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Mathematical modeling and computational analysis of hepatitis B virus transmission using the higher-order Galerkin scheme

  • Attaullah , Salah Boulaaras EMAIL logo , Aasim Ullah Jan , Tahir Hassan and Taha Radwan
Published/Copyright: November 18, 2024
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Abstract

Hepatitis B, a liver disease caused by the hepatitis B virus (HBV), poses a significant public health burden. The virus spreads through the exchange of bodily fluids between infected and susceptible individuals. Hepatitis B is a complex health challenge for individuals. In this research, we propose a nonlinear HBV mathematical model comprising seven compartments: susceptible, latent, acutely infected, chronically infected, carrier, recovered, and vaccinated individuals. Our model investigates the dynamics of HBV transmission and the impact of vaccination on disease control. Using the next-generation matrix approach, we derive the basic reproduction number R 0 and determine the disease-free equilibrium points. We establish the global and local stability of the model using the Lyapunov function. The model is numerically solved using the higher-order Galerkin time discretization technique, and a comprehensive sensitivity analysis is carried out to investigate the impact of all physical parameters involved in the proposed nonlinear HBV mathematical model. A comparison was made of the accuracy and dependability with the findings produced using the Runge–Kutta fourth-order (RK4) approach. The findings highlight the critical need for vaccination, particularly among the exposed class, to facilitate rapid recovery and mitigate the spread of HBV. The results of this study provide valuable insights for public health policymakers and inform strategies for hepatitis B control and elimination.

1 Introduction

Hepatitis B, a severe and potentially fatal viral infection of the liver, represents a considerable challenge to global health. The hepatitis B virus (HBV) is the primary cause for this disease, which can result in both acute and chronic liver damage, leading to significant morbidity and mortality. HBV transmission predominantly occurs through the exchange of bodily fluids, such as blood, semen, and vaginal secretions, with adults generally encountering a self-limiting infection. However, a considerable number of individuals may progress to chronic hepatitis B, potentially resulting in liver cirrhosis, hepatocellular carcinoma, and various other serious complications. The precision of HBV diagnosis and screening is critical for identifying individuals with acute or chronic infections, as well as facilitating prompt interventions and preventive measures. Mathematical modeling is utilized as a fundamental tool for elucidating the dynamics and attributes of diverse diseases. Numerous groups of researchers have constructed models for various diseases, including human immunodeficiency virus (HIV) infection, hepatitis B, cancer, and infectious diseases, facilitating more comprehensive comprehension, prediction, and management of their dissemination and effects. Yavuz et al. [1] introduced a novel fractional model that explained the behaviors of the HBV. The study involved the modeling, equilibria, stabilities, and the analysis of existence and uniqueness pertaining to the model, which was afterward solved numerically employing the Adams–Bashforth scheme. Mustapha et al. [2] developed a systematic deterministic mathematical model that illustrates the transmission dynamics of HBV. The model parameters were estimated utilizing actual data from South Africa through the application of the nonlinear least-squares curve fitting method. The numerical analysis conducted confirmed that minimizing the transition of chronically infected children to adulthood through treatment is essential for the eradication of hepatitis B in South Africa. Naik et al. [3] carried out an investigation into the global dynamics of a fractional-order model for the hepatitis C virus (HCV), incorporating an effective treatment strategy. The model’s fixed points were identified, followed by a comprehensive stability analysis. The fractional Adams method was employed in obtaining the numerical solutions of the model. In the end, they validated the numerical simulations compared to the theoretical and numerical results. Din and Abidin [4] performed an investigation into a recently developed model for hepatitis B infection, utilizing the Atangana–Baleanu–Caputo fractional order derivative. The Ulam–Hyers-type stability was achieved, along with a qualitative analysis of the corresponding solution, through the application of a well-established principle from fixed point theory. The results obtained have been verified by numerical verification through MATLAB. Bolaji et al. [5] implemented a deterministic compartmental co-infection model to elucidate the effects of tuberculosis (TB) infection on the co-infection dynamics of the two diseases, particularly in environments where treatment for TB is readily accessible. The four-dimensional systems of ordinary differential equations (ODEs) constructed by Joshi et al. [6] quantify the impact of burnt and recycled plastic on air pollution. The well-posedness and qualitative features were explored. The plastic waste model’s reproduction number and local/global stability were thoroughly examined. Naik et al. [7] conducted a thorough investigation and analysis of the fractional-order epidemic model concerning the mutual influence in HIV/HCV co-infection. Farman et al. [8] explored an unconditionally convergent semi-analytical method utilizing recent evolutionary computational techniques, alongside evolutionary Padé approximation (EPA), for addressing the complexities of a nonlinear hepatitis B model. Naik et al. [9] performed an analysis of a fractal-fractional operator within the context of an epidemic model, specifically pertaining to COVID-19 modeling, and examined the variations in the infection rate across society. Attaullah et al. [10] formulated a higher-order Galerkin time discretization and conducted numerical comparisons for two models of HIV infection. In order to substantiate the findings, the model was assessed through the application of the Runge–Kutta fourth-order (RK4) method. Furthermore, they examined the impact of diverse physical attributes by altering their values and analyzing them through graphical representations. Jan et al. [11] developed a model for the dynamics of asthma, incorporating smoking and environmental factors within the fractional Caputo–Fabrizio (CF) framework to elucidate its dynamic behavior. Attaullah et al. [12] examined the dynamical behavior of HIV infection, incorporating the influence of a variable source term via the Galerkin method, and elucidated the characteristics of HIV infection. HBV remains a pressing global health challenge, prompting researchers to investigate treatment responses and identify susceptibility factors to inform prevention and intervention strategies. Several researchers looked at how well hepatitis B patients responded to treatment and tried to figure out who was most likely to get infected. They put a lot of effort into making a mathematical model to help them understand how HBV spreads. They attempted to enhance the existing knowledge of hepatitis B by providing detailed mathematical frameworks that illustrate the disease’s transmission dynamics, guide public health policy, and refine treatment approaches. They discussed comprehension of the intricate relationships among HBV transmission, host immunity, and treatment outcomes, thereby addressing a critical public health challenge and enhancing patient outcomes. Mohideen and Lakshmi [13] presented a stochastic gradient algorithm to find the co-connection and to find the resulting accuracy of acute as well as chronic prediction of patients. Din et al. [14] developed a model of HBV under computational fluid dynamics and used domain polynomials to find out the numerical results of the proposed model. Reza et al. [15] suggested the dynamics of patients with HBV vaccination and treatments. The spread of the disease may be reduced by vaccination and spreading awareness. Shang and Kao [16] discussed and summarized the relevant issues of HBV. Nana et al. [17] focused on the treatment model of liver disease and critically investigated the dynamics of the proposed model. Okosun et al. [18] investigated the dynamics of local as well as global stability of HBV by using the Lyapunov function. Lashari et al. [19] investigated direct and indirect transmissions by using the backward bifurcation technique. Forde et al. [20] presented an optimal control strategy for controlling the immunity response against the HBV and showed that high vaccination induces immunity to control the infection. Ntaganda et al. [21] used the fuzzy logic strategy for hepatitis B by applying an optimal control technique and considering infants up to the age of 12 months. Zhang et al. [22] suggested a model for the transmission of HBV in high endemic areas with vertical transmission. Global stability for the HBV model was derived via the Lyapunov function. Anna and Susanna [23] summarized the HBV therapies with limitations, novel approaches and therapeutic points for the cure of HBV. Van den et al. [24] demonstrated the basic reproduction number R 0 for compartmental transmission of infection. Zou et al. [25] proposed a mathematical model to prevail hepatitis B transmission in China by taking R 0 = 2.406 . Reza et al. [26] discussed the vaccination and treatment for the hepatitis B dynamical infection. A R 0 was also derived and analyzed for the infection-free steady state. Hews et al. [27] considered the model as explicit time delay in the production of HBV by providing the lamivudine therapy which showed best agreement with clinical data. Ntaganda [28] presented the HBV dynamics control problem by using Pontryagin’s maximum principle as well as a direct approach. Armbruster and Brandeau [29] evaluated the effect and cost of the chronic infection for different screening levels and contact tracing. Hattaf et al. [30] aimed at the usage of optimal control for the system of the ODE model of hepatitis B disease. Optimal control was derived by using Pontryagin’s maximum principle. Ntaganda and Gahamanyi [31] employed the fuzzy logic technique to determine the optimal control solution. A numerical comparison was derived through the direct method. Bhattacharyya and Ghosh [32] suggested that hepatitis B infection vaccination and antiviral treatment are necessary to be in a proper ratio to take control of HBV. Li et al. [33] discussed the infection for both vertical and horizontal transmission of hepatitis B for the host population and the basic reproduction number R 0 for the vertical transmission. Zou et al. [34] proposed that immunization is very necessary to control the HBV infection, especially for those who are at high risk of this infection. Haq et al. [35] focused on vector-borne diseases by the direct method taking the population as constant. Haq et al. [36] studied the approximate solution with the help of Laplace transformation and used the RK-4 method to find the numerical solution of the proposed model. Pang et al. [37] presented the susceptible infectious removed (SIR) epidemic model by considering the effects of vaccination to control the infection of the HBV. Liu et al. [38] discussed the SIR model with a nonlinear incidence rate and used the Lyapunov function to derive global stability. Zaman et al. [39] used the RK-4 method to find the numerical solution for the proposed model for HBV. Zeb et al. [40] presented the smoking model by using the non-standard finite difference method. RK-4 and ODE45 were used to find out the numerical results. Rahman et al. [41] showed global stability at different equilibrium points, and the numerical solutions were shown graphically. Zaman et al. [42] proposed an optimal control technique to study infected individuals, and the dynamical behavior of HBV R 0 was derived. Khan and Zaman [43] presented Lyapunov function theory to derive global stability. The basic reproduction number R 0 was derived via the next-generation matrix method.

