Kawasaki-multisystem inflammatory syndrome in children in the delayed period of coronavirus infection (covid-19): modern state of the problem and possible new approaches to treatment (plasmapheresis)

The novel coronavirus (SARS-CoV-2) has produced millions of infections and deaths worldwide. It is believed that adaptive immunity to the virus occurs although with variation in its pattern and duration. While uncommon, confirmed reinfection with the novel coronavirus has been reported. Telemedicine has emerged as a viable tool for the delivery of healthcare in lieu of in-person patient contact. The variable and occasionally rapid course of clinical disease raises safety concerns of using telemedicine in the clinical management of acute infection with the novel coronavirus. We present a case of novel coronavirus infection in an immunocompetent individual with obstructive sleep apnea (OSA) who failed to manifest an adaptive immune response to acute infection and was subsequently reinfected. The case highlights the use of telemedicine in managing novel coronavirus respiratory disease and the potential role of OSA as a disease facilitator.

AbstractThe risk of serious complications and the fatality rate due to COVID-19 pandemic have proven particularly higher in older persons, putting a further strain in healthcare system as we dramatically observed.COVID-19 is not exclusively gerophile (géro “old” and philia “love”) as young people can be infected, even if older people experience more severe symptoms and mortality due to their greater frailty. Indeed, frailty could complicate the course of COVID-19, much more than the number of years lived. As demonstration, there are centenarians showing remarkable capacity to recover after coronavirus infection.We hypothesize that centenarian’s portfolio could help in identifying protective biological mechanisms underlying the coronavirus infection.The human leukocyte antigen (HLA) is one of the major genetic regions associated with human longevity, due to its central role in the development of adaptive immune response and modulation of the individual’s response to life threatening diseases. The HLA locus seems to be crucial in influencing susceptibility and severity of COVID-19.In this hypothesis, we assume that the biological process in which HLA are involved may explain some aspects of coronavirus infection in centenarians, although we cannot rule out other biological mechanisms that these extraordinary persons are able to adopt to cope with the infection.

Introduction: COVID-19, caused by the new coronavirus or SARSCoV-2, has a high capacity for dissemination, which brings about an emergency scenario in public health. It manifests itself in a multifaceted manner, with a great variability in the profile of the affected population, which may be associated with biological, social and economic factors. Objective: To know the epidemiological profile of the population affected by COVID-19, in order to promote better assistance.   Methods: This is a literature review, starting in 2020, using the SciELO, PubMed, Google Scholar, DATASUS databases and the website of the Brazilian Institute of Geography and Statistics (IBGE).   Results: Studies show a higher prevalence of SARS-CoV-2 infection in men, in the age group after the fourth decade of life and among whites.   Discussion: The first studies showed a prevalence of coronavirus infection in males. One of the hypotheses drawn was that men present more cardiopulmonary diseases and smoke more. Another study shows that women's lower susceptibility to infection is due to the X chromosome and sex hormones, which are essential for the innate and adaptive immune response. As for the age group, most studies show a higher prevalence after the fourth decade of life, due to increased expression of angiotensin 2 receptors (ACE2), hormonal changes in aging and associated comorbidities.   Conclusion: Studies show with greater assertiveness a predominance of involvement by COVID-19 in males, individuals from the fourth decade of life and in whites. However, it is important to investigate the epidemiological profile in order to offer better assistance and prevention.

The article is devoted to the peculiarities of clinical manifestations and the severity of a new coronary virus infection in a university student transferred to an observatory organized in a hotel-type hostel to prevent the spread of COVID-19 among students living in hostels. The data on the epidemiological history of the patient, the results of clinical observation and examination are provided. The tactics of managing a patient with a suspected of COVID-19 on an outpatient basis, symptoms that determine the indications for hospitalization, the results of examination and treatment in a hospital, and further observation at the observatory are considered. A new coronavirus infection can lead to a rapid deterioration in the condition of young patients, which does not correlate with indicators indicating lung damage on the 5th day of the disease. Persistent hyperthermia and severe weakness with anorexia can be indicators of the complicated course of the disease, including the development of hyperactive inflammatory syndrome. Hypochromic anemia can be another disease, which is an unfavorable background for the development of COVID-19. The course of the new coronavirus infection in young patients requires careful attention and further study.

Both coronavirus disease 2019 (COVID-19) and mycobacterial immune reconstitution inflammatory syndrome (IRIS) in patients with HIV-1 infection result from immunopathology that is characterized by increased production of multiple pro-inflammatory chemokines and cytokines associated with activation of myeloid cells (monocytes, macrophages and neutrophils). We propose that both conditions arise because innate immune responses generated in the absence of effective adaptive immune responses lead to monocyte/macrophage activation that is amplified by the emergence of a pathogen-specific adaptive immune response skewed towards monocyte/macrophage activating activity by the immunomodulatory effects of cytokines produced during the innate response, particularly interleukin-18. In mycobacterial IRIS, that disease-enhancing immune response is dominated by a Th1 CD4+ T cell response against mycobacterial antigens. By analogy, it is proposed that in severe COVID-19, amplification of monocyte/macrophage activation results from the effects of a SARS-CoV-2 spike protein antibody response with pro-inflammatory characteristics, including high proportions of IgG3 and IgA2 antibodies and afucosylation of IgG1 antibodies, that arises from B cell differentiation in an extra-follicular pathway promoted by activation of mucosa-associated invariant T cells. We suggest that therapy for the hyperinflammation underlying both COVID-19 and mycobacterial IRIS might be improved by targeting the immunomodulatory as well as the pro-inflammatory effects of the ‘cytokine storm’.

