ABSTRACT
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.
ABSTRACT
The coronavirus disease 2019 (COVID-19) is a respiratory disease caused by a virus called the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this paper, we analyze a within-host SARS-CoV-2/HIV coinfection model. The model is made up of eight ordinary differential equations. These equations describe the interactions between healthy epithelial cells, latently infected epithelial cells, productively infected epithelial cells, SARS-CoV-2 particles, healthy CD 4 + T cells, latently infected CD 4 + T cells, productively infected CD 4 + T cells, and HIV particles. We confirm that the solutions of the developed model are bounded and nonnegative. We calculate the different steady states of the model and derive their existence conditions. We choose appropriate Lyapunov functions to show the global stability of all steady states. We execute some numerical simulations to assist the theoretical contributions. Based on our results, weak CD 4 + T cell immunity in SARS-CoV-2/HIV coinfected patients causes an increase in the concentrations of productively infected epithelial cells and SARS-CoV-2 particles. This may lead to severe SARS-CoV-2 infection in HIV patients. This result agrees with many studies that discussed the high risk of severe infection and death in HIV patients when they get SARS-CoV-2 infection. On the other hand, increasing the death rate of infected epithelial cells during the latency period can reduce the severity of SARS-CoV-2 infection in HIV patients. More studies are needed to understand the dynamics of SARS-CoV-2/HIV coinfection and find better ways to treat this vulnerable group of patients.
ABSTRACT
Coronavirus disease 2019 (COVID-19) is a new respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It started in China and spread quickly to all continents. This virus has changed the life style and the education system in many countries. As for other viruses, mathematical models have been rated as a useful tool to support the research on COVID-19. In this work, we develop a reaction–diffusion model to describe the within-host dynamics of SARS-CoV-2 in cancer patients. This model studies the interactions between nutrient, healthy epithelial cells, cancer cells, SARS-CoV-2 particles, and immune cells. The model incorporates the spatial mobility of the cells and viruses. The model includes parameters for measuring the effect of lymphopenia on SARS-CoV-2/cancer patients. We verify the basic features of the model’s solutions including the uniqueness, nonnegativity and boundedness. We list all equilibrium points of the proposed model. We show the global stability and the local instability of the most meaningful equilibria. We display some numerical simulations to enhance our theoretical results. The results indicate that diffusion can have a clear effect at the beginning of SARS-CoV-2 infection. Lymphopenia in SARS-CoV-2/cancer patients impairs the immune responses against cancer and SARS-CoV-2, and worsens the health state of patients. [ABSTRACT FROM AUTHOR] Copyright of International Journal of Biomathematics is the property of World Scientific Publishing Company and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
ABSTRACT
The world is going through a critical period due to a new respiratory disease called coronavirus disease 2019 (COVID-19). This disease is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Mathematical modeling is one of the most important tools that can speed up finding a drug or vaccine for COVID-19. COVID-19 can lead to death especially for patients having chronic diseases such as cancer, AIDS, etc. We construct a new within-host SARS-CoV-2/cancer model. The model describes the interactions between six compartments: nutrient, healthy epithelial cells, cancer cells, SARS-CoV-2 virus particles, cancer-specific CTLs, and SARS-CoV-2-specific antibodies. We verify the nonnegativity and boundedness of its solutions. We outline all possible equilibrium points of the proposed model. We prove the global stability of equilibria by constructing proper Lyapunov functions. We do some numerical simulations to visualize the obtained results. According to our model, lymphopenia in COVID-19 cancer patients may worsen the outcomes of the infection and lead to death. Understanding dysfunctions in immune responses during COVID-19 infection in cancer patients could have implications for the development of treatments for this high-risk group.