The effective technique for examining the dynamics of various diseases as they arise in real-world situations is mathematical modeling. Various extensively utilized models have been implemented by biologists and mathematicians to understand the dynamics of how infectious diseases propagate through populations. Mathematical modeling serves as a highly versatile technique, yielding insightful findings pertinent to the realm of health care. The following points outline the primary aims of the research:

  1. Establish a novel mathematical model for HBV with vaccination and treatment rate. The model is solved using higher-order Galerkin Scheme.

  2. To find the basic reproduction number R 0 by implementing the next-generation matrix approach.

  3. To find the model stability by using the Lyapunov function.

  4. To discuss the local and global stability to assess the most sensitive parameters of disease transmission.

  5. In order to confirm the validity and accuracy of the proposed scheme, the model is solved using the classical RK and compared the results obtained from both schemes.

2 Proposed mathematical model for HBV infection

In this section, the HBV mathematical model is considered. We divide the system into seven compartments, i.e., susceptible individuals denoted by S ( t ) , exposed individuals termed L ( t ) , people with acute infection identified by A ( t ) , individuals with chronic HBV infection represented by B(t), carriers of HBV infection denoted by C(t), recovered population characterized as R ( t ) , and lastly the vaccinated individuals represented by V ( t ) . The parameters used in the presented model are as follows: Λ represents the birth rate, ψ represents the carrier transmission rate of HBV, γ 1 demonstrates rate of increase from acute to chronic, γ 2 is the rate at which individuals move to recovery from the carrier class, d 0 and d 1 represent the biological and provoked risks of mortality from hepatitis, respectively, while a describes the rate at which people shifts from latent to acute class, η represents the rate of vertically infected individuals, ξ represents the fraction of effectively immunization, and β represents the transmission rate of HBV infection. The graphical representation of the proposed model is given in Figure 1. The proposed model is as follows (Table 1):

S ̇ = Λ ξ ( 1 η C ) T + ζ V β S A T δ β S B T ψ β S C T ( d 0 + υ ) S ,

L ̇ = β S A T + δ β S B T + ψ β S C T ( d 0 + α ) L ,

A ̇ = α L ( d 0 + γ 1 + φ 1 ) A ,

(1) B ̇ = γ 1 A ( d 0 + d 1 + φ 2 ) B ,  

C ̇ = Λ ξ η C T ( d 0 + φ 3 ) C ,

R ̇ = φ 1 A + φ 2 B + φ 3 C d 0 R ,

V ̇ = Λ ( 1 ξ ) T + v S ( d 0 + ζ ) V ,

and the initial conditions are given as

Figure 1 
               Pictorial representation of the proposed model.
Figure 1

Pictorial representation of the proposed model.