This article deals with the dynamics of the innate and adaptive immune response to severe acute respiratory syndrome coronavirus 2 (SARSCoV2) infection. SARSCoV2 is the viral factor that causes the current global coronavirus pandemic disease 2019 (COVID2019). In terms of person-to-person transmission, it is contacted by inhaling the sneeze droplets of infected people. Severe acute respiratory syndrome Coronavirus 2 attacks lung cells first in its binding mechanism because there are many conservative receptor entries, such as angiotensin converting enzyme 2. The presence of this virus in host cells triggers a variety of protective immune responses, resulting in leads to pneumonia and acute respiratory distress syndrome. In the SarsCoV2 infection process, virus replication, immune response, and inflammatory response are dynamic events that can change rapidly; leading to different results, involving the dynamic expression of pro-inflammatory genes, peaking after the lowest point of respiratory function and leading to a cytokine storm, research on the interleukin 1 (IL1) pathway has shown that it is a factor related in severe respiratory diseases. The weakened expression of cytokines associated with mild infections will also delay T cell immunity to SARSCoV2, thereby prolonging the infection time; this indicates that such afebrile (afebrile) infections and undifferentiated COVID19 cases may promote the virus in the community Spread. This review aims to provide a general overview of the dynamics involved in the human immune response to this viral infection. It also includes a brief description of its structure, discovery history and pathogenesis to facilitate the understanding of this article.

: Coronavirus infection 2019 (COVID-19) primarily has a respiratory system and multi-systemic involvement. Respiratory and gastrointestinal symptoms are predominantly seen in children. In adults, few COVID-19 cases are reported with cutaneous manifestations. Although children are less severely affected by COVID-19, there is increasing evidence for skin involvement, which is in the form of chilblain (e.g., lesions, vesicular, and maculopapular) and erythema multiforme (e.g., rash). Also, few COVID-19 cases are presented with a clinical picture of atypical Kawasaki disease and toxic shock syndrome, later defined as pediatric multisystem inflammatory syndrome (PMIS). The present study aims to summarize various skin lesions with COVID-19.

ABSTRACTGenomic material from many neurotropic RNA viruses (e.g., measles virus [MV], West Nile virus [WNV], Sindbis virus [SV], rabies virus [RV], and influenza A virus [IAV]) remains detectable in the mouse brain parenchyma long after resolution of the acute infection. The presence of these RNAs in the absence of overt central nervous system (CNS) disease has led to the suggestion that they are viral remnants, with little or no potential to reactivate. Here we show that MV RNA remains detectable in permissive mouse neurons long after challenge with MV and, moreover, that immunosuppression can cause RNA and protein synthesis to rebound, triggering neuropathogenesis months after acute viral control. Robust recrudescence of viral transcription and protein synthesis occurs after experimental depletion of cells of the adaptive immune response and is associated with a loss of T resident memory (Trm) lymphocytes within the brain. The disease associated with loss of immune control is distinct from that seen during the acute infection: immune cell-depleted, long-term-infected mice display severe gait and motor problems, in contrast to the wasting and lethal disease that occur during acute infection of immunodeficient hosts. These results illuminate the potential consequences of noncytolytic, immune-mediated viral control in the CNS and demonstrate that what were once considered “resolved” RNA viral infections may, in fact, induce diseases later in life that are distinct from those caused by acute infection.IMPORTANCEViral infections of neurons are often not cytopathic; thus, once-infected neurons survive, and viral RNAs can be detected long after apparent viral control. These RNAs are generally considered viral fossils, unlikely to contribute to central nervous system (CNS) disease. Using a mouse model of measles virus (MV) neuronal infection, we show that MV RNA is maintained in the CNS of infected mice long after acute control and in the absence of overt disease. Viral replication is suppressed by the adaptive immune response; when these immune cells are depleted, viral protein synthesis recurs, inducing a CNS disease that is distinct from that observed during acute infection. The studies presented here provide the basis for understanding how persistent RNA infections in the CNS are controlled by the host immune response, as well as the pathogenic consequences of noncytolytic viral control.

X-linked inhibitor of apoptosis (XIAP) deficiency is a rare inborn error of immunity first described in 2006. XIAP deficiency is characterised by immune dysregulation and a broad spectrum of clinical manifestations, including haemophagocytic lymphohistiocytosis (HLH), inflammatory bowel disease (IBD), hypogammaglobulinemia, susceptibility to infections, splenomegaly, cytopaenias, and other less common autoinflammatory phenomena. Since the first description of the disease, many XIAP deficient patients have been identified and our understanding of the disease has grown. Over 90 disease causing mutations have been described and more inflammatory disease manifestations, such as hepatitis, arthritis, and uveitis, are now well-recognised. Recently, following the introduction of reduced intensity conditioning (RIC), outcomes of allogeneic haematopoietic stem cell transplantation (HSCT), the only curative treatment option for XIAP deficiency, have improved. The pathophysiology of XIAP deficiency is not fully understood, however it is known that XIAP plays a role in both the innate and adaptive immune response and in immune regulation, most notably through modulation of tumour necrosis factor (TNF)-receptor signalling and regulation of NLRP3 inflammasome activity. In this review we will provide an up to date overview of both the clinical aspects and pathophysiology of XIAP deficiency.