ABSTRACT
In this paper, a reaction-diffusion COVID-19 model is proposed to explore how vaccination-isolation strategies affect the development of the epidemic. First, the basic dynamical properties of the system are explored. Then, the system's asymptotic distributions of endemic equilibrium under different conditions are studied. Further, the global sensitivity analysis of R 0 is implemented with the aim of determining the sensitivity for these parameters. In addition, the optimal vaccination-isolation strategy based on the optimal path is proposed. Meantime, social cost C ( m , σ ) , social benefit B ( m , σ ) , threshold R 0 ( m , σ ) three objective optimization problem based on vaccination-isolation strategy is explored, and the maximum social cost ( M S C ) and maximum social benefit ( M S B ) are obtained. Finally, the instance prediction of the Lhasa epidemic in China on August 7, 2022, is made by using the piecewise infection rates ß 1 ( t ) , ß 2 ( t ) , and some key indicators are obtained as follows: (1) The basic reproduction numbers of each stage in Lhasa, China are R 0 ( 1 : 8 ) = 0.4678 , R 0 ( 9 : 20 ) = 2.7655 , R 0 ( 21 : 30 ) = 0.3810 and R 0 ( 31 : 100 ) = 0.7819 ; (2) The daily new cases of this epidemic will peak at 43 on the 20th day (August 26, 2022); (3) The cumulative cases in Lhasa, China will reach about 640 and be cleared about the 80th day (October 28, 2022). Our research will contribute to winning the war on epidemic prevention and control.
ABSTRACT
Co-infections with respiratory viruses were reported in hospitalized patients in several cases. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza A virus (IAV) are two respiratory viruses and are similar in terms of their seasonal occurrence, clinical manifestations, transmission routes, and related immune responses. SARS-CoV-2 is the cause of coronavirus disease 2019 (COVID-19). In this paper, we study the dynamic behaviors of an influenza and COVID-19 co-infection model in vivo. The role of humoral (antibody) immunity in controlling the co-infection is modeled. The model considers the interactions among uninfected epithelial cells (ECs), SARS-CoV-2-infected ECs, IAV-infected ECs, SARS-CoV-2 particles, IAV particles, SARS-CoV-2 antibodies, and IAV antibodies. The model is given by a system of delayed ordinary differential equations (DODEs), which include four time delays: (i) a delay in the SARS-CoV-2 infection of ECs, (ii) a delay in the IAV infection of ECs, (iii) a maturation delay of newly released SARS-CoV-2 virions, and (iv) a maturation delay of newly released IAV virions. We establish the non-negativity and boundedness of the solutions. We examine the existence and stability of all equilibria. The Lyapunov method is used to prove the global stability of all equilibria. The theoretical results are supported by performing numerical simulations. We discuss the effects of antiviral drugs and time delays on the dynamics of influenza and COVID-19 co-infection. It is noted that increasing the delay length has a similar influence to that of antiviral therapies in eradicating co-infection from the body.
ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel respiratory virus that causes coronavirus disease 2019 (COVID-19). Symptoms of COVID-19 range from mild to severe illness. It was observed that disease progression in COVID-19 patients depends on their immune response, especially in elderly patients whose immune system suppression may put them at increased risk of infection. Human T-cell lymphotropic virus type-I (HTLV-I) attacks the CD4+ T cells (T cells) of the immune system and leads to immune dysfunction. Co-infection with HTLV-I and SARS-CoV-2 has been reported in recent studies. Modeling HTLV-I and SARS-CoV-2 co-infection can be a helpful tool to understand the in-host co-dynamics of these viruses. The aim of this study was to construct a model that characterizes the in-host dynamics of HTLV-I and SARS-CoV-2 co-infection. By considering the mobility of the viruses and cells, the model is represented by a system of partial differential equations (PDEs). The system contains two independent variables, time t and position x, and seven dependent variables for representing the densities of healthy epithelial cells (ECs), latent SARS-CoV-2-infected ECs, active SARS-CoV-2-infected ECs, SARS-CoV-2, healthy T cells, latent HTLV-I-infected T cells and active HTLV-I-infected T cells. We first studied the fundamental properties of the solutions of the system, then deduced all steady states and proved their global properties. We examined the global stability of the steady states by constructing appropriate Lyapunov functions. The analytical results were illustrated by performing numerical simulations. We discussed the effect of HTLV-I infection on COVID-19 progression. The results suggest that patients with HTLV-I have a weakened immune response;consequently, their risk of COVID-19 infection may be increased.
ABSTRACT
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
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
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
The COVID-19 epidemic has infected millions of people and cast a shadow over the global economic recovery. To explore the epidemic's transmission law and provide theoretical guidance for epidemic prevention and control. In this paper, we investigate a novel SEIR-A reaction-diffusion COVID-19 system with direct and aerosol transmission. First, the solution's positivity and boundedness for the system are discussed. Then, the system's the basic reproduction number is defined. Further, the uniform persistence of disease when R 0 > 1 is explored. In addition, the system equilibrium's global stability based on R 0 is demonstrated. Next, the system's NSFD scheme is investigated and the discrete system's positivity, boundedness, and global properties are studied. Meantime, global sensitivity analysis on threshold R 0 is investigated. Interestingly, the effects of three strategies, including vaccination, receiving treatment, and wearing a mask, are evaluated numerically. The results suggest that the above three strategies can effectively control the peak and final scale of infection and shorten the duration of the epidemic. Finally, theoretical simulations and instance predictions are used to give several key indicators of the epidemic, including threshold R 0 , peak, time to peak, time to clear cases, and final size. The instance prediction results are as follows: (1) The basic reproduction numbers of Yangzhou and Putian in China are R 0 = 2.5107 and R 0 = 1.8846 , respectively. (2) This epidemic round in Yangzhou will peak at 56 new daily confirmed cases on the 9th day (August 5), and Putian will peat at 37 new daily confirmed cases on the 6th day (September 15). (3) The final scale of infections in Yangzhou and Putian reached 570 and 205 cases, respectively. (4) The Yangzhou epidemic is expected to be completely cleared on the 25th day (August 21). In addition, the Putian epidemic will continue for 15 days and be cleared on September 24. The analysis results mean that we should improve our immunity by actively vaccinating, reducing the possibility of aerosol transmission by wearing masks. In particular, people should maintain proper social distance, and the government should strengthen medical investment and COVID-19 project research.
ABSTRACT
The mathematical modeling and analysis of within-host or between-host coronavirus disease 2019 (COVID-19) dynamics are considered robust tools to support scientific research. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of COVID-19. This paper proposes and investigates a within-host COVID-19 dynamics model with latent infection, the logistic growth of healthy epithelial cells and the humoral (antibody) immune response. Time delays can affect the dynamics of SARS-CoV-2 infection predicted by mathematical models. Therefore, we incorporate four time delays into the model: (i) delay in the formation of latent infected epithelial cells, (ii) delay in the formation of active infected epithelial cells, (iii) delay in the activation of latent infected epithelial cells, and (iv) maturation delay of new SARS-CoV-2 particles. We establish that the model's solutions are non-negative and ultimately bounded. This confirms that the concentrations of the virus and cells should not become negative or unbounded. We deduce that the model has three steady states and their existence and stability are perfectly determined by two threshold parameters. We use Lyapunov functionals to confirm the global stability of the model's steady states. The analytical results are enhanced by numerical simulations. The effect of time delays on the SARS-CoV-2 dynamics is investigated. We observe that increasing time delay values can have the same impact as drug therapies in suppressing viral progression. This offers some insight useful to develop a new class of treatment that causes an increase in the delay periods and then may control SARS-CoV-2 replication.