Table 1

Parameters involved in the proposed HBV infection model (cited from the study of Khan and Zaman [43])

Notations Meaning Values
Λ Birth rate 0.00219
β Disease spread rate 0.04
ψ Carrier infection rate 0.02
φ 1 Acute recovery rate 0.01
φ 2 Chronic recovery rate 0.02
φ 3 Carrier recovery rate 0.14
γ 1 Rate of change from acute to chronic 0.33
λ Carrier vaccination rate 0.02
d 0 Natural death rate 0.03
d 1 Death rate due to chronic infection 0.02
η Rate of vertically infected individuals 0.33
α Latent to acute class transmission rate 0.09
ξ Newborn without effective immunization 0.20

S 0 , L 0 , A 0 , B 0 , C 0 , R 0 , V 0 .

3 Continuous Galerkin Petrov method for the HBV model

In this section, we implement the Galerkin scheme, particularly the cGP(2) scheme (see previous studies [44,45,46,47,48,49,50,51,52,53] for detailed information) to tackle numerically the system of ODEs that mathematically characterize the aforementioned model. By implementing the standard form of the ODEs, we implement the Galerkin scheme to approximate the solutions, leading to a thorough examination of the model’s dynamics and behavior. Let us suppose

ρ 1 ( t ) = S ( t ) , ρ 2 ( t ) = L ( t ) , ρ 3 ( t ) = A ( t ) , ρ 4 ( t ) = B ( t ) , ρ 5 ( t ) = C ( t ) , ρ 6 ( t ) = R ( t ) , ρ 7 ( t ) = V ( t ) ,

initially at time t = 0.

ρ 1 ( 0 ) = S ( 0 ) , ρ 2 ( 0 ) = L ( 0 ) , ρ 3 ( 0 ) = A ( 0 ) , ρ 4 ( 0 ) = B ( 0 ) ,

ρ 5 ( 0 ) = C ( 0 ) , ρ 6 ( 0 ) = R ( 0 ) , ρ 7 ( 0 ) = V ( 0 ) .

For ϱ : K = [ P , Q ] S & K = [ P , Q ] function for positive t > 0 ,

d t ρ ( t ) = ε ( t , ρ ( t ) ) t K = [ P , Q ] ρ ( 0 ) = ρ 0 ,

where d h ρ ( h ) is the time derivative. ρ ( t ) = ( ρ 1 ( t ) , ρ 2 ( t ) , ρ 3 ( t ) , ρ 4 ( t ) , ρ 5 ( t ) , ρ 6 ( t ) , ρ 7 ( t ) ) S at time t = 0, and ε = ( ε 1 , ε 2 , ε 3 , ε 4 , ε 5 , ε 6 , ε 7 ) is non-linear defined as ε : K ×   S S .   S

The formulation of problem of (3.12) is as follows: find ρ X such that ρ ( 0 ) = ρ 0 and

(2) F d t ρ ( t ) , ϑ ( t ) d t = F ε t , ϑ ( t ) d t for all ϑ Y ,

in which X′ suggests the optimal solutions, Y′ serves for experiment, when F = [ P , Q ] describes its time. Assuming the domain E ( F , S ) = E O ( J , S ) as the space of linear equations ρ : F S interconnect with the norm to explain the operation t ρ ( t ) .

Square the integral function Ł 2 ( F   , S ) discontinuous functions manifested as

Ł 2 ( F , S ) = { ρ : [ 0 , S ] S : ρ Ł 2 ( F , S )   < }

ρ Ł 2 ( F , S )   = F ρ ( t ) S 2 d t 1 2 .

So, attempting to discretize the Galerkin time, we prevalently partition the period interval J into N subphases. F n = [ t n 1 , t ] , where n = 1 , 2 , 3 , N , and 0 = t 0 < t 1 < . t N 1 < t n = S . The time linearization component is given the symbol, and so the extreme time will just be illustrated with this sign τ = max 1 n N τ n , where τ n = t n t n 1 time intervals of J n . Now, we will estimate the continuous answer off a function a τ : F S , which is piecewise polynomial of a certain order w.r.t. time. Then,

  X   τ l = { a E ( F S ) : ρ | J n H l ( F n , S ) for all F n G τ } ,

where H l ( F n , S ) = { ρ : F n S , ρ ( t ) = j = 0 l U j t j , for all t F n , U j S , f } , and the Y τ k , get

  Y τ l = { S Ł 2 ( F , S ) : S | F n H l 1 ( F n , S )   F n G τ } ,

with ρ τ   X τ l , i.e., ρ τ ( 0 ) = 0

(3) f d t ρ τ ( t ) , ϑ τ   ( t ) d t = f ε ( h , ρ τ ( t ) ) , ϑ τ   ( t ) d t ϑ τ   Y τ l .

As the discrete test space, Y τ l is discontinuous and complicated and can be solved in a time marching operation where successively local problems on the time intervals are resolved. So, we go for the test function

f n d t ρ τ ( t ) , ϑ ψ ( t ) d t = f n ε ( t , ρ τ ( t ) ) , ϑ ψ ( t ) d t ϑ V and ψ H ( F n ) .

