Autoimmune diseases post-COVID 19 infection in children in intensive care unit: A case series.

SARS-CoV2 primarily affects the respiratory system but a hyperinflammatory response leading to multisystem inflammatory syndrome - children (MIS-C), immune dysfunction and various autoimmune manifestations has also been noted. Autoimmunity depends on various factors, including genetic predisposition, environmental factors, immune dysregulation and infections acting as triggers like Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, hepatitis B. Molecular mimicry, bystander T-cell activation and persistence of viral infection are the main mechanisms behind these manifestations. We present here 3 cases of newly diagnosed connective tissue disease with high titers of COVID19 immunoglobulin G antibody in children. A 9-year-old girl with fever, oliguria and malar rash (prior history of sore throat) and a 10-year-old girl with fever for 2 weeks and choreoathetoid movements were diagnosed as systemic lupus erythematosus (SLE) nephritis (stage 4) and neuropsychiatric SLE, respectively as per European League Against Rheumatism / American College of Rheumatology 2019 criteria. An 8-year-old girl with fever, joint pain and respiratory distress (a recent contact with a positive COVID19 patient) presented with altered sensorium, Raynaud's phenomenon noted, and eventually diagnosed as mixed connective tissue disease as per Kusukawa criteria. The immune-mediated manifestations post-COVID infection are a de-novo phenomenon which necessitates further workup as not many studies exist in the pediatric population.

Rheumatic manifestations and autoimmunity associated with COVID-19

A broad spectrum of complications following COVID-19 has been documented in adults, including the new onset of autoimmune-related manifestations and rheumatic diseases. Numerous case studies, reviews, and clinical trials have been published regarding the relationship between COVID-19 and the generation of autoantibodies that may cause rheumatic and autoimmune diseases. The currently suggested pathophysiology that leads to the new onset of such disorders may include well-established mechanisms, such as molecular mimicry and hyperstimulation of the immune system. The prevailing conditions documented following COVID-19 include, yet are not limited to, rheumatoid arthritis, myositis, antiphospholipid antibodies, ITP, and thyroid dysfunction. This chapter will summarize the current documentation of the broad-spectrum rheumatic diseases and autoimmune manifestations mediated by a SARS-CoV-2 infection. © 2023 Elsevier Inc. All rights reserved.

COVID-19: A Great Mime or a Trigger Event of Autoimmune Manifestations?

Viruses can induce autoimmune diseases, in addition to genetic predisposition and environmental factors. Particularly, coronaviruses are mentioned among the viruses implicated in autoimmunity. Today, the world's greatest threat derives from the pandemic of a new human coronavirus, called "severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the responsible agent of coronavirus disease 2019 (COVID-19). First case of COVID-19 was identified in Wuhan, the capital of Hubei, China, in December 2019 and quickly spread around the world. This review focuses on autoimmune manifestations described during COVID-19, including pro-thrombotic state associated with antiphospholipid antibodies (aPL), acute interstitial pneumonia, macrophage activation syndrome, lymphocytopenia, systemic vasculitis, and autoimmune skin lesions. This offers the opportunity to highlight the pathogenetic mechanisms common to COVID-19 and several autoimmune diseases in order to identify new therapeutic targets. In a supposed preliminary pathogenetic model, SARS-CoV-2 plays a direct role in triggering widespread microthrombosis and microvascular inflammation, because it is able to induce transient aPL, endothelial damage and complement activation at the same time. Hence, endothelium might represent the common pathway in which autoimmunity and infection converge. In addition, autoimmune phenomena in COVID-19 can be explained by regulatory T cells impairment and cytokines cascade.

The JANUS of chronic inflammatory and autoimmune diseases onset during COVID-19 - A systematic review of the literature.

The diverse clinical manifestations of COVID-19 is emerging as a hallmark of the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection. While the initial target of SARS-CoV-2 is the respiratory tract, it is becoming increasingly clear that there is a complex interaction between the virus and the immune system ranging from mild to controlling responses to exuberant and dysfunctional multi-tissue directed autoimmune responses. The immune system plays a dual role in COVID-19, being implicated in both the anti-viral response and in the acute progression of the disease, with a dysregulated response represented by the marked cytokine release syndrome, macrophage activation, and systemic hyperinflammation. It has been speculated that these immunological changes may induce the loss of tolerance and/or trigger chronic inflammation. In particular, molecular mimicry, bystander activation and epitope spreading are well-established proposed mechanisms to explain this correlation with the likely contribution of HLA alleles. We performed a systematic literature review to evaluate the COVID-19-related autoimmune/rheumatic disorders reported between January and September 2020. In particular, we investigated the cases of incident hematological autoimmune manifestations, connective tissue diseases, antiphospholipid syndrome/antibodies, vasculitis, Kawasaki-like syndromes, acute arthritis, autoimmune-like skin lesions, and neurologic autoimmune conditions such as Guillain-Barré syndrome. We screened 6263 articles and report herein the findings of 382 select reports which allow us to conclude that there are 2 faces of the immune response against SARS-CoV-2, that include a benign virus controlling immune response and a many faceted range of dysregulated multi-tissue and organ directed autoimmune responses that provides a major challenge in the management of this viral disease. The number of cases for each disease varied significantly while there were no reported cases of adult onset Still disease, systemic sclerosis, or inflammatory myositis.