Sepsis-associated severe interleukin-6 storm in critical coronavirus disease 2019

Huang, Lan; Zhao, Xuan; Qi, Yu; Li, Hong; Ye, Guanchao; Liu, Yafei; Zhang, Yi; Gou, Jianjun

doi:10.1038/s41423-020-00522-6

Cited by 35 publications

(28 citation statements)

References 10 publications

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“…Additional experiments are needed to validate the effect of the IL6-201 isoform on IL-6 protein activity in SARS-CoV-2-infected lung tissues. However, elevated IL-6 was observed in more than half of COVID-19 patients 68 and was associated with COVID-19 complications, progression and poor prognosis, respiratory failure, sepsis, and mortality risk [69][70][71][72][73] . Our observations suggest the possibility that isoform switching, as well as upregulation of gene expression, may contribute to this IL-6 elevation.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis

Ferrarini

Rebollo

et al. 2021

Commun Biol

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The novel betacoronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a worldwide pandemic (COVID-19) after emerging in Wuhan, China. Here we analyzed public host and viral RNA sequencing data to better understand how SARS-CoV-2 interacts with human respiratory cells. We identified genes, isoforms and transposable element families that are specifically altered in SARS-CoV-2-infected respiratory cells. Well-known immunoregulatory genes including CSF2, IL32, IL-6 and SERPINA3 were differentially expressed, while immunoregulatory transposable element families were upregulated. We predicted conserved interactions between the SARS-CoV-2 genome and human RNA-binding proteins such as the heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) and eukaryotic initiation factor 4 (eIF4b). We also identified a viral sequence variant with a statistically significant skew associated with age of infection, that may contribute to intracellular host–pathogen interactions. These findings can help identify host mechanisms that can be targeted by prophylactics and/or therapeutics to reduce the severity of COVID-19.

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Section: Discussionmentioning

confidence: 99%

Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis

Ferrarini

Rebollo

et al. 2021

Commun Biol

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“…SARS-CoV-2 can invade various cell types, resulting in organ-specific impairment; similarly, the virus can elicit a wholebody response mediated by an uncontrolled inflammatory process. [49][50] In vivo and in vitro studies have been helpful in furthering our understanding of the molecular and cellular mechanisms of disease causation, and epidemiologic studies have been beneficial in discovering novel signs and symptoms that are unique to the disease and may have important diagnostic significance.…”

Section: Discussionmentioning

confidence: 99%

“…48 Moderate to severe COVID-19 can also trigger a widespread inflammation and immune response activation evidenced by high levels of expression of IL-6, IL-1β, interferon γ, interferon-γ-inducible protein 10, and monocyte chemoattractant protein 1-proinflammatory cytokines associated with activated T-helper type-1 cell activation. 49 Accumulated evidence and clinical studies also show that individuals with severe COVID-19 generally experience cytokinerelease syndrome or cytokine storm, which plays a crucial role in disease progression and is considered a major cause of COVID-19-associated ARDS and multiorgan dysfunction syndrome. 50 High levels of IL-6, the main mediator of inflammatory and immune response to viral challenge, are also seen in patients who have severe presentation and are being investigated as an important prognosticator for negative outcomes in COVID-19.…”

Section: Sars-cov-2 Pathophysiologymentioning

confidence: 99%

Comprehensive Review of Cardiovascular Involvement in COVID-19

Cajanding

2021

AACN Advanced Critical Care

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COVID-19 has emerged as one of the most devastating and clinically significant infectious diseases of the last decade. It has reached global pandemic status at an unprecedented pace and has placed significant demands on health care systems worldwide. Although COVID-19 primarily affects the lungs, epidemiologic reports have shown that the disease affects other vital organs of the body, including the heart, vasculature, kidneys, brain, and the hematopoietic system. Of importance is the emerging awareness of the effects of COVID-19 on the cardiovascular system. The current state of knowledge regarding cardiac involvement in COVID-19 is presented in this article, with particular focus on the cardiovascular manifestations and complications of COVID-19 infection. The mechanistic insights of disease causation and the relevant pathophysiology involved in COVID-19 as they affect the heart are explored and described. Relevant practice essentials and clinical management implications for patients with COVID-19 with a cardiac pathology are presented in light of recent evidence.

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“…In general, IL-6 elevation has associated with cardiovascular complications such as atherosclerosis, MI, and heart failure. IL-6 and other cytokines are key components of the human body host defense system against infection, yet high levels of these cytokines in a hyperinflammatory response can lead to CRS (99,100). Cytokine release syndrome can be a fatal complication due to exaggerated inflammatory response in COVID-19, partially mediated by immune cells fighting the viral infection by increasing inflammatory cytokines via activation of intracellular NF-κB (101), but also in large part mediated by the ACE2 and AT1 receptors, which are generally highly expressed on epithelial cells in the lung and endothelium (20,(102)(103)(104).…”

Section: Cytokine Release Syndromementioning

confidence: 99%

Pandemic Perspective: Commonalities Between COVID-19 and Cardio-Oncology

Brown

Zaharova

Mason

et al. 2020

Front. Cardiovasc. Med.

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Overlapping commonalities between coronavirus disease of 2019 (COVID-19) and cardio-oncology regarding cardiovascular toxicities (CVT), pathophysiology, and pharmacology are special topics emerging during the pandemic. In this perspective, we consider an array of CVT common to both COVID-19 and cardio-oncology, including cardiomyopathy, ischemia, conduction abnormalities, myopericarditis, and right ventricular (RV) failure. We also emphasize the higher risk of severe COVID-19 illness in patients with cardiovascular disease (CVD) or its risk factors or cancer. We explore commonalities in the underlying pathophysiology observed in COVID-19 and cardio-oncology, including inflammation, cytokine release, the renin-angiotensin-aldosterone-system, coagulopathy, microthrombosis, and endothelial dysfunction. In addition, we examine common pharmacologic management strategies that have been elucidated for CVT from COVID-19 and various cancer therapies. The use of corticosteroids, as well as antibodies and inhibitors of various molecules mediating inflammation and cytokine release syndrome, are discussed. The impact of angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) is also addressed, since these drugs are used in cardio-oncology and have received considerable attention during the COVID-19 pandemic, since the culprit virus enters human cells via the angiotensin converting enzyme 2 (ACE2) receptor. There are therefore several areas of overlap, similarity, and interaction in the toxicity, pathophysiology, and pharmacology profiles in COVID-19 and cardio-oncology syndromes. Learning more about either will likely provide some level of insight into both. We discuss each of these topics in this viewpoint, as well as what we foresee as evolving future directions to consider in cardio-oncology during the pandemic and beyond. Finally, we highlight commonalities in health disparities in COVID-19 and cardio-oncology and encourage continued development and implementation of innovative solutions to improve equity in health and healing.

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Sepsis-associated severe interleukin-6 storm in critical coronavirus disease 2019

Cited by 35 publications

References 10 publications

Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis

Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis

Comprehensive Review of Cardiovascular Involvement in COVID-19

Pandemic Perspective: Commonalities Between COVID-19 and Cardio-Oncology

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