Similarly, for the cGP(k) method:

ρ | F n H l ( F n , S ) ,

i.e.,

ρ τ ρ τ ( t n 1 ) = υ n 1 ,

(4) k = 0 l w j d t ρ τ ( t n , j ) ψ ( t n , j ) = k = 0 l w j ε ( t n , j , ρ τ ( t n , j ) ) ψ ( t n , j )  ψ H k 1 ( F n ) .

For estimating ρ τ | t n , replace

ρ τ ( t ) = j = 0 l U n j ϑ n , j ( t ) t F n ,

where other components of S and another real-valued mechanism comprising their weighting U n j . The Lagrange partial derivatives t n , j F n meet the conditions having ( l + 1 ) adequate nodal positions.

ϑ n , j ( t n , j ) = Δ i , j for i , = 0 , 1 , 2 , l . and j = 0 , 1 , 2 , l .

Δ i , j , Kronecker delta is given by

(5) Δ i , j = one : i = j zero : i j ,

let t n , 0 = t n 1 , stands for the equation’s fundamental assumptions, i.e.,

U n 0 = ρ | F n ( t n 1 ) , if n 2 ,

U n 0 = ρ 0 , if n = 1 .

The points t n , 1 , t n , 2 , , t t n , l are being taken from the GauB -Lobatto formula at F n interval for d t ρ τ , having

(6) d t ρ τ = k = 0 l U n j ϑ n , j ( t ) , for all t F n .

Thus, we have

F n d t ρ τ ( t ) , ϑ ψ ( t ) d t = F j = 0 l U n j , ϑ ϑ j ( t ) ψ ( t ) d t .

In a straight forward manner, we arrive at the following

(7) F n d t ρ τ ( t ) , ϑ ψ ( t ) d t = j = 0 l U n j , ϑ ,

with the basic ϑ n , j H k ( F n ) function having

(8) ρ n : k F n , with k = [ 1 , 1 ] ρ n t ˆ = t n + t n 1 2 + τ n 2 t ˆ F n t ˆ k , n = from 1 to N .

Designate basic functions having

ϑ ˆ j ( t ˆ i ) = Δ i , j , i , j = 0 , 1 , 2 , , l .

Now, defining basic real J n the time interval by

ϑ n , j t = ϑ ˆ j ( t ) with t ˆ = α n 1 ( t ) = 2 τ n t + t n 1 t n 2 k .

In a similar fashion, we create the most appropriate comparative wavelet coefficients for the sample basic functions   φ n , i , i.e., ψ ˆ i H l 1 ( k ) ,

(9) ψ n , i ( t ) = ψ ˆ i ( ρ n 1 ( t ) t F n

By using the Galerkin method, we get φ H l 1 and ϑ S ,

J ˆ n j = 0 l U n j , ϑ ˆ j ( t ˆ ) ψ ˆ ( t ) d t ˆ = τ n 2 J ˆ n ε ρ n ( t ˆ ) , j = 0 l U n j ( t ) , ϑ ψ ˆ ( t ˆ ) d t ˆ ϑ S .

This implies that

(10) μ = 0 l ρ μ ^ j = 0 l U n j , ϑ ϕ ˆ j ( t ˆ μ ψ ˆ ( t ˆ μ ) = τ n 2 μ = 0 l   ρ μ ^ ε ρ n t ˆ μ , j = 0 l U n j ( t μ ) , ϑ ψ ˆ ( t ˆ μ ) .

Here, α μ ^ are the weights and t ˆ μ [ 1 , 1 ] are the integration prong with t ˆ 0 = 1 and t ˆ l = 1

(11) ψ ˆ i ( t ˆ μ ) = ( ρ μ ^ ) 1 δ i , μ   .

Let J ˆ n be cGP(k), and undetermined U n j S j = 1 , 2 , 3 , , l , thus

(12) j = 0 l ρ ˆ i , j U n j = t n 2 { ε ( t n , i , U n j ) + α i ε ( t n , 0 , U n 0 ) } .

For U n 0 = U n 1 l and n greater than 1 and U 1 0 = ρ 0 for n equal to 1, with z i , j

(13) ψ ¯ i , j = ϑ ˆ j ( t ˆ μ ) + α i ϑ ˆ j ( t ˆ μ ) , t n , μ = ρ n ( t ˆ μ ) and α i = ρ 0 ^ ψ ˆ i ( t ˆ μ ) .

Once we have broken this system, the initial value is set for the current time interval

J ˆ n + 1 to U n + 1 0 = U n l .

cGP (1) Method:

According to GauB -Lobatto two-point formulae,

t n , 0 = t n 1 , h n , 1 = t n & ρ 0 ^ = ρ 1 ^ = 1 ,

ψ ˆ 0 ( t ˆ ) = 01 , can have sign U n 1 = ρ τ ( t n ) S , i.e.,

(14) U n 1 = U n 0 + t n 2 { ε ( t n , U n 1 ) + ε ( t n 1 , U n 0 ) } .

cGP(2) Method:

Now, the three-point GauB-Lobatto method which is also known as the Simpson rule is used for defining the basic function with weights α 0 ^ = α 2 ^ = 1 / 3 , α 1 ^ = 4 / 3 and t 0 ^ = 1 , t 1 ^ = 0 , t 2 ^ = 1 .

Then, we have

ψ i , j = 5 2 1 1 4 2 3 2 , ϕ i = 1 2 1 , i = 1 , 2 and   j = 0 , 1 , 2 .

So, the system is to be solved for the U n 1 , U n 2 V for the known U n 0 = U n 1 2 which becomes

(15) α 1 , 1 U n 1 + α 1 , 2 U n 2 = α 1 , 0 U n 0 + τ n 2 { F ( τ n , 1 , U n 1 ) + β 1 F ( τ n , 1 , U n 0 ) } ,  

(16) α 2 , 1 U n 1 + α 2 , 2 U n 2 = α 2 , 0 U n 0 + τ n 2 { F ( τ n , 2 , U n 2 ) + β 2 F ( τ n , 2 , U n 0 ) } .  

