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Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2022 Jul 23;203:741–766. doi: 10.1016/j.matcom.2022.07.012

Global stability and analysing the sensitivity of parameters of a multiple-susceptible population model of SARS-CoV-2 emphasising vaccination drive

R Prem Kumar a,b,, PK Santra c, GS Mahapatra a
PMCID: PMC9308141  PMID: 35911951

Abstract

The study explores the dynamics of a COVID-19 epidemic in multiple susceptible populations, including the various stages of vaccination administration. In the model, there are eight human compartments: completely susceptible; susceptible with dose-1 vaccination; susceptible with dose-2 vaccination; susceptible with booster dose vaccination; exposed; infected with and without symptoms, and recovered compartments. The biological feasibility of the model is analysed. The threshold value, R0, is derived using the next-generation matrix. The stability analysis of the equilibrium points was performed locally and globally using the threshold parameter of the model. The conditions determining disease persistence is obtained. The model is subjected to sensitivity analysis, and the most sensitive parameters are identified. Also, MATLAB is used to verify the mathematical outcomes of the system’s dynamic behaviour and suggests that necessary steps should be taken to keep the spread of the omicron variant infectious disease under control. The findings of this study could aid health officials in their efforts to combat the spread of COVID-19.

Keywords: Boundedness, Basic reproduction number, Stability, Sensitivity, Vaccination

1. Introduction

SARS-CoV-2 or Coronavirus-19 was officially declared a global epidemic in March 2020, affecting and changing human life worldwide. It has only been recently that many countries have started investigating the origins of the new coronavirus. Some of its characteristics complicate the detection of epidemic breakouts; among them is the large number of people who are asymptomatic but can infect others. Furthermore, the number of hospitalised patients with COVID-19 increases asymmetrically with age; it is almost innocuous for teenagers and young adults. However, it is hazardous for the elderly, especially in conjunction with other conditions; it has caused more than 105 deaths in Italy, accounting for more than 3 million infections; The average age of COVID-19 patients who died in Italy was 81. Social distancing, face masks, lock-downs, self-isolation/quarantine, contact tracing, and vaccination administration are all effective techniques for avoiding the spread of this virus. The Centers for Disease Control and Prevention have designated this pandemic as a public health issue. Approximately six feet apart, droplets are the means of transmission caused by coughing, sneezing, and talking. The Spanish Flu (1918 to 1920) and the Ebola epidemic (2014 to 2016) are examples of historical pandemics that have impacted human health and economic development [1], [2], [3], [4]

The Indian government has approved four vaccinations: Covishield, Covaxin, Sputnik V, and spikevax. The Indian government began vaccinating individuals with the help of the National Expert Group on COVID-19 Vaccine Administration (NEGVAC), intending to vaccinate 300 million people in 180 days and complete the process by August 2021. The vaccination was administered to people in three phases. The first phase vaccination programme, which began on January 16, 2021, was only for health and front-line workers and was completed by April 3, 2021. The phase two vaccination programme began on March 1, 2021, and was mainly for people over 45 years old with other health complications and 60+year-old adults. Finally, the Phase 3 vaccination programme was opened to all adults over 18 years on May 1, 2021, after the second wave hit the country in April 2021 [5], [6], [7], [8].

There were many variants of COVID-19 as announced by WHO, namely the alpha variant spreading to many countries in late 2020, the variant beta(B.1.351) dominant in many parts of southern Africa, the Gamma variant (P.1) dominant in the U.S and Brazil in January 2021, the Delta variant (B.1.617.2) dominant in many countries including India from December 2020, variant Mu(B.1.621) dominant in South Africa and other countries from January 2021, R.1 variant dominant in Japan in March 2021, omicron variant(B1.1.529) dominant in South Africa, India and U.S from November 2021 onwards [9].

A model for tracking and predicting the intensity of the virus is required to plan for future outbreaks and alert administrations and communities about what can be done today to prevent transmission and infection. We can model and track current outbreak trends to prepare for future breakouts. This measure will help prevent the next coronavirus outbreak from being as severe. Global health decisions are made better with mathematical models that allow us to understand epidemiological patterns. Epidemic transmission patterns remain challenging to predict because a mathematical system is contingent on the presence of its solutions. Data is frequently skewed, delayed, or erroneous, and obtaining quality data is one of the most challenging tasks. Furthermore, traditional epidemic models assume that epidemic transmission occurs without interventions, a rare event. Keeping track of daily activities and travel, which intertwine with the spread of infection, makes it more challenging. Furthermore, there are far too many occurrences in hospitals where the interaction rate is more significant than in the general population. This cannot be ignored anyhow. Another difficulty here is estimating the epidemic model’s parameters. To fully understand, capture, and predict the transmission of infectious illnesses, epidemiologists must continue to use mathematical models. Recently, there has been much research and development into understanding and predicting COVID-19. Using mathematical formulations to model the transmission of infectious diseases like COVID-19 is a well-established approach to analysing individuals and their infections in communities. Several studies have been published examining the dynamics of the COVID-19 epidemic worldwide [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [30], [32], [35], [36], [37], [38], [39], [41], [42], [43], [44], [45], [46], [47], [48], [49], [50], [52], [53], [54], [55], [57], [58], [59], [60], [61], [62], [63], [64], [65], [66], [67], [68], [69], [70], [71], [72], [73], [74], [75], [76], [77], [78], [79], [80], [81], [82], [83]. Vaccination’s impact on the spread of COVID-19 has been the subject of several articles [40], [51]. During the second wave of COVID-19, mathematical models involving multiple susceptible compartments with each susceptible compartment containing individuals at varying phases of vaccination were the least explored. We present a compartmental mathematical model that includes multiple susceptible compartments corresponding to distinct vaccination stages.

The mathematical model is described and formalised in Section 2. The Section 3 examines the model’s essential characteristics. The system’s equilibrium points are determined in Section 3.3, and the criteria for its existence are specified. The disease-free equilibrium is discussed in Section 4, and the endemic equilibrium point is examined in Section 5. A bifurcation analysis is conducted in Section 6. In Section 7, the sensitivity analysis is carried out, and the parameter with the most sensitivity index is identified. The parameter estimation is performed in Section 8. The numerical simulations are performed in Section 9 and finally, in Section 10, all of the results have been summarised.

