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Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and influenza A virus (IAV) are two respiratory viruses and are similar concerning seasonal occurrence, transmission routes, clinical manifestations, and related immune responses. Recent studies showed that a substantial number of patients infected by SARS‐CoV‐2 were also coinfected with IAV. In this paper, we study the global properties of SARS‐CoV‐2 and IAV coinfection model in vivo. The role of humoral (antibody) immunity in controlling the coinfection is modeled. The model tracks uninfected epithelial cells, latent SARS‐CoV‐2‐infected epithelial cells, latent IAV‐infected epithelial cells, active SARS‐CoV‐2‐infected epithelial cells, active IAV‐infected epithelial cells, free SARS‐CoV‐2 particles, free IAV particles, SARS‐CoV‐2‐specific antibodies and IAV‐specific antibodies. The model includes six distributed‐time delays, two delays for the formation of latent SARS‐CoV‐2‐infected and latent IAV‐infected cells; two delays for the reactivation of latent SARS‐CoV‐2‐infected cells and latent IAV‐infected cells; and two delays for the maturation of new released SARS‐CoV‐2 and IAV virions. The regeneration and death of the uninfected epithelial cells are considered. We first examine the basic qualitative properties of the model, then we calculate all equilibria and prove their global stability. The global stability of equilibria is established using the Lyapunov method. The theoretical findings are demonstrated via numerical simulations. The importance of considering humoral immunity in the coinfection dynamics model is discussed. It is found that without modeling the humoral immunity, the case of IAV and SARS‐CoV‐2 coexistence will not occur. We discuss the effect of time delays on the dynamics of SARS‐CoV‐2 and IAV coinfection. It is noted that increasing the time delay length has similar impact as antiviral therapies. [ABSTRACT FROM AUTHOR]

Background. The impact of SARS-CoV-2 infection alongside with influenza and RSV, the major viral agents in pediatric disordes, may be an important concern to the healthcare system. Clinical outcomes of the interaction are unknown. The aim of this systematic review is to contribute at establishing the prevalence of the co-infection, its clinical outcomes and potential risk factors. Methods. A systematical literature search was performed for papers published in PubMed, Scopus, Web of Science, Pedro and Cochrane Library, from January 2020 - the beginning of the COVID 19 pandemic - to June 2023. Our review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methods. Studies were eligible for inclusion if they approached the co-infection COVID 19 and influenza or RSV, and were available in English. Due to the fact that studies conducted on pediatric population are scarce, we included patients of all ages. Results. Out of 159 articles found, 12 were eligible for inclusion. The prevalence of co-infection was between 5% and 12 % for influenza viruses and 10% for RSV. The most common symptoms were high-grade fever, cough, headache, and shortness of breath and the most frequent complications were pneumonia and respir-atory distress. In terms of laboratory findings, co-infected patients presented with signifi-cant lymphopenia and pronounced inflammatory response, as well as a progressive ten-dency towards pneumonia and respiratory distress. Regarding the clinical outcomes of co-infection, the majority of articles indicated that simultaneous infection with SARS-CoV-2 and influenza predisposes to a more severe course of the disease(s), with a longer length of hospital stay and an increased risk of death. Conclusion. Our study underlines that the frequency of such co-infections, although not very high, predisposes to more frequent hos-pitalisations and a longer length of stay, complications including admission to intensive care and more severe outcomes, including life-threatening events. It is therefore essential to determine the epidemiological impact of such an interaction nowadays, in order to in-form and adjust treatment and control and prevention strategies, for limiting co-infection between major respiratory viruses. Due to the lack of studies on children, we were unable to identify specific features of co-infections in this population. Therefore, more studies are needed to evaluate the paediatric population and consequently, our doctoral research en-deavour is warranted. [ABSTRACT FROM AUTHOR]

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]

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 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]

The world has been suffering from the coronavirus disease 2019 (COVID‐19) since late 2019. COVID‐19 is caused by a virus called the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). The human immunodeficiency virus (HIV) coinfection with SARS‐CoV‐2 has been reported in many patients around the world. This has raised the alarm for the importance of understanding the dynamics of coinfection and its impact on the lives of patients. As in other pandemics, mathematical modeling is one of the important tools that can help medical and experimental studies of COVID‐19. In this paper, we develop a within‐host SARS‐CoV‐2/HIV coinfection model. The model consists of six ordinary differential equations. It depicts the interactions between uninfected epithelial cells, infected epithelial cells, free SARS‐CoV‐2 particles, uninfected CD4+ T cells, infected CD4+ T cells, and free HIV particles. We confirm that the solutions of the developed model are biologically acceptable by proving their nonnegativity and boundedness. We compute all possible steady states and derive their positivity conditions. We choose suitable Lyapunov functions to prove the global asymptotic stability of all steady states. We run some numerical simulations to enhance the global stability results. Based on our model, weak CD4+ T cell immune response or low CD4+ T cell counts in SARS‐CoV‐2/HIV coinfected patient increase the concentrations of infected epithelial cells and SARS‐CoV‐2 viral load. This causes the coinfected patient to suffer from severe SARS‐CoV‐2 infection. This result agrees with many studies which showed that HIV patients are at greater risk of suffering from severe COVID‐19 when infected. More studies are needed to understand the nature of SARS‐CoV‐2/HIV coinfection and the role of different immune responses during infection. [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]

Tuberculosis is still an important medical and social problem. In recent years, great strides have been made in the fight against M. tuberculosis, especially in the Russian Federation. However, the emergence of a new coronavirus infection (COVID-19) has led to the long-term isolation of the population on the one hand and to the relevance of using personal protective equipment on the other. Our knowledge regarding SARS-CoV-2-induced inflammation and tissue destruction is rapidly expanding, while our understanding of the pathology of human pulmonary tuberculosis gained through more the 100 years of research is still limited. This paper reviews the main molecular and cellular differences and similarities caused by M. tuberculosis and SARS-CoV-2 infections, as well as their critical immunological and pathomorphological features. Immune suppression caused by the SARS-CoV-2 virus may result in certain difficulties in the diagnosis and treatment of tuberculosis. Furthermore, long-term lymphopenia, hyperinflammation, lung tissue injury and imbalance in CD4+ T cell subsets associated with COVID-19 could propagate M. tuberculosis infection and disease progression. [ABSTRACT FROM AUTHOR]