3.1 RK scheme

This well-known scheme is established by Kutta having an order of four (see Eikenbery et al. [27] for details).

4 Comparative analysis of Galerkin and RK schemes

In this section, we conduct a comprehensive comparative analysis of the numerical outcomes obtained using the RK4-method and cGP(2)-method for solving the HIV model. Both numerical schemes are implemented for the model using a computer code written in MATLAB, and simulations are performed over a time span of t [ 0 , 1 ] . The accuracy of the Galerkin method is assessed by comparing its solutions with those obtained using the RK4 method at various time points within the specified interval. The results are visualized in Figures 28, which depict the temporal evolution of susceptible, latent, acutely infected, chronically infected , carrier, recovered, and vaccinated populations, respectively. A thorough examination of the graphical output reveals that the Galerkin method exhibits excellent agreement with the RK method, demonstrating its reliability and accuracy in approximating solutions to the HIV model. Furthermore, the proposed approach is shown to be a trustworthy tool for finding approximate solutions to real-world problems, particularly in the context of mathematical modeling of infectious diseases.

Figure 2 
               Comparison of RK4 and cGP(2) results for susceptible population 
                     
                        
                        
                           S
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                           .
                        
                        S(t).
Figure 2

Comparison of RK4 and cGP(2) results for susceptible population S ( t ) .

Figure 3 
               Comparison of RK4 and cGP(2) results for latent population 
                     
                        
                        
                           L
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                           .
                        
                        L(t).
Figure 3

Comparison of RK4 and cGP(2) results for latent population L ( t ) .

Figure 4 
               Comparison of RK4 and cGP(2) results for acutely infected individuals 
                     
                        
                        
                           A
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                        
                        A(t)
                     
                  .
Figure 4

Comparison of RK4 and cGP(2) results for acutely infected individuals A ( t ) .

Figure 5 
               Comparison of RK4 and cGP(2) results for chronically infected individuals 
                     
                        
                        
                           B
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                        
                        B(t)
                     
                  .
Figure 5

Comparison of RK4 and cGP(2) results for chronically infected individuals B ( t ) .

Figure 6 
               Comparison of RK4 and cGP(2) results for carrier-infected individuals 
                     
                        
                        
                           C
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                        
                        C(t)
                     
                  .
Figure 6

Comparison of RK4 and cGP(2) results for carrier-infected individuals C ( t ) .

Figure 7 
               Comparison of RK4 and cGP(2) results for recovered population 
                     
                        
                        
                           R
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                        
                        R(t)
                     
                  .
Figure 7

Comparison of RK4 and cGP(2) results for recovered population R ( t ) .

Figure 8 
               Comparison of RK4 and cGP(2) results for vaccinated population 
                     
                        
                        
                           V
                           
                              
                                 (
                                 
                                    t
                                 
                                 )
                              
                           
                           .
                        
                        V(t).
Figure 8

Comparison of RK4 and cGP(2) results for vaccinated population V ( t ) .

Furthermore, we investigated the influence of parameter ξ on the dynamical behavior of the model, which describes the temporal evolution of the susceptible, latent, acutely infected, chronically infected, carrier, recovered, and vaccinated populations. The results are presented graphically in Figures 915, respectively. These figures illustrate how the parameter ξ affects the dynamics of each population, providing valuable insights into the impact of this parameter on the spread of the disease and the effectiveness of vaccination strategies.

Figure 9 
               Dependence of susceptible population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 9

Dependence of susceptible population as a function of varying “ ξ ”.

Figure 10 
               Dependence of latent population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 10

Dependence of latent population as a function of varying “ ξ ”.

Figure 11 
               Dependence of acutely infected population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 11

Dependence of acutely infected population as a function of varying “ ξ ”.

Figure 12 
               Dependence of chronically infected population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 12

Dependence of chronically infected population as a function of varying “ ξ ”.

Figure 13 
               Dependence of carrier infected population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 13

Dependence of carrier infected population as a function of varying “ ξ ”.

Figure 14 
               Dependence of recovered population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 14

Dependence of recovered population as a function of varying “ ξ ”.

Figure 15 
               Dependence of vaccinated population as a function of varying “
                     
                        
                        
                           ξ
                        
                        \xi 
                     
                  ”.
Figure 15

Dependence of vaccinated population as a function of varying “ ξ ”.

Furthermore, the analysis results in Figures 915 demonstrate a unifying pattern, indicating that the concentrations of susceptible, latent, acutely infected, chronically infected, carrier, recovered, and vaccinated individuals all exhibit a growing trend corresponding to an increase in the value of parameter ξ . In particular:

  1. The population of susceptible (Figure 9) demonstrates a consistent increase in concentration as the parameter ξ escalates, signifying a greater number of individuals vulnerable to infection.

  2. The latent population (Figure 10) demonstrates an increasing concentration as the parameter ξ increases, indicating a larger number of individuals in the latent phase of infection.

  3. The population experiencing acute infection (Figure 11) exhibits a significant rise in concentration as the parameter ξ increases, suggesting a greater number of individuals affected by acute infection.

  4. The population with chronic infections (Figure 12) exhibits a comparable trend, where an increase in parameter ξ corresponds to a greater concentration of individuals affected by chronic infections.

  5. The carrier population (Figure 13) demonstrates an increase in concentration as the parameter ξ increases, indicating a larger number of individuals harboring the infection.

  6. The data presented in Figure 14 illustrate a notable increase in concentration corresponding to the increase of parameter ξ , suggesting a greater number of individuals successfully recovering from infection.

  7. The data regarding the vaccinated population (Figure 15) reveal a significant increase in concentration as the parameter ξ increases, indicating a greater number of individuals receiving vaccination.

The empirical findings indicate that parameter ξ significantly influences the dynamics of the model, as higher values correspond to an increased number of individuals within each category.