2. Construction of novel COVID-19 model

The COVID-19 model’s population is organised into eight classes, namely, the susceptible population without vaccination (S0), the susceptible population vaccinated with dose 1 (S1), the susceptible population vaccinated with dose 2 (S2), susceptible population with a booster dose (S3), exposed population (E), infected and asymptomatic population to omicron variant induced COVID-19 disease (IA), infected and symptomatic population to omicron variant induced COVID-19 disease (IS) and the recovered population from omicron variant induced COVID-19 disease (R). The following assumptions are included in the model:

The total population M=S0+S1+S2+S3+E+IA+IS+R is assumed to be constant, while the individual compartment populations vary over time. It is assumed that dose-1 vaccination is given to non-vaccinated susceptible individuals, dose-2 vaccination is given to dose-1 vaccinated susceptible individuals, and a booster dose vaccination is given to dose-2 vaccinated individuals. The omicron variant viral infection is assumed to exclusively affect those who have not had either dose-1 or dose-2 of vaccination, and it does not affect people who have received a booster dose. Individuals’ disease-related deaths were assumed to occur mainly in the infected but symptomatic compartment, and only natural death occurs in the remaining compartments. It is assumed that when non-vaccinated individuals have contact with infected but asymptomatic individuals, they get exposed to the infection with the transmission coefficient given by β1S0IA. When susceptible dose-1 vaccinated individuals have contact with infected but asymptomatic individuals, they get exposed to the infection with the transmission coefficient given by β2S1IA. When susceptible dose-2 vaccinated individuals have contact with infected but asymptomatic individuals, they get exposed to the infection with the transmission coefficient given by β3S2IA. It is assumed that those who recover will be immune to the disease for the rest of their lives. It is supposed that the people who are exposed to the infection are asymptomatic of the disease after testing positive for the disease and moves to an asymptomatic infected compartment with the transmission coefficient given by γE and following the appearance of symptoms, the infected individual transfers to the symptomatic infected compartment, with δ1IA as the transmission coefficient. The individuals who are recovered from both asymptomatic and symptomatic infections due to supportive care treatments available for COVID-19 disease in hospitals under isolation are recovered and moved to the recovered compartment with a transmission coefficient given by δ2IA and σ1IS respectively. Symptomatic infected individuals are assumed to be isolated and undergo supportive care treatments in hospitals, so these individuals do not spread the disease. The omicron variant-induced COVID-19 pandemic model is formulated as below.

S0˙=Λβ1S0IA(α1+ξ)S0.S1˙=α1S0β2S1IA(α2+ξ)S1.S2˙=α2S1β3S2IA(α3+ξ)S2.S3˙=α3S2ξS3.Ė=(β1S0+β2S1+β3S2)IA(γ+ξ)E.IA˙=γE(δ1+δ2+ξ)IA.IS˙=δ1IA(σ1+σ2+ξ)IS.=δ2IA+σ1ISξR. (1)

The preliminary conditions are given by

0<Si(0)<,0E(0),IA(0),IS(0),R(0)<,i=0,1,2,3. (2)

In our model, the flow diagram of the omicron virus transmission in the human population is presented in Fig. 1.

Fig. 1.

Fig. 1

Virus transmission diagram of the system (1).

3. The fundamental characteristics of the model

3.1. The characteristic of non-negativity in solutions

It is essential to show that for all time t0, each solution of system (1) with preliminary conditions (2) remains non-negative.

Theorem 1

For anyt0, each solution of system(1)with preliminary conditions (2) is non-negative.

Proof

Using the first equation of (1) with initial condition (2), we get

S0˙=Λ(β1IA+c1)S0>(β1IA+c1)S0. (3)

As a result, after integrating, we obtain,

S0(t)>S0(0)e0t(β1IA+c1)dt>0. (4)

Similarly from the remaining equations of (1) utilising the initial conditions (2), we get

S1(t)>S1(0)e0t(β2IA+c2)dt>0,S2(t)>S2(0)e0t(β3IA+c3)dt>0,S3(t)>S3(0)eξt>0,E(t)E(0)ec4t0,IA(t)IA(0)ec5t0,IS(t)IS(0)ec6t0,R(t)R(0)eξt0. (5)

where c1=α1+ξ, c2=α2+ξ, c3=α3+ξ, c4=γ+ξ, c5=δ1+δ2+ξ, c6=σ1+σ2+ξ. Hence, 0<Si(t)<,0E(t),IA(t),IS(t),R(t)<,i=0,1,2,3. □

3.2. Invariant region and uniform boundedness of solutions

We will now prove that all of system (1)’s solutions are bounded uniformly and there exist solutions to system (1) of R+8 in a positively invariant region.

Theorem 2

The system(1)’s solutions with preliminary conditions (2) are bounded uniformly in R+8 and are confined to the region ={(S0,S1,S2,S3,E,IA,IS,R)R+8:0<MΛξ} as t , where M=S0+S1+S2+S3+E+IA+IS+R .

Proof

Let M=S0+S1+S2+S3+E+IA+IS+R, where M=M(t) is the total population at time t. For m>0 we have,

dMdt+mM=Λ(ξm)σ2ISΛ. (6)

if and only if mξ. Using differential inequality theory [31], we can arrive at the following conclusion:

0<MΛm1emt+M(0)emt. (7)

which yields 0<MΛm as t with mξ. Hence system (1)’s solutions with preliminary conditions (2) starting in R+8 are bounded uniformly and limited to the region ={(S0,S1,S2,S3,E,IA,IS,R)R+8:0<M(t)Λm}, where mξ. As a result, the closed region is positively invariant, and all system (1)’s solutions are bounded uniformly. □

Remark 1

All of system (1)’s solutions with preliminary conditions (2) have non-negative components in for t 0 and are globally attracted in R+8. As a result, the system (1) with preliminary conditions (2) defined on ={(S0,S1,S2,S3,E,IA,IS,R)R+8:0<M(t)Λm}, where mξ is well-posed mathematically and epidemiologically. We will investigate the dynamics of system (1) without the recovered compartment defined on the invariant region Δ={(S0,S1,S2,S3,E,IA,IS)R+7:0<M(t)Λm}, where mξ, because the recovered compartment of individuals is independent of other compartments.

3.3. The system’s equilibrium points

The equilibrium points for the system (1) are as follows

  • 1.

    Disease free equilibrium (DFE) point P0=(S00,S10,S20,S30,E0,IA0,IS0), where, S00=Λc1,S10=Λα1c1c2,S20=Λα1α2c1c2c3,S30=Λα1α2α3ξc1c2c3,E0=0,IA0=0,IS0=0. Here, c1=α1+ξ, c2=α2+ξ, c3=α3+ξ, c4=γ+ξ, c5=δ1+δ2+ξ, c6=σ1+σ2+ξ

  • 2.
    Endemic equilibrium (EE) point P1=(S0,S1,S2,S3,E,IA,IS), where S0=Λc1+β1IA,S1=Λα1(c1+β1IA)(c2+β2IA),S2=Λα1α2(c1+β1IA)(c2+β2IA)(c3+β3IA),S3=Λα1α2α3(c1+β1IA)(c2+β2IA)(c3+β3IA)ξE=β2c3(α1+IAβ1)+α1α2β3+(α1+IAβ1)β2β3IA+c2β1(c3+IAβ3)ΛIAc4(c1+β1IA)(c2+β2IA)(c3+β3IA),IS=δ1IAc6 From the sixth equation of (1) after simplification, we get the polynomial equation
    k3IA3+k2IA2+k1IA+k0=0. (8)
    where
    k0=c1c2c3c4c51(c2c3β1+c3α1β2+α1α2β3)Λγc1c2c3c4c5,k1=c4c5c2c3β1+c1c3β2+c1c2β3γΛc3β1β2+c2β1β3+α1β2β3,k2=c4c5c3β1β2+c2β1β3+c1β2β3β1β2β3γΛ,k3=c4c5β1β2β3. (9)
    Clearly, k3>0 and if we set R0=(c2c3β1+c3α1β2+α1α2β3)Λγc1c2c3c4c5, then k0<0 whenever R0>1. The above polynomial in IA has three roots and by Descartes rule of sign, the polynomial has either one or three positive real roots for all possible combination of signs of k1 and k2. As a result, the polynomial (8) always has at least one positive root if R0>1. Hence if R0>1 then IA>0 always and hence S0,S1,S2,S3,E,IS belong to R+. As a result P1 always exists if R0>1.

