This article develops a within-host viral kinetics model of SARS-CoV-2 under the Caputo fractional-order operator. We prove the results of the solution’s existence and uniqueness by using the Banach mapping contraction principle. Using the next-generation matrix method, we obtain the basic reproduction number. We analyze the model’s endemic and disease-free equilibrium points for local and global stability. Furthermore, we find approximate solutions for the non-linear fractional model using the Modified Euler Method (MEM). To support analytical findings, numerical simulations are carried out.

In this article, a non-integer nonlinear mathematical model for toxoplasmosis disease in human and cat population is proposed and studied. The basic concepts of the model's dynamic are given. The study of qualitative dynamics is done by the basic threshold parameter $R_0$. Local and global stabilities are done and the system's disease free equilibrium point is an attractor when $R_0<1$. Besides of it, endemic equilibrium point is an attractor when $R_0>1$. The sensitivity analysis of $R_0$ shows which parameter has positive/negative impact on the model. Numerical simulation of the model for the parameters occurred in threshold parameter is also discussed. The techniques of Adams Bashforth Moulton will be considered to justify all the derived theoretical results which will help in understanding to study the effect of various parameters to both the transient and steady-state dynamics of the disease infection.

In this article, a mathematical model of the COVID-19 pandemic with control parameters is introduced. The main objective of this study is to determine the most effective model for predicting the transmission dynamic of COVID-19 using a deterministic model with control variables. For this purpose, we introduce three control variables to reduce the number of infected and asymptomatic or undiagnosed populations in the considered model. Existence and necessary optimal conditions are also established. The Grünwald-Letnikov non-standard weighted average finite difference method (GL-NWAFDM) is developed for solving the proposed optimal control system. Further, we prove the stability of the considered numerical method. Graphical representations and analysis are presented to verify the theoretical results.

In this study, asymptotic analysis of an HIV-1 epidemic model with distributed intracellular delays is proposed. One delay term represents the latent period which is the time when the target cells are contacted by the virus particles and the time the contacted cells become actively infected and the second delay term represents the virus production period which is the time when the new virions are created within the cell and are released from the cell. The infection free equilibrium and the chronic-infection equilibrium have been shown to be locally asymptotically stable by using Rouths Hurwiths criterion and general theory of delay differential equations. Similarly, by using Lyapunov functionals and LaSalle’s invariance principle, it is proved that if the basic reproduction ratio is less than unity, then the infection-free equilibrium is globally asymptotically stable, and if the basic reproduction ratio is greater than unity, the chronic-infection equilibrium is globally asymptotically stable. Finally, numerical results with conclusion are discussed.

In this research article, a new mathematical model of delayed differential equations is developed which discusses the interaction among CD4T cells, human immunodeficiency virus (HIV), and recombinant virus with cure rate. The model has two distributed intracellular delays. These delays denote the time needed for the infection of a cell. The dynamics of the model are completely described by the basic reproduction numbers represented byR0,R1, andR2. It is shown that ifR0<1, then the infection-free equilibrium is locally as well as globally stable. Similarly, it is proved that the recombinant absent equilibrium is locally as well as globally asymptotically stable if1<R0<R1. Finally, numerical simulations are presented to illustrate our theoretical results. Our obtained results show that intracellular delay and cure rate have a positive role in the reduction of infected cells and the increasing of uninfected cells due to which the infection is reduced.