4.1 Basic reproduction number R 0

The R 0 is applied to work out the power of sickness, i.e., illness spread among a given population. This number simply represents the transmissibility of an infection. Now, let

ϒ = ( L ( t ) , A ( t ) , B ( t ) , C ( t ) ) . So, from the model, we obtain

(17) d ϒ d t = U ¯ V ¯ ,

where U ¯ and V ¯ are defined in Eq. (1) as

U ¯ = β A ( t ) S ( t ) T + δ β B ( t ) S ( t ) T + ψ β C ( t ) S ( t ) T 0 0 0 , V ¯ = v 1 v 2 v 3 v 4 ,

where

v 1 = ( d 0 + α ) L , v 2 = L ( d 0 + γ 1 + φ 1 ) A ,

v 3 = γ 1 A ( d 0 + d 1 + φ 2 ) B , v 4 = ξ η C T ( d 0 + φ 3 ) C .

Now, we have to find the Jacobean of U ¯ and V ¯ at the disease-free equilibrium point, thus we will obtain

U = 0 β S 0 δ β S 0 ψ β S 0 0 0 0 0 0 0 0 0 0 0 0 0 ,

V = α + d 0 0 0 0 α γ 1 + φ 1 + d 0 0 0 0 γ 1 d 0 + d 1 + φ 2 0 0 0 0 d 0 + φ 3 ξ η Λ T ,

V 1 = 1 α + d 0 0 0 0 α ( α + d 0 ) ( γ 1 + φ 1 + d 0 ) 1 ( γ 1 + φ 1 + d 0 ) 0 0 α γ 1 ( α + d 0 ) ( γ 1 + φ 1 + d 0 ) ( d 0 + d 1 + φ 2 ) γ 1 ( γ 1 + φ 1 + d 0 ) ( d 0 + d 1 + φ 2 ) 1 ( d 0 + d 1 + φ 2 ) 0 0 0 0 1 ( d 0 + φ 3 ξ η Λ T ) .

Thus, R 0 is the spectral radius of χ ¯ = U V 1 , that is, R o = ρ ( U V 1 ) and thus R o of the proposed model (1) becomes

R 0 = r 1 + r 2 + r 3 ,

where

r 1 = α β S 0 ( α + d 0 ) ( γ 1 + φ 1 + d 0 ) ,

r 2 = α β δ γ 1 S 0 ( α + d 0 ) ( γ 1 + φ 1 + d 0 ) ( d 0 + d 1 + φ 2 ) ,

and

r 3 = α β ψ γ 1 S 0 ( α + d 0 ) ( γ 1 + φ 1 + d 0 ) ( d 0 + φ 3 ξ η T ) .

4.2 Local stability analysis

The following findings have been demonstrated for our suggested model’s local stability with disease-free and endemic equilibria.

Theorem 2: If R 0 < 1 , then the above model (1) is locally asymptotically stable at disease-free equilibrium point U 0 , and if R 0 > 1 , then this will be the unstable saddle point.

Proof: For the given equation, the characteristic equation of the Jacobian matrix J ( t ) at disease-free equilibrium U 0 point has the form

(18) P ( λ ) = ( λ + d 0 ) ( λ + d 0 + v + φ ) ( λ 4 + x 1 λ 3 + x 2 λ 2 + x 3 λ + x 4 ) = 0 ,

where

x 1 = x 22 + x 33 + x 44 + x 55 ,

x 2 = x 22 x 33 ( 1 r 1 ¯ ) + x 44 x 55 + x 33 x 55 + x 33 x 44 + x 22 x 44 + x 22 x 55 ,

x 3 = x 55 x 33 x 22 ( 1 r 1 ¯ ) + x 33 x 44 x 55 1 x 22 x 55 r 2 ¯ + x 22 x 44 x 55 ( 1 r 2 ¯ ) + x 22 x 33 x 44 ( 1 r 1 ¯ ) ,

x 4 = α δ β γ 1 S 0 x 55 + α ψ γ 1 β S 0 a 44 + x 22 x 33 x 55 α β S 0 x 44 a 44 α ψ β γ 1 S 0 a 44 .

So, if R 0 < 1 , we obtain that 0 < r ¯ i < 1 , for i = 1 , 2 , 3 . So, for i = 1 , 2 , 3 , 4 , x i > 0 and so x 1 x 2 x 3 > x 3 2 + x 2 2 a 4 . The disease-free equilibrium point is a saddle point that is consistently unstable, as defined by the Routh–Hurwitz assumptions, together all roots of the characteristic polynomials P ( λ ) have nonzero portions. For R o >1, the solution described really does have positive and negative eigenvalues.

Theorem 3 If R 0 < 1 , then the infectious equilibrium point U 0 is locally asymptotically stable by model (1), otherwise for R 0 >1 it is unstable.

Proof: The Jacobean matrix around U 1 will have this echelon form

(19) J 1 = u 11 0 u 13 u 14 u 15 ζ 0 u 22 u 23 u 24 u 25 ζ u 21 0 0 u 33 u 32 0 α u 21 0 0 0 u 44 u 45 α u 21 0 0 0 0 u 55 α ζ u 21 v 0 0 0 0 u 66 .

The eigenvalues of the Jacobean matrix have been simplified and rearranged as J 1 which is

λ 1 = u 11 ,

λ 2 = u 22 ,

λ 3 = u 11 u 22 u 33 + α u 13 ( u 11 u 21 ) ,

λ 4 = 1 γ 1 α u 13 u 44 ( u 11 u 22 u 33 + u 11 u 21 ) ,

λ 5 = 1 γ 1 α u 13 u 44 ( u 11 u 22 u 33 + u 11 u 21 ) + α u 14 ( u 11 u 21 ) ,

λ 6 = 1 γ 1 α u 13 u 44 ( u 11 u 22 u 33 + u 11 u 21 ) α ζ v u 14 u 44 u 53 ( v + d 0 ) β γ 1 ζ u 44 + β u 45 ( γ γ 1 + u 44 ) .

