Computational modeling of fractional COVID-19 model by Haar wavelet collocation Methods with real data.

This study explores the use of numerical simulations to model the spread of the Omicron variant of the SARS-CoV-2 virus using fractional-order COVID-19 models and Haar wavelet collocation methods. The fractional order COVID-19 model considers various factors that affect the virus's transmission, and the Haar wavelet collocation method offers a precise and efficient solution to the fractional derivatives used in the model. The simulation results yield crucial insights into the Omicron variant's spread, providing valuable information to public health policies and strategies designed to mitigate its impact. This study marks a significant advancement in comprehending the COVID-19 pandemic's dynamics and the emergence of its variants. The COVID-19 epidemic model is reworked utilizing fractional derivatives in the Caputo sense, and the model's existence and uniqueness are established by considering fixed point theory results. Sensitivity analysis is conducted on the model to identify the parameter with the highest sensitivity. For numerical treatment and simulations, we apply the Haar wavelet collocation method. Parameter estimation for the recorded COVID-19 cases in India from 13 July 2021 to 25 August 2021 has been presented.

Effect of Macrophages and Latent Reservoirs on the Dynamics of HTLV-I and HIV-1 Coinfection

Human immunodeficiency virus type 1 (HIV-1) and human T-lymphotropic virus type I (HTLV-I) are two retroviruses that have a similar fashion of transmission via sharp objects contaminated by viruses, transplant surgery, transfusion, and sexual relations. Simultaneous infections with HTLV-I and HIV-1 usually occur in areas where both viruses have become endemic. CD4+T cells are the main targets of HTLV-I, while HIV-1 can infect CD4+T cells and macrophages. It is the aim of this study to develop a model of HTLV-I and HIV-1 coinfection that describes the interactions of nine compartments: susceptible cells of both CD4+T cells and macrophages, HIV-1-infected cells that are latent/active in both CD4+T cells and macrophages, HTLV-I-infected CD4+T cells that are latent/active, and free HIV-1 particles. The well-posedness, existence of equilibria, and global stability analysis of our model are investigated. The Lyapunov function and LaSalle's invariance principle were used to study the global asymptotic stability of all equilibria. The theoretically predicted outcomes were verified by utilizing numerical simulations. The effect of including the macrophages and latent reservoirs in the HTLV-I and HIV-1 coinfection model is discussed. We show that the presence of macrophages makes a coinfection model more realistic when the case of the coexistence of HIV-1 and HTLV-I is established. Moreover, we have shown that neglecting the latent reservoirs in HTLV-I and HIV-1 coinfection modeling will lead to the design of an overflow of anti-HIV-1 drugs.

Global Dynamics of a Within-Host COVID-19/AIDS Coinfection Model with Distributed Delays

Acquired immunodeficiency syndrome (AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV). Among people with AIDS, cases of COVID-19 have been reported in many countries. COVID-19 (coronavirus disease 2019) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this manuscript, we are going to present a within-host COVID-19/AIDS coinfection model to study the dynamics and influence of the coinfection between COVID-19 and AIDS. The model is a six-dimensional delay differential equation that describes the interaction between uninfected epithelial cells, infected epithelial cells, free SARS-CoV-2 particles, uninfected CD4+ T cells, infected CD4+ T cells, and free HIV-1 particles. We demonstrated that the proposed model is biologically acceptable by proving the positivity and boundedness of the model solutions. The global stability analysis of the model is carried out in terms of the basic reproduction number. Numerical simulations are carried out to investigate that if COVID-19/AIDS coinfected individuals have a poor immune response or a low number of CD4+ T cells, then the viral load of SARS-CoV-2 and the number of infected epithelial cells will rise. On the contrary, the existence of time delays can rise the number of uninfected CD4+ T cells and uninfected epithelial cells, thus reducing the viral load within the host.