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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]

We highlighted in this current paper similar prolonged respiratory presentation with COVID-19 pneumonia in four severely immunocompromised patients currently being treated with anti-CD20 monoclonal antibodies (mAbs), such as ocrelizumab and rituximab, for multiple sclerosis or rheumatoid polyarthritis. Real-time reverse transcription-polymerase chain reaction on a nasopharyngeal swab specimen was negative in all patients. SARS-CoV-2 infection was confirmed from bronchoalveolar lavage fluid. A high titer of post-vaccine COVID-19 convalescent plasma was administered with complete recovery in all patients. [ABSTRACT FROM AUTHOR]

Cellular immunity against SARS-CoV-2 is an important component of the immune response to the virus. At present, two such tests based on interferon-gamma release (interferon-γ release assays, IGRAs) are available—Quan-T-Cell SARS-CoV-2 by EUROIMMUN and T-SPOT.COVID by Oxford Immunotec. In this paper, we compared the results of these two tests in 90 subjects employed at the Public Health Institute Ostrava who had previously undergone COVID-19 infection or were vaccinated against that disease. To the best of our knowledge, this is the first head-to-head comparison of these two tests evaluating T-cell-mediated immunity against SARS-CoV-2. In addition, we also evaluated humoral immunity in the same individuals using the in-house virus neutralization test and IgG ELISA assay. The evaluation yielded similar results for both IGRAs, with Quan-T-Cell appearing to be insignificantly (p = 0.08) more sensitive (all 90 individuals were at least borderline positive) than T-SPOT.COVID (negative results found in five patients). The overall qualitative (presence/absence of immune response) agreement of both tests with virus neutralization test and anti-S IgG was also excellent (close or equal to 100% in all subgroups, with the exception of unvaccinated Omicron convalescents, a large proportion of whom, i.e., four out of six subjects, were IgG negative while at least borderline positive for T-cell-mediated immunity measured by Quan-T). This implies that the evaluation of T-cell-mediated immunity is a more sensitive indicator of immune response than the evaluation of IgG seropositivity. This is true at least for unvaccinated patients with a history of being infected only by the Omicron variant, but also likely for other groups of patients. [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 immune response plays a crucial role in preventing diseases, such as infections. There are two types of immune responses, specific and innate immunity, each of which consists of two components: cellular immunity and humoral immunity. Dysfunction in any immune system component increases the risk of developing certain diseases. Systemic lupus erythematosus (SLE), an autoimmune disease in the human body, develops an immune response against its own components. In these patients, due to underlying immune system disorders and receipt of immunosuppressive drugs, the susceptibility to infections is higher than in the general population and is the single largest cause of mortality in this group. COVID-19 infection, which first appeared in late 2019, has caused several concerns in patients with SLE. However, there is no strong proof of additional risk of developing COVID-19 in patients with SLE, and in some cases, studies have shown less severity of the disease in these individuals. This review paper discusses the immune disorders in SLE and COVID-19. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Currently, SARS-CoV-2 spike receptor-binding-domain (RBD)-based vaccines are considered one of the most effective weapons against COVID-19. During the first step of assessing vaccine immunogenicity, a mouse model is often used. In this paper, we tested the use of five experimental animals (mice, hamsters, rabbits, ferrets, and chickens) for RBD immunogenicity assessments. The humoral immune response was evaluated by ELISA and virus-neutralization assays. The data obtained show hamsters to be the least suitable candidates for RBD immunogenicity testing and, hence, assessing the protective efficacy of RBD-based vaccines. [ABSTRACT FROM AUTHOR]

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing COVID-19 is associated with excessive inflammation, as a main reason for severe condition and death. Increased inflammatory cytokines and humoral response to SARS-CoV-2 correlate with COVID-19 immunity and pathogenesis. Importantly, the levels of pro-inflammatory cytokines that increase profoundly in systemic circulation appear as part of the clinical pictures of two overlapping conditions, sepsis and the hemophagocytic syndromes. Both conditions can develop lethal inflammatory responses that lead to tissue damage, however, in many patients hemophagocytic lymphohistiocytosis (HLH) can be differentiated from sepsis. This is a key issue because the life-saving aggressive immunosuppressive treatment, required in the HLH therapy, is absent in sepsis guidelines. This paper aims to describe the pathophysiology and clinical relevance of these distinct entities in the course of COVID-19 that resemble sepsis and further highlights two effector arms of the humoral immune response (inflammatory cytokine and immunoglobulin production) during COVID-19 infection. [ABSTRACT FROM AUTHOR]

Summary: The factors responsible for the spectrum of coronavirus 19 (COVID‐19) disease severity and the genesis and nature of protective immunity against COVID‐19 remain elusive. Multiple studies have investigated the immune responses to COVID‐19 in various populations, including those without evidence of COVID‐19 infection. Information regarding innate and adaptive immune responses to the novel severe respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has evolved rapidly. Data are accumulating defining disease phenotypes that aid in rational and informed development of new therapeutic approaches for the treatment of patients infected with SARS‐CoV‐2 and the development of novel vaccines. In this paper, data on important innate immune responses are summarized, including cytokines, specifically interleukin (IL)‐6 and complement, and potential treatments are explored. Adaptive immune responses and derivative therapeutics such as monoclonal antibodies directed at spike proteins are also examined. Finally, data on real‐time assessments of adaptive immune responses are explored, which include CD4+/CD8+ T cells, natural killer (NK) T cells, memory B cells and T follicular cells with specificities for COVID‐19 peptides in infected and normal individuals. Data of two novel vaccines have been released, both showing > 95% efficacy in preventing SARS‐CoV‐2 infection. Analysis of humoral and cellular responses to the vaccines will determine the robustness and durability of protection. In addition, long‐term assessment of SARS‐CoV‐2 memory B and T cell‐mediated immune responses in patients recovering from an infection or those with cross‐reactive immunological memory will help to define risk for future SARS‐CoV infections. Finally, patients recovering from SARS‐CoV‐2 infection may experience prolonged immune activation probably due to T cell exhaustion. This will be an important new frontier for study. This review summarizes published data on the relevant innate and adaptive immune responses to SARS‐CoV‐2. Data characterizing innate and adaptive immune responses have rapidly led to informed therapeutic interventions, including vaccine development and recognition of dysfunctional immune responses that are likely responsible for post‐COVID‐19 autoimmunity. [ABSTRACT FROM AUTHOR]

Since its outbreak in December 2019, the coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), led to an enormous rise in scientific response with an excess of COVID-19-related studies on the pathogenesis and potential therapeutic approaches. Solid organ transplant (SOT) recipients are a heterogeneous population with long-lasting immunosuppression as a joining element. Immunocompromised patients are a vulnerable population with a high risk of severe infections and an increased infection-related mortality rate. It was postulated that the hyperinflammatory state due to cytokine release syndrome during severe COVID-19 could be alleviated by immunosuppressive therapy in SOT patients. On the other hand, it was previously established that T cell-mediated immunity, which is significantly weakened in SOT recipients, is the main component of antiviral immune responses. In this paper, we present the current state of science on COVID-19 immunology in relation to solid organ transplantation with prospective therapeutic and vaccination strategies in this population. [ABSTRACT FROM AUTHOR]