From here, we obtain that λ 1 , λ 2 , λ 3 , λ 4 λ 5 , λ 6 has negative real parts and λ 3 , λ 5 are negative if u 22 u 33 > α β S 1 and u 44 S 1 > δ B 1 .

4.3 Global stability

Utilizing the Lyapunov functional hypothesis and a geometrical approach, the global stability of the current estimated model has been demonstrated. Here, we would like to utilize the Lypanavo operating concept to verify the global stability of every disease-free equilibrium position U 0 , while we would want to establish the global stability of an endemic equilibrium point U 1 in a geometrical manner. Prior to discussing the results, it is essential to note that our anticipated concept is asymptotically stable everywhere as defined by the following fundamental theorem.

Theorem 1: If R 0 < 1 , at the disease-free equilibrium point U 0 , model (1) is globally asymptotically stable; otherwise, it is unstable.

Proof: Using Lyapunov function theory, we illustrate the global stability of Eq. (1) at the disease-free equilibrium point. To do this, we take into consideration the following Lyapunov function, such that

(20) U ( t ) = 1 2 [ ( S S 0 ) + L ( t ) + A ( t ) + B ( t ) + C ( t ) + R ( t ) + ( V V 0 ) ] 2 + λ 1 S ( t ) + λ 2 L ( t ) + λ 3 A ( t ) + λ 4 B ( t ) + λ 5 C ( t ) + λ 6 R ( t ) + λ 7 V ( t ) .

For i = 1 , 2 , 3 , , 7 , where λ i are positive constants. Now, after differentiating U ( t ) w.r.t. time, we have

(21) d U d t = [ ( S S 0 ) + L ( t ) + A ( t ) + B ( t ) + C ( t ) + R ( t ) + ( V V 0 ) ] ( Λ d 0 T ( t ) d 1 B ( t ) ) + λ 1 d S d t + λ 2 d L d t + λ 3 d A d t + λ 4 d B d t + λ 5 d C d t + λ 6 d V d t .

Now, if we choose the positive parameters λ i = ( α + d o ) ( d o + d 1 + φ 2 ) for i = 1, 2, 3, 5, 7 and λ 4 = α β δ S o along with the solution of model (1), we will obtain

(22) d U d t = [ ( S S 0 ) + L ( t ) + A ( t ) + B ( t ) + C ( t ) + R ( t ) + ( V V 0 ) ] × ( Λ d 0 T ( t ) d 1 B ( t ) )   q 4 q 2 ( Λ ξ η C ( t ) d 0 L ( t ) q 4 q 2 q 3 ( 1 r 2 ¯ ) A ( t ) α β δ γ 1 q 4 S 0 B ( t ) + ( Λ d 0 S ( t ) d 0 V ( t ) ) q 4 q 2 .

Now, since T ( t ) Λ d 0 , this implies S ( t ) Λ d 0 . Thus, using S 0 + V 0 = Λ d 0 and S ( t ) Λ d 0 in Eq. (20), we will obtain

(23) d U  d t [ ( S S 0 ) + L ( t ) + A ( t ) + B ( t ) + C ( t ) + R ( t ) + ( V V 0 ) ] × ( d 0 T ( t ) S ( t ) + d 1 B ( t ) ) q 4 q 2 ( Λ ξ η C ( t ) + d 0 L ( t ) ) q 4 q 2 q 3 ( 1 r 2 ¯ ) A ( t ) α β δ γ 1 q 4 S 0 B ( t ) d 0 ( ( S ( t ) + V ( t ) ) ( S 0 + V 0 ) q 4 q 2 .

Now, if R 0 < 1 , then 0 < r i ¯ < 1 , for i = 1 , 2 , 3 ; therefore, d U d t is negative and d U d t = 0 , if S = S 0 , L = L 0 , A = A 0 , B = B 0 , C = C 0 , R = R 0 , V = V 0 . Thus, the biggest compact invariant set is the singleton set { U 0 }, so by LaSalle’s invariant principle we obtain that the sickness-free equilibrium point U 0 is globally asymptotically stable.

5 Conclusions

Hepatitis B, a severe and widespread liver infection worldwide, represents a considerable challenge to public health. Although it is both treatable and preventable, it leads to around one million deaths each year. The virus can be transmitted through direct interaction with contaminated blood or bodily fluids, with maternal transmission during childbirth and the sharing of personal items with an infected person being prevalent methods of spread. This study presents the development of a mathematical model aimed at exploring the dynamics of hepatitis B transmission. The population is categorized into seven distinct subclasses: susceptible, latent, acute and chronically infected, carrier, recovered, and vaccinated. Implementing the Galerkin scheme, we conducted an analysis of the model and calculated the fundamental reproduction number R 0 through the next-generation matrix method. Subsequently, we identified the disease-free equilibrium points and assessed both the global and local stability of the model through application of the Lyapunov function. To confirm the accuracy of the presented scheme, the results are compared with those obtained from the classical RK scheme. The findings indicate that the Galerkin aligns well with RK-4 results for adequately small sizes, thereby affirming the precision of our methodology. All computations were executed utilizing MATLAB, and the graphical outcomes are displayed. This research enhances our comprehension of the transmission dynamics of hepatitis B and underscores the critical role of vaccination and preventive measures in mitigating the proliferation of the disease. Future investigations are entitled to concentrate on the estimation and validation of parameters through utilization of empirical data, thereby guiding public health policy and refining intervention strategies.

This novel contribution provides a comprehensive framework for understanding HBV transmission dynamics, enabling medical researchers to:

  1. Identify high-risk individuals and stages of infection,

  2. Characterize the impact of vaccination strategies on HBV transmission,

  3. Optimize intervention approaches to control the spread of HBV,

  4. Inform public health policy with data-driven insights.

5.1 Limitations of the present study

The proposed model’s limitations include the assumption of a homogenous population, the lack of coinfection, and parameter uncertainty. It fails to account for age-specific transmission, regional heterogeneity, mutation, or evolution. Intervention techniques and stochasticity are not clearly addressed.