4. Stability analysis on DFE

4.1. Next generation matrix method

The mean number of secondary infections induced by a single infection is known as the Basic Reproduction Number (BRN). It is one of the most important threshold values for mathematically expressing a virus infection’s spread.

At a given point P=(S0,S1,S2,S3,E,IA,IS), the Jacobian matrix of the system (1) is given by J(P) as follows:

J(P)=(β1IA+c1)0000β1S00α1(β2IA+c2)000β2S100α2(β3IA+c3)00β3S2000α3ξ000β1IAβ2IAβ3IA0c4(β1S0+β2S1+β3S2)00000γc5000000δ1c6 (10)

P0’s stability corresponds to eigenvalues of J(P)’s characteristic equation at P0 being of negative real parts, as confirmed by the BRN computed using the next-generation matrix approach. Let us assume x=(E,IA,IS,S0,S1,S2,S3)T and hence the system (1) is expressed as

x˙=FV. (11)

where

F(x)=β1S0+β2S1+β3S2000000

and

V(x)=c4EγE+c5IAδ1IA+c6ISΛ+β1S0IA+c1S0α1S0+β2S1IA+c2S1α2S1+β3S2IA+c3S2α3S2+ξS3.

The Jacobian matrices of F(x) and V(x) at P0 are as follows.

F=0Λ(β1c2c3+β2α1c3+β3α1α2)c1c2c30000000

and

V=c400γc500δ1c6.

The next generation matrix for system (1)is given by

FV1=γΛ(β1c2c3+β2α1c3+β3α1α2)c1c2c3c4c5(β1c2c3+β2α1c3+β3α1α2)Λc1c2c3c50000000

The spectral radius ρ(FV1) of FV1 is the BRN given as follows:

R0=γΛ(β1c2c3+β2α1c3+β3α1α2)c1c2c3c4c5. (12)

where c1=α1+ξ, c2=α2+ξ, c3=α3+ξ, c4=γ+ξ, c5=δ1+δ2+ξ.

4.2. The analysis of P0’s local stability

In this part, we investigate the local asymptotic stability (LAS) of the disease-free equilibrium point P0.

Theorem 3

The point P0 of system (1) is LAS whenever R0<1 and is unstable if R0>1 .

Proof

The jacobian matrix evaluated at P0 of the system (1) is

J(P0)=c10000β1Λc10α1c2000β2α1Λc1c200α2c300β3Λα1α2c1c2c3000α3ξ0000000c4(β1Λc1+β2α1Λc1c2+β3α1α2Λc1c2c3)00000γc5000000δ1c6 (13)

J(P0) has the following characteristic equation

|J(P0)λI|=0. (14)

Hence, we get the polynomial in λ, say

(λ+c1)(λ+ξ)(λ+c2)(λ+c6)(λ+c3)(c2c3β1+c3α1β2+α1α2β3)γΛc1c2c3(λ+c4)(λ+c5)=0. (15)

The five eigen values of the characteristic equation are given by λ=c1<0, λ=ξ, λ=c2<0, λ=c6<0 and λ=c3<0. The remaining two eigen values of the characteristic equation are given by the equation

(c2c3β1+c3α1β2+α1α2β3)γΛc1c2c3(λ+c4)(λ+c5)=0. (16)

After simplifying the above equation, we get

λ2+a1λ+a2=0. (17)

where

a1=c4+c5.a2=c4c51(c2c3β1+c3α1β2+α1α2β3)γΛc1c2c3c4c5=c4c5(1R0). (18)

Clearly a1>0 but a2>0 if and only if R0<1. Hence, P0 is LAS if R0<1 and unstable if R0>1 according to Hurwitz–Routh criterion [29]. □

4.3. The analysis of P0’s global stability

We analyse the global asymptotic stability (GAS) of P0 based on the value of R0 using the conditions in Castillo-Chavez method [34] in this section. To prove the GAS of P0, the feasible region Δ1={(S0,S1,S2,S3,E,IA,IS)Δ:S0S00,S1S10,S2S20} is used. Firstly, the region Δ1’s positively invariant property is established.

Theorem 4

For the omicron system (1) , the region Δ1={(S0,S1,S2,S3,E,IA,IS)Δ:S0S00,S1S10,S2S20} is a positively invariant set.

Proof

From system (1), we obtain

S0˙=Λβ1S0IAc1S0Λc1S0. (19)

Hence we get,

S0(t)S00(S00S0(0))ec1t. (20)

If S0(0)Δ1, then S0(0)S00. Therefore S0(t)S00(S00S0(0))ec1tS00 t0. Similarly, we deduce from second and third equations of system (1), S1(t)S10 and S2(t)S20, t0 if the initial conditions Si(0)Δ1 for i=1,2. As a result, the region Δ1 is positively invariant set which attracts all of the system (1) solutions in R+7. □

Theorem 5

If R0<1 , P0 is GAS in Δ1 .

Proof

The system (1) is written as

X˙=K(X,I).I˙=L(X,I). (21)

Where, dot denotes differentiation with respect to t in this context and X=(S0,S1,S2,S3)T, I=(E,IA,IS)T,

K(X,I)=Λβ1S0IAc1S0α1S0β2S1IAc2S1α2S1β3S2IAc3S2α3S2ξS3,L(X,I)=(β1S0+β2S1+β3S2)IAc4EγEc5IAδ1IAc6IS

Furthermore

A=c4β1S00+β2S10+β3S200γc500δ1c6,Lˆ(X,I)=β1(S00S0)+β2(S10S1)+β3(S20S2)IA00
K(X,I)|I=0=Λc1S0α1S0c2S1α2S1c3S2α3S2ξS3,L(X,I)|I=0=000,whereA=DIL(X,0),L(X,I)=AILˆ(X,I)

Solving the system dXdt=K(X,0), we get S0(t)=Λc1+(S0(0)Λc1)ec1t and hence limtS0(t)=S00 and similarly from the other equations of dXdt=K(X,0), we get limtS1(t)=S10, limtS2(t)=S20 and limtS3(t)=S30. The solutions of dXdt=K(X,0) do not depend on the initial conditions Si(0), i=0,1,2,3. As a result, the asymptotic nature of the solutions Si(t), i=0,1,2,3 is independent of the preliminary conditions in Δ1, ensuring the global asymptotic stability of the equilibrium point X=(Λc1,α1Λc1c2,α1α2Λc1c2c3,Λα1α2,α3ξc1c2c3) and hence the first condition of the Castillo-Chavez method [34] is satisfied. Further in Δ1, S0S00, S1S10, S2S20 and hence

β1(S00S0)+β2(S10S1)+β3(S20S2)0. (22)

This implies that

Lˆ(X,I)0. (23)

which satisfies the second condition of the Castillo-Chavez method [34]. As a result, P0 is GAS if R0<1. □

5. Stability analysis of EE

In this section, we analyse the local asymptotic stability (LAS) and global asymptotic stability (GAS) of the endemic equilibrium (EE) point P1.

