Search

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Mycobacterium tuberculosis (Mtb) coinfection has been observed in a number of nations and it is connected with severe illness and death. The paper studies a reaction–diffusion within-host Mtb/SARS-CoV-2 coinfection model with immunity. This model explores the connections between uninfected epithelial cells, latently Mtb-infected epithelial cells, productively Mtb-infected epithelial cells, SARS-CoV-2-infected epithelial cells, free Mtb particles, free SARS-CoV-2 virions, and CTLs. The basic properties of the model's solutions are verified. All equilibrium points with the essential conditions for their existence are calculated. The global stability of these equilibria is established by adopting compatible Lyapunov functionals. The theoretical outcomes are enhanced by implementing numerical simulations. It is found that the equilibrium points mirror the single infection and coinfection states of SARS-CoV-2 with Mtb. The threshold conditions that determine the movement from the monoinfection to the coinfection state need to be tested when developing new treatments for coinfected patients. The impact of the diffusion coefficients should be monitored at the beginning of coinfection as it affects the initial distribution of particles in space. [ABSTRACT FROM AUTHOR]

The aim of the present paper is to formulate two new mathematical models to describe the co-dynamics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and human T-cell lymphotropic virus type-I (HTLV-I) in a host. The models characterizes the interplaying between seven compartments, uninfected ECs, latently SARS-CoV-2-infected ECs, actively SARS-CoV-2-infected ECs, free SARS-CoV-2 particles, uninfected CD4 + T cells, latently HTLV-I-infected CD4 + T cells and actively HTLV-I-infected CD4 + T cells. The models incorporate five intracellular time delays: (i) two delays in the formation of latently SARS-CoV-2-infected ECs and latently HTLV-I-infected CD4 + T cells, (ii) two delays in the reactivation of latently SARS-CoV-2-infected ECs and latently HTLV-I-infected CD4 + T cells, and (iii) maturation delay of new SARS-CoV-2 virions. We consider discrete-time delays and distributed-time delays in the first and second models, respectively. We first investigate the properties of the model's solutions, then we calculate all equilibria and study their global stability. The global asymptotic stability is examined by constructing Lyapunov functionals. The analytical findings are supported via numerical simulation. The impact of time delays on the coinfection progression is discussed. We found that, increasing time delays values can have an antiviral treatment-like impact. Our developed coinfection model can contribute to understand the SARS-CoV-2 and HTLV-I co-dynamics and help to select suitable treatment strategies for COVID-19 patients with HTLV-I. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new virus which infects the respiratory system and causes the coronavirus disease 2019 (COVID-19). The coinfection between malaria and COVID-19 has been registered in many countries. This has risen an urgent need to understand the dynamics of coinfection. In this paper, we construct a reaction–diffusion in-host malaria/COVID-19 model. The model includes seven-dimensional partial differential equations that explore the interactions between seven compartments, healthy red blood cells (RBCs), infected RBCs, free merozoites, healthy epithelial cells (ECs), infected ECs, free SARS-CoV-2 particles, and antibodies. The biological validation of the model is confirmed by establishing the nonnegativity and boundedness of the model's solutions. All equilibrium points with the corresponding existence conditions are calculated. The global stability of all equilibria is proved by picking up appropriate Lyapunov functionals. Numerical simulations are used to enhance and visualize the theoretical results. We found that the equilibrium points show the different cases when malaria and SARS-CoV-2 infections occur as mono-infection or coinfection. The shared antibody immune response decreases the concentrations of SARS-CoV-2 and malaria merozoites. This can have an important role in reducing the severity of SARS-CoV-2 if the immune response works effectively. [ABSTRACT FROM AUTHOR]

Studies have reported several cases with respiratory viruses coinfection in hospitalized patients. Influenza A virus (IAV) mimics the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) with respect to seasonal occurrence, transmission routes, clinical manifestations and related immune responses. The present paper aimed to develop and investigate a mathematical model to study the dynamics of IAV/SARS-CoV-2 coinfection within the host. The influence of SARS-CoV-2-specific and IAV-specific antibody immunities is incorporated. The model simulates the interaction between seven compartments, uninfected epithelial cells, SARS-CoV-2-infected cells, IAV-infected cells, free SARS-CoV-2 particles, free IAV particles, SARS-CoV-2-specific antibodies and IAV-specific antibodies. The regrowth and death of the uninfected epithelial cells are considered. We study the basic qualitative properties of the model, calculate all equilibria and investigate the global stability of all equilibria. The global stability of equilibria is established using the Lyapunov method. We perform numerical simulations and demonstrate that they are in good agreement with the theoretical results. The importance of including the antibody immunity into the coinfection dynamics model is discussed. We have found that without modeling the antibody immunity, the case of IAV and SARS-CoV-2 coexistence is not observed. Finally, we discuss the influence of IAV infection on the dynamics of SARS-CoV-2 single-infection and vice versa. [ABSTRACT FROM AUTHOR]