5.2 Future research directions

In further research, we plan to address the aforementioned limitations in order to improve the model accuracy and generalizability. This research endeavors to extend the Galerkin scheme’s applicability to novel models, encompassing the integration of awareness dissemination and epidemic propagation developed by Kabir et al. [54], examining the interplay between information diffusion and disease transmission in multilayer networks developed by Kabir and Tanimoto [55], and evaluating the economic and epidemiological implications of hybrid strategies in voluntary vaccination policies developed by Kabir et al. [56], thereby contributing to the advancement of mathematical modeling in infectious disease research.

Future research directions also include parameter estimation and validation using real-world data, extension of the model to incorporate additional risk factors, and exploration of optimal control strategies to eradicate HBV. This study’s findings have the potential to significantly impact HBV research and public health initiatives, ultimately contributing to the reduction of HBV-related morbidity and mortality worldwide.

Acknowledgements

The researchers would like to thank the Deanship of Graduate Studies and Scientific Research at Qassim University for financial support (QU-APC-2024-9/1).

  1. Funding information: The researchers would like to thank the Deanship of Graduate Studies and Scientific Research at Qassim University for financial support (QU-APC-2024-9/1).

  2. Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission. Conceptualization, validation, writing – original draft, A, S.B, and A.J.; investigation, T.H. and T.R.; writing – review and editing, S.B.; supervision and project administration, S.B. and T.R. All authors have read and agreed to the published version of the manuscript.

  3. Conflict of interest: There are no competing interest regarding this research work.

  4. Data availability statement: There are no data associated with the current study.

  5. Institutional review board statement: There are no ethical issues in this work. All the authors actively participated in this research and approved it for publication.

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Received: 2024-07-22
Revised: 2024-09-19
Accepted: 2024-10-15
Published Online: 2024-11-18

© 2024 the author(s), published by De Gruyter

This work is licensed under the Creative Commons Attribution 4.0 International License.

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  42. Variable sampling time discrete sliding mode control for a flapping wing micro air vehicle using flapping frequency as the control input
  43. Error analysis of arbitrarily high-order stepping schemes for fractional integro-differential equations with weakly singular kernels
  44. Solitary and periodic pattern solutions for time-fractional generalized nonlinear Schrödinger equation
  45. An unconditionally stable numerical scheme for solving nonlinear Fisher equation
  46. Effect of modulated boundary on heat and mass transport of Walter-B viscoelastic fluid saturated in porous medium
  47. Analysis of heat mass transfer in a squeezed Carreau nanofluid flow due to a sensor surface with variable thermal conductivity
  48. Navigating waves: Advancing ocean dynamics through the nonlinear Schrödinger equation
  49. Experimental and numerical investigations into torsional-flexural behaviours of railway composite sleepers and bearers
  50. Novel dynamics of the fractional KFG equation through the unified and unified solver schemes with stability and multistability analysis
  51. Analysis of the magnetohydrodynamic effects on non-Newtonian fluid flow in an inclined non-uniform channel under long-wavelength, low-Reynolds number conditions
  52. Convergence analysis of non-matching finite elements for a linear monotone additive Schwarz scheme for semi-linear elliptic problems
  53. Global well-posedness and exponential decay estimates for semilinear Newell–Whitehead–Segel equation
  54. Petrov-Galerkin method for small deflections in fourth-order beam equations in civil engineering
  55. Solution of third-order nonlinear integro-differential equations with parallel computing for intelligent IoT and wireless networks using the Haar wavelet method
  56. Mathematical modeling and computational analysis of hepatitis B virus transmission using the higher-order Galerkin scheme
  57. Mathematical model based on nonlinear differential equations and its control algorithm
  58. Bifurcation and chaos: Unraveling soliton solutions in a couple fractional-order nonlinear evolution equation
  59. Space–time variable-order carbon nanotube model using modified Atangana–Baleanu–Caputo derivative
  60. Minimal universal laser network model: Synchronization, extreme events, and multistability
  61. Valuation of forward start option with mean reverting stock model for uncertain markets
  62. Geometric nonlinear analysis based on the generalized displacement control method and orthogonal iteration
  63. Fuzzy neural network with backpropagation for fuzzy quadratic programming problems and portfolio optimization problems
  64. B-spline curve theory: An overview and applications in real life
  65. Nonlinearity modeling for online estimation of industrial cooling fan speed subject to model uncertainties and state-dependent measurement noise
  66. Quantitative analysis and modeling of ride sharing behavior based on internet of vehicles
  67. Review Article
  68. Bond performance of recycled coarse aggregate concrete with rebar under freeze–thaw environment: A review
  69. Retraction
  70. Retraction of “Convolutional neural network for UAV image processing and navigation in tree plantations based on deep learning”
  71. Special Issue: Dynamic Engineering and Control Methods for the Nonlinear Systems - Part II
  72. Improved nonlinear model predictive control with inequality constraints using particle filtering for nonlinear and highly coupled dynamical systems
  73. Anti-control of Hopf bifurcation for a chaotic system
  74. Special Issue: Decision and Control in Nonlinear Systems - Part I
  75. Addressing target loss and actuator saturation in visual servoing of multirotors: A nonrecursive augmented dynamics control approach
  76. Collaborative control of multi-manipulator systems in intelligent manufacturing based on event-triggered and adaptive strategy
  77. Greenhouse monitoring system integrating NB-IOT technology and a cloud service framework
  78. Special Issue: Unleashing the Power of AI and ML in Dynamical System Research
  79. Computational analysis of the Covid-19 model using the continuous Galerkin–Petrov scheme
  80. Special Issue: Nonlinear Analysis and Design of Communication Networks for IoT Applications - Part I
  81. Research on the role of multi-sensor system information fusion in improving hardware control accuracy of intelligent system
  82. Advanced integration of IoT and AI algorithms for comprehensive smart meter data analysis in smart grids
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