5.1. The analysis of P1’s local stability

Theorem 6

The EE point P1 of the system (1) is LAS if R0>1 and all of the conditions in the proof are met.

Proof

The Jacobian matrix of system (1) at P1 is

J(P1)=(c1+β1IA)0000β1S00α1(c2+β2IA)000β2S100α2(c3+β3IA)00β3S2000α3ξ000β1IAβ2IAβ3IA0c4β1S0+β2S1+β3S200000γc5000000δ1c6 (24)

The determinantal equation of (24) is given by

|J(P1)τI|=0. (25)

Hence we get the polynomial in τ, say

(τ+c6)(τ+ξ)(τ5+B1τ4+B2τ3+B3τ2+B4τ+B5)=0. (26)

The two latent roots of (26) are τ=c6<0 and τ=ξ<0. The remaining latent roots of (26) are analysed using the polynomial equation

τ5+B1τ4+B2τ3+B3τ2+B4τ+B5=0. (27)

The coefficients of (27) are as follows:

B1=c1+c2+c3+c4+c5+IA(β1+β2+β3)>0.
B2=c3c4+c3c5+c3IAβ1+c4IAβ1+c5IAβ1+c3IAβ2+c4IAβ2+c5IAβ2+IA2β1β2+c4IAβ3+c5IAβ3+IA2β1β3+IA2β2β3+c2(c3+c4+c5+IA(β1+β3))+c1(c2+c3+c4+c5+IA(β2+β3))>0.
B3=c1c2c3+c1c2c4+c1c3c4+c2c3c4+c1c2c5+c1c3c5+c2c3c5+c2c3IAβ1+c2c4IAβ1+c3c4IAβ1+c2c5IAβ1+c3c5IAβ1+IAS0γβ12+c1c3IAβ2+c1c4IAβ2+c3c4IAβ2+c1c5IAβ2+c3c5IAβ2+IAS1γβ22+c3IA2β1β2+c4IA2β1β2+c5IA2β1β2+c1c2IAβ3+c1c4IAβ3+c2c4IAβ3+c1c5IAβ3+c2c5IAβ3+IAS2γβ32+c2IA2β1β3+c4IA2β1β3+c5IA2β1β3+c1IA2β2β3+c4IA2β2β3+c5IA2β2β3+IA3β1β2β3>0.
B4=c1c2c3c4+c1c2c3c5+c2c3c4IAβ1+c2c3c5IAβ1+c2IAβ12S0γ+c3IAβ12S0γ+c1c3c4IAβ2+c1c3c5IAβ2+c1IAβ22S1γ+c3IAβ22S1γ+c3c4IA2β1β2+c3c5IA2β1β2+IA2β1β2γ(S0β1+S1β2)+c1c2c4IAβ3+c1c2c5IAβ3+c1IAβ32S2γ+c2IAβ32S2γ+c2c4IA2β1β3+c2c5IA2β1β3+IA2β1β3γ(S0β1+S2β3)+c1c4IA2β2β3+c1c5IA2β2β3+IA2β2β3γ(S1β2+S2β3)+c4IA3β1β2β3+c5IA3β1β2β3+IAS0α1β1β2γ+IAS1α2β2β3γ>0.
B5=c4c5IA3β1β2β3+IA2(c3β1β2γ(S0β1+S1β2)+c2β1β3γ(S0β1+S2β3)+c1β2β3(S1β2+S2β3)γ+(S0α1+S1α2)β1β2β3γ)+IA(S0α1β1(c3β2+α2β3)γ+c1c2β3(S2β3γ)+c1β2(c3S1β2γ+S1α2β3γ)+c2c3β12S0γ)>0.

The Hurwitz–Routh criterion [29] states that the polynomial (27) has all five roots be either negative or have roots with negative real parts if and only if the determinants of all Hurwitz matrices H1,H2,H3,H4,H5 are positive, i.e., 

|Hi|>0fori=1,2,3,4,5. (28)

where H1=(B1), H2=B11B3B2, H3=B110B3B2B1B5B4B3, H4=B1100B3B2B11B5B4B3B200B5B4and

H5=B11000B3B2B110B5B4B3B2B100B5B4B30000B5

The determinants of the Hurwitz matrices are given as follows:

|H1|=B1.|H2|=B1B2B3.|H3|=B32B12B4+B1(B2B3+B5).|H4|=B4(B1B2B3+B32+B12B4)+(B1B22+B2B3+2B1B4)B5B52.|H5|=B5(B4(B1B2B3+B32+B12B4)B2B3B5+B1(B222B4)B5+B52). (29)

But the EE point P1 exists if R0>1 and hence P1 is LAS if R0>1 and satisfies the conditions |Hi|>0, i=1,2,3,4,5. □

5.2. The analysis of P1’s global stability

In this part, the global asymptotic stability (GAS) of endemic equilibrium (EE) point is analysed.

Theorem 7

If R0>1 , the EE point P1 is GAS if P<Q . The expressions of P and Q are specified in the proof.

Proof

Let us create a suitable Lyapunov function as follows:

L(S0,S1,S2,S3,E,IA,IS)=[S0S0+S0log(S0S0)]+[S1S1+S1log(S1S1)]+[S2S2+S2log(S2S2)]+[S3S3+S3log(S3S3)]+[EE+Elog(EE)]+[IAIA+IAlog(IAIA)]+[ISIS+ISlog(ISIS)]. (30)

Then

dLdt=(S0S0S0)dS0dt+(S1S1S1)dS1dt+(S2S2S2)dS2dt+(S3S3S3)dS3dt+(EEE)dEdt+(IAIAIA)dIAdt+(ISISIS)dISdt=(Λβ1S0IAc1S0)(S0S0S0)+(α1S0β2S1IAc2S1)(S1S1S1)+(α2S1β3S2IAc3S2)(S2S2S2)+(α3S2ξS3)(S3S3S3)+((β1S0+β2S1+β3S2)IAc4E)(EEE)+(γEc5IA)(IAIAIA)+(δ1IAc6IS)(ISISIS). (31)

Using the endemic equilibrium point P1 in (1), we get,

Λβ1S0IAc1S0=0.α1S0β2S1IAc2S1=0.α2S1β3S2IAc3S2=0.α3S2ξS3=0.(β1S0+β2S1+β3S2)IAc4E=0.γEc5IA=0.δ1IAc6IS=0. (32)

and using (32) in (31), we get,

dLdt=PQ. (33)

where

P=[β1(IAS0+IAS0)+β2(IAS1+IAS1)+α1S1(S0S1+S0S1)+α2S2(S1S2+S1S2)+β3S2S2(IAS2+IAS2)+α3S3(S2S3+S2S3)+(β1S0+β2S1+β3S2)IA+IAEE(β1S0+β2S1+β3S2)+γIA(EIA+EIA)+δ1IS(IAIS+IAIS)].
Q=[(S0S0)2β1IA+c1S0+β1(IAS0+IAS0)+(S1S1)2β2IA+c2S1+β2(IAS1+IAS1)+α1S1(S0S1+S1S0)+(S2S2)2β3IA+c3S2+α2S2(S1S2+S2S1)+β3S2S2(IAS2+IAS2)+ξS3(S3S3)2+α3S3(S2S3+S2S3)+c4E(EE)2+IAEE(β1S0+β2S1+β3S2)+(β1S0+β2S1+β3S2)IA+c5IA(IAIA)2+γIA(EIA+EIA)+c6IS(ISIS)2+δ1IS(IAIS+IAIS)]. (34)

and with P>0 and Q>0. Thus L˙=PQ<0 iff P<Q and L˙=0 if and only if Si=Si,E=E,IA=IA,IS=IS for i=0,1,2,3. The EE point P1 exists if and only if R0>1, and the singleton set {P1} is the biggest compact invariant set in {(S0,S1,S2,S3,E,IA,IS)Δ:dLdt=0}. According to LaSalle’s invariance principle [56], the EE point {P1} is GAS in Δ if P<Q. □

6. Bifurcation analysis

The Castilla-Chavez and Song [33] approach is used to study the bifurcation nature of system (1).

