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The coronavirus disease 2019 (COVID-19) is a respiratory disease that appeared in 2019 caused by a virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is still spreading and causing deaths around the world. There is a real concern of SARS-CoV-2 coinfection with other infectious diseases. Tuberculosis (TB) is a bacterial disease caused by Mycobacterium tuberculosis (Mtb). SARS-CoV-2 coinfection with TB has been recorded in many countries. It has been suggested that the coinfection is associated with severe disease and death. Mathematical modeling is an effective tool that can help understand the dynamics of coinfection between new diseases and well-known diseases. In this paper, we develop an in-host TB and SARS-CoV-2 coinfection model with cytotoxic T lymphocytes (CTLs). The model investigates the interactions between healthy epithelial cells (ECs), latent Mtb-infected ECs, active Mtb-infected ECs, SARS-CoV-2-infected ECs, free Mtb, free SARS-CoV-2, and CTLs. The model's solutions are proved to be nonnegative and bounded. All equilibria with their existence conditions are calculated. Proper Lyapunov functions are selected to examine the global stability of equilibria. Numerical simulations are implemented to verify the theoretical results. It is found that the model has six equilibrium points. These points reflect two states: the mono-infection state where SARS-CoV-2 or TB occurs as a single infection, and the coinfection state where the two infections occur simultaneously. The parameters that control the movement between these states should be tested in order to develop better treatments for TB and COVID-19 coinfected patients. Lymphopenia increases the concentration of SARS-CoV-2 particles and thus can worsen the health status of the coinfected patient. [ABSTRACT FROM AUTHOR]

In this paper, we propose and study a Middle East respiratory syndrome coronavirus (MERS-CoV) infection model with cytotoxic T lymphocyte (CTL) immune response and intracellular delay. This model includes five compartments: uninfected cells, infected cells, viruses, dipeptidyl peptidase 4 (DPP4), and CTL immune cells. We obtained an immunity-inactivated reproduction number R 0 and an immunity-activated reproduction number R 1 . By analyzing the distributions of roots of the corresponding characteristic equations, the local stability results of the infection-free equilibrium, the immunity-inactivated equilibrium, and the immunity-activated equilibrium were obtained. Moreover, by constructing suitable Lyapunov functionals and combining LaSalle's invariance principle and Barbalat's lemma, some sufficient conditions for the global stability of the three types of equilibria were obtained. It was found that the infection-free equilibrium is globally asymptotically stable if R 0 ≤ 1 and unstable if R 0 > 1 ; the immunity-inactivated equilibrium is locally asymptotically stable if R 0 > 1 > R 1 and globally asymptotically stable if R 0 > 1 > R 1 and condition (H1) holds, but unstable if R 1 > 1 ; and the immunity-activated equilibrium is locally asymptotically stable if R 1 > 1 and is globally asymptotically stable if R 1 > 1 and condition (H1) holds. [ABSTRACT FROM AUTHOR]

Human T-lymphotropic virus type I (HTLV-I) and human immunodeficiency virus (HIV) are two famous retroviruses that share similarities in their genomic organization, and differ in their life cycle as well. It is known that HTLV-I and HIV have in common a way of transmission via direct contact with certain body fluids related to infected patients. Thus, it is not surprising that a single-infected person with one of these viruses can be dually infected with the other virus. In the literature, many researchers have devoted significant efforts for modeling and analysis of HTLV or HIV single infection. However, the dynamics of HTLV/HIV dual infection has not been formulated. In the present paper, we formulate an HTLV/HIV dual infection model. The model includes the impact of the Cytotoxic T lymphocyte (CTLs) immune response, which is important to control the dual infection. The model describes the interaction between uninfected CD 4 + T cells, HIV-infected cells, HTLV-infected cells, free HIV particles, HIV-specific CTLs, and HTLV-specific CTLs. We establish that the solutions of the model are non-negative and bounded. We calculate all steady states of the model and deduce the threshold parameters which determine the existence and stability of the steady states. We prove the global asymptotic stability of all steady states by utilizing the Lyapunov function and Lyapunov–LaSalle asymptotic stability theorem. We solve the system numerically to illustrate the our main results. In addition, we compared between the dynamics of single and dual infections. [ABSTRACT FROM AUTHOR]

A severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to morbidity and mortality. SARS-CoV-2 infects the epithelial cells of the respiratory tract and causes coronavirus disease 2019 (COVID-19). The immune system's response plays a significant role in viral progression. This article develops and analyzes a system of partial differential equations (PDEs), which describe the in-host dynamics of SARS-CoV-2 under the effect of cytotoxic T-lymphocyte (CTL) and antibody immune responses. The model characterizes the interplay between six compartments, healthy epithelial cells (ECs), latent infected ECs, active infected ECs, free SARS-CoV-2 particles, CTLs, and antibodies. We consider the logistic growth of healthy ECs. We first investigate the properties of the model's solutions, then, we calculate all steady states and determine the conditions of their existence and global stability. The global asymptotic stability is examined by constructing Lyapunov functions. The analytical findings are supported via numerical simulations. [ABSTRACT FROM AUTHOR]