The Multifaceted Manifestations of Multisystem Inflammatory Syndrome during the SARS-CoV-2 Pandemic

Abstract

The novel coronavirus SARS-CoV-2, which has similarities to the 2002–2003 severe acute respiratory syndrome coronavirus known as SARS-CoV-1, causes the infectious disease designated COVID-19 by the World Health Organization (Coronavirus Disease 2019). Although the first reports indicated that activity of the virus is centered in the lungs, it was soon acknowledged that SARS-CoV-2 causes a multisystem disease. Indeed, this new pathogen causes a variety of syndromes, including asymptomatic disease; mild disease; moderate disease; a severe form that requires hospitalization, intensive care, and mechanical ventilation; multisystem inflammatory disease; and a condition called long COVID or postacute sequelae of SARS-CoV-2 infection. Some of these syndromes resemble previously described disorders, including those with no confirmed etiology, such as Kawasaki disease. After recognition of a distinct multisystem inflammatory syndrome in children, followed by a similar syndrome in adults, various multisystem syndromes occurring during the pandemic associated or related to SARS-CoV-2 began to be identified. A typical pattern of cytokine and chemokine dysregulation occurs in these complex syndromes; however, the disorders have distinct immunological determinants that may help to differentiate them. This review discusses the origins of the different trajectories of the inflammatory syndromes related to SARS-CoV-2 infection.

Evaluation of 34 Cytokines and Vitamin D Status Reveal A Sexually-Dimorphic Active Immune Response to SARS-CoV-2

“…More importantly, our results showed that male patients had significantly higher serum concentrations of VEGF, IFNγ, IL-13, and IL-5 than female patients. This is in line with previous studies demonstrating a stronger response in cytokines and chemokines in SARS-CoV-2-infected male than in female patients [ 6 , 13 ]. Differences in the expression of cytokines and chemokines secondary to infection are partially yet substantially controlled by sex hormones, which modulate the innate immune function at various stages of human life concurrent with hormonal changes.…”

“…SARS-CoV-2 infection induces over-production of pro-inflammatory cytokines and chemokines as a defense mechanism against the viral infection. On the other hand, a dysregulation, i.e., hyper-inflammation, results in cytokine release syndrome (CRS) leading to apoptosis of immune cells, impaired cytotoxic function, and tissue damage [ 13 ]. More importantly, our results showed that male patients had significantly higher serum concentrations of VEGF, IFNγ, IL-13, and IL-5 than female patients.…”

“…In fact, hyperinflammation caused by cytokine release syndrome (CRS), as well as upregulation of inflammatory cytokines [ 4 ], are associated with the severity of COVID-19 disease [ 4 , 9 ]. Likewise, significant elevation of the pro-inflammatory cytokine profile has been reported as a key player in the severity and eventual death of patients with SARS-CoV [ 10 ], MERS-CoV [ 11 ], and SARS-CoV-2 diseases [ 7 , 10 , 11 , 12 , 13 , 14 ]. Furthermore, data from COVID-19 patients indicated high circulating levels of IL-10 and IL-4, which are protective against inflammation [ 15 ].…”

COVID-19 Heart Lesions in Children: Clinical, Diagnostic and Immunological Changes

“…It has the high transmissibility and moreover, the ability to escape from immune response, caused by vaccination or natural infection [ 16 ]. In addition, its pathogenicity is much lower and it causes less hospitalization, lethal outcomes and severe cases [ 17 , 18 ]. However, it should be noted, in comparison with Delta variant, Omicron increased a number of hospitalizations among children aged 5–11 [ 19 , 20 ].…”

Modulation of redox-sensitive transcription factors with polyphenols as pathogenetically grounded approach in therapy of systemic inflammatory response

“…Due to an aggregation of uncleaved angiotensin II, the stimulated inflammatory cells cause cytokines synthesis and secretion (cytokine storming), leading to widespread tissue injuries [ 38 ]. In some cases severe acute respiratory syndrome coronavirus can form the HGSIP (elevated CRP, fibrinogen, procalcitonin, D-dimer, ferritin, IL-6, erythrocyte sedimentation rate, elevated neutrophils, reduced lymphocytes, low albumin), whose consequences include Multisystem Inflammatory Syndrome (MIS) affected children (MIS-C) and adults (MIS-A) with inflammation of a variety of organ systems, including the heart, lungs, brain, kidneys, gastrointestinal system, skin, and eyes [ [39] , [40] , [41] ]. However, criterial signs of the SIRS may be absent.…”