Theorem 8

The system (1) has forward bifurcation at β1=β1 (i.e. at R0=1 ) whenever a<0 , where expression for β1 and a are given in the proof.

Proof

Let Si=xi+1 for i=0,1,2,3, E=x5, IA=x6, IS=x7. The transformed system becomes

x1˙=Λβ1x1x6c1x1.x2˙=α1x1β2x2x6c2x2.x3˙=α2x2β3x3x6c3x3.x4˙=α3x3ξx4.x5˙=(β1x1+β2x2+β3x3)x6c4x5.x6˙=γx5c5x6.x7˙=δ1x6c6x7. (35)

where c1=α1+ξc2=α2+ξ,c3=α3+ξ,c4=γ+ξ,c5=δ1+δ2+ξ,c6=σ1+σ2+ξ. The transmission rate of the non-vaccinated susceptible population is considered as the bifurcation parameter with the restriction R0=1. Hence we get

β1=c1c2c3c4c5γΛc3α1β2γΛα1α2β3γΛc2c3. (36)

The transformed system has the disease free equilibrium point P0=(x10,x20,x30,x40,x50,x60,x70), where x10=Λc1, x20=Λα1c1c2, x30=Λα1α2c1c2c3, x40=Λα1α2α3ξc1c2c3, x50=0, x60=0, x70=0. J(P0), provided in Eq. (13), is the linearisation matrix of the transformed system at P0. At β1=β1(R0=1), the jacobian of system (35) has one zero eigenvalue, while the other eigenvalues have a negative real part. As a result, the dynamics of the transformed system near β1=β1(R0=1) are studied using the central manifold theory [33]. The necessary calculations as per the central manifold theory [33] is as follows. W=(w1,w2,w3,w4,w5,w6,w7)T is the right eigenvector for J(P0) when R0=1 is computed using J(P0)W=0 and hence

w1=γΛ(c3α1β2+α1α2β3)c1c2c3c4c5c12c2c3c5w5,w2=α1(c1c2c3c4c5+γΛ(c1c3β2+c3α1β2+α1α2β3))c12c22c3c5w5,
w3=α1α2(c1c2c3c4c5+γΛ(c1c3β2+c3α1β2+c1c2β3+α1α2β3))c12c22c32c5w5,w6=γc5w5,w7=γδ1c5c6w5
w4=α1α2α3(c1c2c3c4c5+γΛ(c1c3β2+c3α1β2+c1c2β3+α1α2β3))ξc12c22c32c5w5.

V=(v1,v2,v3,v4,v5,v6,v7) is the left eigenvector of jacobian matrix J(P0) when R0=1 is computed using V.J(P0)=0 and hence we get, vi=0 for i=1,2,3,4,7, v6=c4γv5. Then, v5 is calculated to ensure that condition V.W=1 is met and hence v5=c5(c4+c5)w5 and v6=c4c5γ(c4+c5)w5. The bifurcation coefficients are given by

a=k,i,j=17vkwiwj2fk(P0,β1)xixj.b=k,i,j=17vkwi2fk(P0,β1)xiβ1. (37)

The following expressions give the bifurcation coefficients a and b after simplification

a=2w5(γΛc2c32c4c5α1β2+γΛc2c3c4c5α1α2β3γ2Λ2c3α1α2β2β3γ2Λ2c2α1α2β32c1c22c32c42c52γ2Λ2c32α1β22)Λc1c22c32c5(c4+c5). (38)
b=γΛc1(c4+c5)>0. (39)

As a result, when a<0, the system (1) at R0=1 experiences forward bifurcation. In forward bifurcation, when R0>1, an unstable disease-free equilibrium coexists with a stable endemic equilibrium point.  □

Fig. 2.

Fig. 2

Bifurcation plot showing the bifurcation point β1(R0=1)=0.29325 at which the forward bifurcation occurs with parameters values from the Table 5.

7. Analysis of sensitivity

A sensitivity study was performed on the system (1) to see how different factors affected OMICRON variant disease transmission in the Indian population. The parameters that have a substantial impact on the system (1)’s BRN are highlighted in this analysis. The health authorities can better manage the spread of the disease by analysing the parameters in relation to the BRN. Sensitivity analysis helps with experiment design, data assimilation, and reduction of complex non-linear models. The normalised forward sensitivity index of R0 that depends differentiably on a parameter m is defined as ΓmR0=R0mmR0. Here R0=γΛ(β1c2c3+β2α1c3+β3α1α2)c1c2c3c4c5, where c1=α1+ξ, c2=α2+ξ, c3=α3+ξ, c4=γ+ξ, c5=δ1+δ2+ξ. Then the sensitivity index of R0 that depends on various parameters of the system (1) is given as follows. ΓΛR0=1>0, Γβ1R0=0.64β10.204+0.64β1>0, Γβ2R0=0.48β20.444+0.48β2>0, Γβ3R0=0.3β30.528+0.3β3>0, ΓξR0=ξ(0.4482+ξ(3.3856+ξ(9.869+ξ(14.21+(10.3+3ξ)ξ))))0.063+ξ(0.6498+ξ(2.6846+ξ(5.739+ξ(6.73+ξ(4.1+ξ)))))<0, ΓγR0=0.3+2.46515×1016γ0.3+γ>0, Γδ1R0=δ11+δ1<0, Γδ2R0=δ21+δ2<0, Γα1R0=(0.829412+3.55271×1016α1)α1(0.3+α1)(1.12941+α1)<0, Γα2R0=(0.18+1.5099×1016α2)α2(0.3+α2)(0.48+α2)<0, Γα3R0=(0.0909091+2.74528×1016α3)α3(0.3+α3)(0.390909+α3)<0 .

From Fig. 4(B), the sensitivity index of β2, say Γβ2R0=Γβ2R0=0.48β20.444+0.48β2 is approximately 0.3 for β2=0.4. The physical meaning of this positive sensitivity index of β2 is that increasing (or decreasing) β2 by 10% increases (or decreases) R0 value by 3%. From Fig. 4(J), the sensitivity index of α3, say Γα3R0=(0.0909091+2.74528×1016α3)α3(0.3+α3)(0.390909+α3) is approximately −0.06 for α3=0.6. The physical meaning of this negative sensitivity index of α3 is that increasing (or decreasing) α3 by 10% decreases (or increases) R0 value by 0.6%. A highly sensitive parameter must be carefully estimated, as a very small variation in that parameter will result to large quantitative changes to the system (1).

Fig. 4.

