10.1038/s41467-021-21118-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Clouston S.A.P., Natale G., Link B.G. Socioeconomic inequalities in the spread of coronavirus-19 in the united states: a examination of the emergence of social inequalities. Soc Sci Med. 2021;268:113554. doi: 10.1016/j.socscimed.2020.113554. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Meyers C., Robison R., Milici J., Alam S., Quillen D., Goldenberg D., Kass R. Lowering the transmission and spread of human coronavirus. J Med Virol. 2021;93(3):1605–1612. doi: 10.1002/jmv.26514. [DOI] [PubMed] [Google Scholar]
  • 5.Mahmoudi M.R., Baleanu D., Mansor Z., Tuan B.A., Pho K.-H. Fuzzy clustering method to compare the spread rate of covid-19 in the high risks countries. Chaos Soliton Fractal. 2020;140:110230. doi: 10.1016/j.chaos.2020.110230. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Roda W.C., Varughese M.B., Han D., Li M.Y. Why is it difficult to accurately predict the COVID-19 epidemic? Infect Dis Modell. 2020 doi: 10.1016/j.idm.2020.03.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Din A., Khan A., Baleanu D. Stationary distribution and extinction of stochastic coronavirus (COVID-19) epidemic model. Chaos Soliton Fractal. 2020;139:110036. doi: 10.1016/j.chaos.2020.110036. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Sohail A., Nutini A. Forecasting the timeframe of coronavirus and human cells interaction with reverse engineering. Progr Biophys Mol Biol. 2020 doi: 10.1016/j.pbiomolbio.2020.04.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Auwaerter P.G. Coronavirus COVID-19 (SARS-2-cov) Johns Hopkins ABX Guide. 2020 [Google Scholar]
  • 10.Nikolich-Zugich J., Knox K.S., Rios C.T., Natt B., Bhattacharya D., Fain M.J. Sars-cov-2 and covid-19 in older adults: what we may expect regarding pathogenesis, immune responses, and outcomes. Geroscience. 2020:1–10. doi: 10.1007/s11357-020-00186-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Chen W.-C. Nonlinear dynamics and chaos in a fractional-order financial system. Chaos Soliton Fractal. 2008;36(5):1305–1314. [Google Scholar]
  • 12.Baleanu D., Jajarmi A., Mohammadi H., Rezapour S. A new study on the mathematical modelling of human liver with caputo–fabrizio fractional derivative. Chaos Solitons Fractal. 2020;134:109705. [Google Scholar]
  • 13.Du H., Zeng Q., Wang C. Modified function projective synchronization of chaotic system. Chaos Soliton Fractal. 2009;42(4):2399–2404. [Google Scholar]
  • 14.Holden A.V., Biktashev V.N. Computational biology of propagation in excitable media models of cardiac tissue. Chaos Soliton Fractal. 2002;13(8):1643–1658. [Google Scholar]
  • 15.Iftikhar M., Iftikhar S., Sohail A., Javed S. Ai-modelling of molecular identification and feminization of wolbachia infected aedes aegypti. Progr Biophys Mol Biol. 2020;150:104–111. doi: 10.1016/j.pbiomolbio.2019.07.001. [DOI] [PubMed] [Google Scholar]
  • 16.Baleanu D., Mohammadi H., Rezapour S. A fractional differential equation model for the COVID-19 transmission by using the caputo–fabrizio derivative. Adv Diff Eqs. 2020;2020(1):1–27. doi: 10.1186/s13662-020-02762-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Baleanu D., Mohammadi H., Rezapour S. A mathematical theoretical study of a particular system of caputo–fabrizio fractional differential equations for the rubella disease model. Adv Diff Eqs. 2020;2020(1):1–19. [Google Scholar]
  • 18.Baleanu D., Mohammadi H., Rezapour S. Analysis of the model of HIV-1 infection of CD4+ CD4{+} t-cell with a new approach of fractional derivative. Adv Diff Equs. 2020;2020(1):1–17. [Google Scholar]
  • 19.Blackwood J.C., Childs L.M. An introduction to compartmental modeling for the budding infectious disease modeler. Lett Biomathe. 2018;5(1):195–221. [Google Scholar]
  • 20.Yu Zhenhua, et al. Journal of Molecular Liquids. 2021 doi: 10.1016/j.molliq.2020.114863. https://www.sciencedirect.com/science/article/pii/S0167732220371051?casa_token=NCU80gz18p8AAAAA:m7HBFWhCrK-iC1nLNVTN1p4aHYiH_q8idUK74VCciZAPRxPvv2FLrmXsIz8xnadBp7r58txq2w [DOI] [PMC free article] [PubMed] [Google Scholar]; In press.
  • 21.Yu Zhenhua, et al. Front. Mol. Biosci. 2021 doi: 10.3389/fmolb.2021.679031. https://www.frontiersin.org/articles/10.3389/fmolb.2020.585245/full [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Al-Utaibi K.A., et al. results in physics. 2021 https://www.sciencedirect.com/science/article/pii/S2211379721004174 [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary Data S1

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

Download video file (182.1KB, mp4)

Articles from Chaos, Solitons, and Fractals are provided here courtesy of Elsevier

RESOURCES