Potential Pathophysiological Mechanisms Underlying Multiple Organ Dysfunction in Cytokine Release Syndrome

Chen, Peixian; Tang, Yan; He, Weixin; Yang, Ruixuan; Lan, Zhien; Chen, Ruirong; Zhang, Peidong

doi:10.1155/2022/7137900

Cited by 12 publications

(12 citation statements)

References 148 publications

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“…It suppresses the activity of Il-6 and Il-1β, thus taming the inflammatory response [78]. It is often excessive cytokine production by an overactive immune system that leads to tissue damage and life-threatening multiple-organ failure [79].…”

Section: A Role For Hsp70 and Diabetesmentioning

confidence: 99%

SARS-CoV-2 Spike Protein in the Pathogenesis of Prion-like Diseases

Seneff

Kyriakopoulos²,

Nigh

et al. 2022

Preprint

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Human prion protein and prion-like protein misfolding are widely recognized as playing a causal role in a large and growing number of neurodegenerative diseases. Here we summarize the compelling evidence that the spike protein of SARS-CoV-2 contains extended amino acid sequences previously established as characteristic of a prion-like protein. This suggests that vaccine-induced spike protein production is synonymous with production of a prion-like protein, and we trace some of the various pathways through which these proteins should be expected to traverse and distribute throughout the body. We describe some of the highly concerning biological consequences that would be expected to occur with increased frequency as a consequence. Specifically, we describe spike-protein contribution, via its prion-like properties, to neuroinflammation and neurodegenerative diseases; to clotting disorders within the vasculature; to suppressed prion protein regulation in the context of widely prevalent insulin resistance; and other health complications it could be expected to induce. We explain why these prion-like characteristics are more relevant to vaccine-related mRNA-induced spike proteins than natural infection with SARS-CoV-2. We conclude with some potentially ominous public health implications and recommendations for investigations of these possibilities.

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Section: A Role For Hsp70 and Diabetesmentioning

confidence: 99%

SARS-CoV-2 Spike Protein in the Pathogenesis of Prion-like Diseases

Seneff

Kyriakopoulos²,

Nigh

et al. 2022

Preprint

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“…Those various alterations and symptoms are, in some individuals, persistent after infection. In the central nervous system, the pathophysiological mechanisms underlying these symptoms are heterogeneous and may also be related to the excessive cytokine release present in COVID-19 [ 138 ], as well as the direct cytopathogenic effects of the virus [ 152 ]. Considering the strict association with the gut microbiota (gut–brain axis) [ 153 ], this could influence neurological alterations and symptoms.…”

Section: Discussionmentioning

confidence: 99%

Multidistrict Host–Pathogen Interaction during COVID-19 and the Development Post-Infection Chronic Inflammation

et al. 2022

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Due to the presence of the ACE2 receptor in different tissues (nasopharynx, lung, nervous tissue, intestine, liver), the COVID-19 disease involves several organs in our bodies. SARS-CoV-2 is able to infect different cell types, spreading to different districts. In the host, an uncontrolled and altered immunological response is triggered, leading to cytokine storm, lymphopenia, and cellular exhaustion. Hence, respiratory distress syndrome (ARDS) and systemic multi-organ dysfunction syndrome (MODS) are established. This scenario is also reflected in the composition of the microbiota, the balance of which is regulated by the interaction with the immune system. A change in microbial diversity has been demonstrated in COVID-19 patients compared with healthy donors, with an increase in potentially pathogenic microbial genera. In addition to other symptoms, particularly neurological, the occurrence of dysbiosis persists after the SARS-CoV-2 infection, characterizing the post-acute COVID syndrome. This review will describe and contextualize the role of the immune system in unbalance and dysbiosis during SARS-CoV-2 infection, from the acute phase to the post-COVID-19 phase. Considering the tight relationship between the immune system and the gut–brain axis, the analysis of new, multidistrict parameters should be aimed at understanding and addressing chronic multisystem dysfunction related to COVID-19.

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“…The inflammatory effects of key cytokines such as IL-1, IL-6, IFN-γ and TNF-α are realized through the appropriate intracellular signaling pathways resulting in the activation of nuclear factor kappa-light-chain-enhancer of activated B cells' (NF-κB), JAK/STAT and MAPK pathways [34,35]. Through various combinations of cytokine receptors and signal transduction pathways, a one signaling molecule may not only participate in one pathway, but also affect the transduction of other pathways.…”

Section: Pathophysiological Mechanisms Of Joint Damage In Sars-cov-2 ...mentioning

confidence: 99%

View of the Pathogenetic Mechanisms of Joint Damage in Coronavirus Disease 2019

Borodin¹,

Tuharov²,

Ostapchenko³

et al. 2022

BTSNUKSB

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The Сoronavirus disease 2019 (COVID-19) pandemic has had an extremely serious impact on the livelihoods of people worldwide. Despite the mainly respiratory manifestations of SARS-CoV-2 infection, its consequences can affect the functioning of most systems of organism, including the musculoskeletal, dysfunction of which is a leading factor in disability of the population. Diseases of the joints are one of the most common pathologie of modernity, which in the last decade are increasingly found in young people and even children. The musculoskeletal symptoms can be observed as isolated clinical signs and expressed regardless of the severity of the viral disease. Chronic fatigue, myalgia, swelling and joint pain may occur during the acute phase of COVID-19 and as short-term or long-term complications, but their prevalence has not been systematically studied. Considering the wide range of clinical manifestations of SARS-CoV-2 infection and the complexity of their pathogenesis, the mechanisms underlying lesions of musculoskeletal system and rheumatological complications remain unclear. Today, the main research in this direction is focused mainly on a complete understanding of the regulatory pathways of immune dysregulation and inflammation. Excessive secretion of pro-inflammatory cytokines, disruption of signal transduction and immune response are the result of the severe impact of SARS-CoV-2 infection on most organs, including joints, as well as the use of corticosteroids for the treatment of patients with COVID-19. The presented review highlights generalized information on the main pathophysiological processes that can occur in the joints as a manifestation of the impact of SARS-CoV-2 infection, and possible key mechanisms which contribute to the progression of pathological changes.

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Potential Pathophysiological Mechanisms Underlying Multiple Organ Dysfunction in Cytokine Release Syndrome

Cited by 12 publications

References 148 publications

SARS-CoV-2 Spike Protein in the Pathogenesis of Prion-like Diseases

SARS-CoV-2 Spike Protein in the Pathogenesis of Prion-like Diseases

Multidistrict Host–Pathogen Interaction during COVID-19 and the Development Post-Infection Chronic Inflammation

View of the Pathogenetic Mechanisms of Joint Damage in Coronavirus Disease 2019

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