Fig. 4

The plot of the sensitivity indices of R0 depends on (A) The disease transmission rate of non-vaccinated susceptible population β1, (B) The disease transmission rate of dose-1 vaccinated susceptible population β2, (C) The disease transmission rate of dose-2 vaccinated susceptible population β3, (D) δ1, the proportion of infected but asymptomatic individuals exposing symptoms, (E) The recovery rate of asymptomatic infected individuals from the disease δ2, (F) The rate of exposed individuals who are asymptomatic to the disease γ, (G) ξ, each population’s natural death rate, (H) The dose-1 vaccination rate α1 administered to non-vaccinated susceptible population, (I) The dose-2 vaccination rate α2 administered to dose-1 vaccinated susceptible population, (J) The booster dose vaccination rate α3 administered to dose-2 vaccinated susceptible population.

From Fig. 3(A), it is evident that the parameter with the most positive sensitivity index relative to R0 is β1, the infection transmission rate among the non-vaccinated susceptible population. The remaining parameters with positive sensitivity are β2,β3 and γ arranged from most sensitive to least sensitive positive index.

Fig. 3.

Fig. 3

Sensitivity index plot of (A) The parameters with positive sensitivity index, and (B) The parameters with negative sensitivity index.

From the Fig. 3(B), it is seen that the most sensitive parameter among the parameters with a negative sensitivity index is δ1, the proportion of the asymptomatic infected population who develop symptoms of the disease and δ2, the recovery rate of asymptomatic infected individuals. The remaining parameters with negative sensitivity are α1, α2 and α3 arranged from most sensitive to least sensitive negative index.

By examining R0’s sensitivity indices in relation to various parameters, it is reasonable to conclude that disease transmission rates β1, β2 and β3 with positive sensitivity indices should be minimised to keep the disease from spreading. Furthermore, vaccination administration rates, specifically α1, α2 and α3 with a negative sensitivity index, should be maximised to prevent the spread of the disease in society.

Solution trajectories for the infected populations, namely IA and IS, are plotted for distinct values of parameters with the same preliminary conditions to identify the sensitive parameters of the system (1). The parameters in the Table 1 with preliminary conditions S0(0)=10,S1(0)=9,S2(0)=8,S3(0)=7,E(0)=6,IA(0)=5,IS(0)=4 are used to numerically simulate system (1). For different values of the disease transmission rate, say β1=0.3, 0.5 and 0.7 of the non-vaccinated susceptible population, S0, the time series of infected human populations are plotted in Figs. 5(A) and 5(B), respectively. The figures clearly show that the number of infected cases in both populations increased as β1 levels increased. As a result, the disease transmission rate β1 among the non-vaccinated susceptible population is crucial to the disease’s spread.

Table 1.

Description of the model parameters.

Parameter Description
Λ The non-vaccinated susceptible population’s recruitment rate.
β1 Non-vaccinated susceptible population’s infection transmission rate.
β2 Disease transmission rate of dose-1 vaccinated susceptible population.
β3 The disease transmission rate of dose-2 vaccinated susceptible population.
α1 The rate of dose-1 vaccination given to non-vaccinated individuals.
α2 The rate of dose-2 vaccination given to dose-1 vaccinated individuals.
α3 The rate of booster dose vaccination given to dose-2 vaccinated individuals.
ξ The proportion of death in all populations.
γ The proportion of the exposed population who are infected without symptoms.
δ1 The proportion of the asymptomatic infected population who develop symptoms of the disease.
δ2 The recovery rate of asymptomatic infected individuals.
σ1 The recovery rate of symptomatic infected individuals.
σ2 The disease-induced death rate of symptomatic infected individuals.

Fig. 5.

Fig. 5

A plot of the infected populations IA and IS over time for β1=0.3,0.5,0.7.

Figs. 6(A) and 6(B) show time series of asymptomatic infected and symptomatic infected human populations for different values of the disease transmission rate among the dose-1 vaccinated susceptible population S1, such as β2=0.3, 0.5, and 0.7. The increase in β2 increases the number of infected cases in both populations, as seen in the figures. As a result, the disease transmission rate β2 within the dose-1 vaccinated susceptible group S1 is critical to the disease’s spread.

Table 2.

Sensitivity values of R0.

Parameters Λ β1 β2 β3 α1 α2 α3 ξ γ δ1 δ2
Sign of sensitivity index of R0

Fig. 6.

Fig. 6

A plot of the infected populations IA and IS over time for β2=0.3,0.5,0.7.

Figs. 7(A) and 7(B) show time series of asymptomatic infected and symptomatic infected human populations for different values of the disease transmission rate among the dose-2 vaccinated susceptible population S2, i.e., β3=0.3, 0.5, and 0.7. The figure shows that the total infected cases in the IA and IS populations do not change much when β3 increases. As a result, the disease does not spread rapidly among the susceptible population who have received both vaccine doses. This emphasises the importance of administering two doses to a susceptible population.

Fig. 7.

Fig. 7

A plot of the infected populations IA and IS over time for β3=0.3,0.5,0.7.

Figs. 8(A) and 8(B) show time series of asymptomatic infected and symptomatic infected human populations for different values of the dose-1 vaccination rate among the non-vaccinated susceptible population S0, such as α1=0.3, 0.5, and 0.7. The figures clearly show that when the dose-1 vaccination rate rises, the number of infected individuals in both populations drops. As a result, the dose-1 vaccination rate among the non-vaccinated susceptible population S0 is critical in limiting disease spread.

Fig. 8.

Fig. 8

A plot of the infected populations IA and IS over time for α1=0.3,0.5,0.7.

Figs. 9(A) and 9(B) show time series of asymptomatic and symptomatic infected human populations for distinct values of the dose-2 vaccination rate within the dose-1 vaccinated susceptible population S1, such as α2=0.3, 0.5, and 0.7. The rise in the dose-2 vaccination rate α2 reduces the number of infected cases in both populations, as seen in the figures. As a result, the dose-2 vaccination rate among the dose-1 vaccinated susceptible population S1 is critical in limiting disease spread.

Fig. 9.

Fig. 9

A plot of the infected populations IA and IS over time for α2=0.3,0.5,0.7.

Figs. 10(A) and 10(B) show time series of asymptomatic and symptomatic infected human populations for various values of the booster dose vaccination rate among the dose-2 vaccinated susceptible population S2, such as α3=0.01, 0.3, and 0.95. It is apparent from these data that are increasing the booster dose vaccination rate α3 in the dose-2 vaccinated susceptible population S2 reduces the number of infected cases in both the populations IA and IS. These results demonstrate the relevance of delivering the booster dose vaccine in addition to the dose-2 vaccination among S2.

Fig. 10.

Fig. 10

A plot of the infected populations IA and IS over time for α3=0.01,0.3,0.95.

Figs. 11(A) and 11(B) show the time series of asymptomatic infected and symptomatic infected human populations for various values of the parameters, δ1= 0.3, 0.5, 0.7 and δ2=0.3, 0.5, 0.7, respectively. The asymptomatic infected population IA drops steadily whenever the rate of infected individuals showing signs of the disease δ1 increases, as shown in Fig. 11(A), and hence, disease spread is minimised. Fig. 11(A) emphasises the need to employ suitable testing methods to detect asymptomatic infected persons. The symptomatic infected population IS is steadily reduced as the rate of infected persons without symptoms recovered from the disease δ2 increases, as shown in Fig. 11(B).

Fig. 11.

Fig. 11

A plot of the infected populations IA and IS over time for δ1=0.3,0.5,0.7 and δ2=0.3,0.5,0.7 respectively.

8. Parameter estimation

The following values of parameters are used to analyse the effect of the OMICRON variant virus in India using our proposed mathematical model. The following approach is employed to estimate some parameter values and the preliminary values of eight populations. According to the most recent WHO data published in 2018 [10], males have a life expectancy of 67.4 years, and females have a life expectancy of 70.3 years, for a total life expectancy of 68.8 years. As a result, each population’s natural mortality rate ξ is estimated to be 1365×68.8=0.00004 deaths per day. According to UNICEF [11], there are approximately 70000 births per day in India. Therefore the recruitment rate Λ is assumed as 70,000 births per day. The values of the parameters α1, α2, and α3 are determined based on the vaccination administration speed, whereas β1, β2, and β3 are chosen hypothetically and adjusted using the least square approach to fit our model with accurate data. The incubation period for COVID-19 disease caused by the Omicron variant virus is 2 to 4 days [12]. As a result, we assume that our model’s incubation time is three days, resulting in the value of the γ=13=0.33 exposed individuals infected every day. Patients with COVID-19 caused by an omicron variant usually recover after five days [13]. As a result, δ2 is considered 15=0.2 infected persons recovering per day. To fit our model with actual data, the parameters δ1, σ1, and σ2 are set hypothetically and changed using the least square approach.

9. Numerical analysis

This section carried out simulation tests to verify the analytically derived results. The proposed OMICRON model (1) has been subjected to simulations portraying local and global stability. The parameter values are taken from the Table 4, Table 5, respectively, for R0<1 and R0>1.

Table 4.

Parameter values for constructing Fig. 12.

Parameters Λ β1 β2 β3 α1 α2 α3 ξ γ δ1 δ2 σ1 σ2
Values 3 0.6 0.3 0.2 0.6 0.5 0.5 0.3 0.3 0.7 0.7 0.3 0.4

Table 5.

Parameter values for constructing Fig. 13.

Parameters Λ β1 β2 β3 α1 α2 α3 ξ γ δ1 δ2 σ1 σ2
Values 5 0.6 0.3 0.2 0.6 0.5 0.5 0.3 0.3 0.7 0.7 0.3 0.4

The DFE point P0(S00,S10,S20,S30,E0,IA0,IS0)’s global and local stability has been numerically simulated and depicted in Fig. 12. The disease free equilibrium is found to be P0(3.33, 2.5, 1.5625, 2.60417, 0, 0, 0) and R0=0.9<1 using the parameter values from Table 4. Hence for various initial conditions on the state variables near the equilibrium point P0, it is seen from the Fig. 12(A) that limtS0(t)=S00=3.33, limtS1(t)=S10=2.5, limtS2(t)=S20=1.5625, limtS3(t)=S30=2.60417, limtE(t)=E0=0, limtIA(t)=IA0=0 and limtIS(t)=IS0=0. From Fig. 12(C), it is seen that the populations S0(t) and IA(t) converge to S00=3.3 and IA0=0 respectively as t for initial points of state variables near P0. Similarly from Figs. 12(D), 12(E), 12(F), 12(G) and 12(H), it is seen that the state variables (S0(t),IS(t))(S00,IS0)=(3.33,0), (S1(t),IA(t))(S10,IA0)=(2.5,0), (S2(t),IA(t))(S20,IA0)=(1.5625,0), (S1(t),IS(t))(S10,IS0)=(2.5,0) and (S2(t),IS(t))(S20,IS0)=(1.5625,0) as t respectively whenever the initial populations are chosen near P0. As stated in Theorem 3, the local stability of P0 whenever R0<1 is verified. From figure Fig. 12(B), it is noticed that for any initial conditions on the state variables S0(t), IA(t) and IS(t) in Δ1, the solution trajectories (S0(t),IA(t),IS(t)) (S00,IA0,IS0)=(3.33,0,0) as t. This convergence can be verified for all possible ordered triples out of the seven state variables. As stated in Theorem 5, P0 is GAS in Δ1 whenever R0<1 is verified.

Fig. 12.

Fig. 12

(A) The local stability of P0 of the omicron model (1) for R0<1, (B) Global stability of disease free equilibrium shown in S0IAIS phase space for R0<1, (C) Susceptible population without vaccination (S0) against infected & asymptomatic population (IA) over time ‘t’ for R0<1, (D) Susceptible population without vaccination (S0) against infected & symptomatic population (IS) over time ‘t’ for R0<1, (E) Susceptible population & vaccinated with dose-1 (S1) against infected & asymptomatic population (IA) over time ‘t’ for R0<1, (F) Susceptible population & vaccinated with dose-2 (S2) against infected & asymptomatic population (IA) over time ‘t’ for R0<1, (G) Susceptible population & vaccinated with dose-1 (S1) against infected & symptomatic population (IS) over time ‘t’ for R0<1 and (H) Susceptible population & vaccinated with dose-2 (S2) against infected & symptomatic population (IS) over time ‘t’ for R0<1.

The global and local stability of the endemic equilibrium P1(S0,S1,S2,S3,E,IA,IS) has been numerically simulated and portrayed in the Fig. 13. The endemic equilibrium point is found to be P1(3.9933, 2.45477, 1.33795, 2.229917, 3.32537, 0.58683, 0.410781) and R0=1.5>1 using the parameter values from Table 5. Hence for various initial conditions on the state variables near the equilibrium point P1, it is seen from the Fig. 13(A) that limtS0(t)=S0=3.9933, limtS1(t)=S1=2.45477, limtS2(t)=S2=1.33795, limtS3(t)=S3=2.229917, limtE(t)=E=3.32537, limtIA(t)=IA=0.58683 and limtIS(t)=IS=0.410781. From Fig. 13(C), it is seen that the populations S0(t) and IA(t) converges to S0=3.9933 and IA=0.58683 respectively as t for initial points of state variable near P1. Similarly from the Figs. 13(D), 13(E), 13(F), 13(G) and 13(H) it is seen that the state variables (S0(t),IS(t))(S0,IS)=(3.9933,0.410781), (S1(t),IA(t))(S1,IA)=(2.45477,0.58683), (S2(t),IA(t))(S2,IA)=(1.33795,0.58683), (S1(t),IS(t))(S1,IS)=(2.45477,0.410781) and (S2(t),IS(t))(S2,IS)=(1.33795,0.410781) as t respectively whenever the initial populations are chosen near P1. Further the necessary and sufficient conditions stated in the Theorem 6, say |H1|=B1=5.44551>0, |H2|=48.2477>0, |H3|=336.786>0, |H4|=902.45>0 and |H5|=355.561>0 with B1=5.44551>0, B2=10.5008>0, B3=8.93463>0, B4=3.25204>0, B5=0.393995>0, are satisfied. As stated in Theorem 6, the LAS of the point P1 is verified whenever R0>1. From Fig. 13(B), it is noticed that for any initial conditions on the state variables S0(t), IA(t) and IS(t) in Δ, the solution trajectories (S0(t),IA(t),IS(t)) (S0,IA,IS)=(3.9933,0.58683,0.410781) as t. This convergence can be verified for all possible ordered triples out of the seven state variables. As stated in Theorem 7, it is verified that P1 is GAS in Δ when R0>1.

Fig. 13.

Fig. 13

(A) The LAS of P1 of the omicron system (1) for R0>1, (B) GAS of P1 shown in S0IAIS phase plane for R0>1, (C) Susceptible population without vaccination (S0) against infected & asymptomatic population (IA) over time ‘t’ for R0>1, (D) Susceptible population without vaccination (S0) against infected & symptomatic population (IS) over time ‘t’ for R0>1, (E) Susceptible population & vaccinated with dose-1 (S1) against infected & asymptomatic population (IA) over time ‘t’ for R0>1, (F) Susceptible population & vaccinated with dose-2 (S2) against infected & asymptomatic population (IA), (G) Susceptible population & vaccinated with dose-1 (S1) against infected & symptomatic population (IS) over time ‘t’ for R0>1 and (H) Susceptible population & vaccinated with dose-2 (S2) against infected & symptomatic population (IS) over time ‘t’ for R0>1.

According to WHO data as of December 28th, 2021, the initial susceptible vaccination populations of dose-1 and dose-2 and active OMICRON-infected populations are assumed to be S1=254121172, S2=585974301, IS=80621, respectively. The remaining initial populations are hypothetically chosen for numerical simulation as follows: S0=520000000, S3=10000, E=15000000, IA=15000000, and R=5000. Table 6 summarises the real-time symptomatic infected populations from 29th December 2021 to 20th February 2022.

Fig. 14.

Fig. 14

The BRN R0 plotted against (a) dose-1 vaccination rate α1, (b) dose-2 vaccination rate α2, (c) booster dose vaccination rate α3, (d) disease transmission rate of non-vaccinated population β1, (e) disease transmission rate of dose-1 vaccinated population β2, (f) disease transmission rate of dose-2 vaccinated population β3, (g) rate of exposed population who are asymptomatic γ, (h) rate of asymptomatic infected population become symptomatic to disease δ1, (j) rate of asymptomatic infected population getting recovered δ2.

Table 6.

Real confirmed COVID-19 infected cases in the Indian population.

Date 29-12-2021 30-12-2021 31-12-2021 1-1-2022 2-1-2022 3-1-2022
Active cases 86158 95214 109995 130000 152690 179098

Date 4-1-2022 5-1-2022 6-1-2022 7-1-2022 8-1-2022 9-1-2022
Active cases 210261 280409 300000 468419 586858 720580

Date 10-1-2022 11-1-2022 12-1-2022 13-1-2022 14-1-2022 15-1-2022
Active cases 835000 951560 1113769 1268309 1414025 1500000

Date 16-1-2022 17-1-2022 18-1-2022 19-1-2022 20-1-2022 21-1-2022
Active cases 1652538 1732831 1827199 1920244 2000000 2109548

Date 22-1-2022 23-1-2022 24-1-2022 25-1-2022 26-1-2022 27-1-2022
Active cases 2183398 2245489 2233040 2200000 2198632 2101766

Date 28-1-2022 29-1-2022 30-1-2022 31-1-2022 1-2-2022 2-2-2022
Active cases 2000490 1881088 1800000 1739187 1617723 1530050

Date 3-2-2022 4-2-2022 5-2-2022 6-2-2022 7-2-2022 8-2-2022
Active cases 1400000 1327735 1221091 1105009 990968 900000

Date 9-2-2022 10-2-2022 11-2-2022 12-2-2022 13-2-2022 14-2-2022
Active cases 786833 693839 606474 533102 450000 419148

Date 15-2-2022 16-2-2022 17-2-2022 18-2-2022 19-2-2022 20-2-2022
Active cases 366256 328933 288099 250000 220186 198128

The infected population IS of the model (1) fits well with the real confirmed infected cases in India from the Table 6 with the parameter values estimated as in the Table 3, as shown in Fig. 15(b).

Table 3.

Parameter values with assumed and real field values used in constructing the Fig. 14, Fig. 15, Fig. 16, Fig. 17.

Parameters Values Source
Λ 70000 [11]
α1 0.0085 assumed
α2 0.012 assumed
α3 0.0001 assumed
β1 2×1010 assumed
β2 2×1010 assumed
β3 1×109 assumed
γ 0.33 [12]
δ1 0.0012 assumed
δ2 0.2 [13]
σ1 0.1 assumed
σ2 0.00001 assumed
ξ 0.00004 [10]

Fig. 15.

Fig. 15

Fitted with real data from Table 6 and values of parameters from Table 3, plot of (a) asymptomatic infected populations (IA) and (b) symptomatic infected populations (IS) against time t.

The infected populations IA and IS of the model (1) decrease when the booster dose vaccination rate α3 increases, as shown in Figs. 16(a) and 16(b). The asymptomatic infected population IA and the symptomatic infected population IS steadily increase when the disease transmission rate β3 among dose-2 vaccinated individuals increases, as shown in Figs. 16(c) and 16(d).

Fig. 16.

Fig. 16

A plot of the infected populations IA and IS over time various values of the booster dose vaccination rate α3 among the dose-2 vaccinated susceptible population S2 and disease transmission rate β3 of dose-2 vaccinated susceptible population S2.

From Figs. 17(a) and 17(b), it is seen that the populations IA and IS of the model (1) increase when the infection rate γ of the exposed individuals E increases. From Figs. 17(c) and 17(d), it is seen that the infected populations IA and IS of the model (1) are reduced when the rate of recovery δ2 of the IA population increases. Therefore, rapid recovery of the IA population from the disease is crucial to reducing the rapid spread of the disease.

Fig. 17.

Fig. 17

For different values of the infection rate γ and the recovered rate from the disease of asymptomatic infected persons δ2, a time-series graph of asymptomatic infected and symptomatic infected populations is shown.

10. Conclusion

A COVID-19 mathematical model was developed for studying the disease transmission dynamics in India when a vaccination program is underway and the omicron variant of the coronavirus is dominant. According to the research, the Omicron system (1)’s DFE is LAS when the basic reproduction number is below one but unstable otherwise. The stability of the equilibrium points was tested after the basic reproduction number, R0, was computed. The system (1) exhibits forward bifurcation at R0=1 when a<0 (38). The sensitivity parameters were calculated using the notion of normalised forward sensitivity. The time-series graphs for various populations with assumed parameter values are created in the numerical analysis section to validate the results of the stability theorems. Different model parameters are determined based on current omicron variant transmission among various susceptible populations, divided into groups based on vaccination dosage. The estimated values are used to examine variations in the value of the threshold parameter, R0, to the model’s most essential parameters. The sensitivity analysis is performed, and the most sensitive parameters are identified. The numerical experiments are carried out using estimated parameter values for real infected cases in the Indian population during the omicron variant virus transmission and vaccination drive in India, and it is found that the model (1)’s symptomatic infected population matches the real infected data well. Finally, some of the key estimated parameters are examined using time series graphs of the model (1)’s infected populations. In future research, we will look at this model with a non-human reservoir compartment for the omicron virus, investigate its dynamics, and compare the results to real-world data.

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