Decontamination of SARS-CoV-2 and other RNA viruses from N95 level meltblown polypropylene fabric using heat under different humidities

Campos, Rafael K.; Jin, Jing; Rafael, Grace; Zhao, Mervin; Liao, Lei; Simmons, Graham; Chu, Steven; Weaver, Scott C.; Chiu, Wah; Cui, Yi

doi:10.1101/2020.08.10.20171728

Cited by 6 publications

(4 citation statements)

References 31 publications

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“…While COVID-19 can affect multiple organs, the lungs are the predominant target of the severity of the immune response and where the cytokine storm originates 3 . To evaluate the relevance of CD80/86 co-stimulation in the lungs during COVID-19 we took advantage of an available single-cell RNA-seq dataset generated from the bronchoalveolar lavage fluid obtained from mild (n = 3) and severe (n = 6) COVID-19 patients and from healthy controls (n = 3) 10 , 11 . Figure 5 A,B show the cell clustering analysis and identification of the marker genes within each cell type, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…In order to corroborate the relevance of the CD80/86 signaling axis in COVID-19, we analyzed single cell RNA-seq data generate from the lungs, the target tissue of severity. For this objective we analyzed a single cell RNA-seq recently generated from bronchoalveolar lavage fluid (BALF) cells from COVID-19 patients and healthy controls (GEO database accession GSE145926) 10 , 11 . Single-cell RNA-seq raw data from BALF samples was generated using the 10× Genomics platform and included 9 COVID-19 patients (n = 6 severe and n = 3 mild).…”

Section: Methodsmentioning

confidence: 99%

“…In severe COVID-19, macrophages in the lungs activate and produce large amounts of proinflammatory cytokines, mainly IL6. Recent evidence suggests that during SARS-CoV-2 infection, resident alveolar macrophages are gradually substituted by monocyte-derived proinflammatory macrophages 10 , 11 . However, how these macrophages are brought to drastically increase the proinflammatory cytokine production in severe COVID-19 is yet not known 5 .…”

Section: Introductionmentioning

confidence: 99%

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Targeting of the CD80/86 proinflammatory axis as a therapeutic strategy to prevent severe COVID-19

Juliá¹,

Bonafonte-Pardàs²,

Gómez³

et al. 2021

Sci Rep

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An excessive immune response known as cytokine storm is the hallmark of severe COVID-19. The cause of this cytokine rampage is yet not known. Based on recent epidemiological evidence, we hypothesized that CD80/86 signaling is essential for this hyperinflammation, and that blocking this proinflammatory axis could be an effective therapeutic approach to protect against severe COVID-19. Here we provide exploratory evidence that abatacept, a drug that blocks CD80/86 co-stimulation, produces changes at the systemic level that are highly antagonistic of the proinflammatory processes elicited by COVID-19. Using RNA-seq from blood samples from a longitudinal cohort of n = 38 rheumatic patients treated with abatacept, we determined the immunological processes that are significantly regulated by this treatment. We then analyzed available blood RNA-seq from two COVID19 patient cohorts, a very early cohort from the epicenter of the pandemic in China (n = 3 COVID-19 cases and n = 3 controls), and a recent and larger cohort from the USA (n = 49 severe and n = 51 mild COVD-19 patients). We found a highly significant antagonism between SARS-CoV-2 infection and COVID-19 severity with the systemic response to abatacept. Analysis of previous single-cell RNA-seq data from bronchoalveolar lavage fluid from mild and severe COVID-19 patients and controls, reinforce the implication of the CD80/86 proinflammatory axis. Our functional results further support abatacept as a candidate therapeutic approach to prevent severe COVID-19.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Targeting of the CD80/86 proinflammatory axis as a therapeutic strategy to prevent severe COVID-19

Juliá¹,

Bonafonte-Pardàs²,

Gómez³

et al. 2021

Sci Rep

View full text Add to dashboard Cite

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“…[43] Single-cell RNA sequencing of bronchoalveolar fluid (BALF) collected from patients with COVID-19 showed an increased proportion of mononuclear macrophages, accounting for 80% of the total number of BALF cells in patients with severe COVID-19. [44] Surprisingly, immunostaining of postmortem tissues from patients who died from COVID-19 revealed that CD169 + lymph node subcapsular and splenic marginal zone macrophage populations expressed ACE2 receptors and that these macrophages contained SARS-CoV-2 nuclear protein (NP). [45] CD68 + NP + macrophages were also observed in the kidneys of COVID-19 patients, and AKI was associated with a significant accumulation of monocytes and macrophages.…”

Section: Immune Response In Covid-19-associated Akimentioning

confidence: 99%

Immune Response in COVID-19-associated Acute Kidney Injury and Maladaptive Kidney Repair

Dong

2023

Integr Med Nephrol Androl

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Acute kidney injury (AKI) is a major disease with substantial short and long-term morbidity and mortality. It is also a critical consequence of coronavirus disease 2019 (COVID-19), which is characterized by a robust immunological response and a cytokine storm. Current COVID-19-AKI prevention and management approaches are largely based on clinical experience, and further research is required to obtain evidence to support current clinical practices and to develop new treatment and care strategies. Several individuals have reported experiencing long-term symptoms indicative of the long COVID syndrome following COVID-19 infection. Evidence of the long-term consequences of COVID-19 on kidneys has also been reported. In this aspect, the kidney has a remarkable capacity for repair after injury. However, when the injury is too severe or persistent, kidney repair is incomplete and maladaptive, potentially leading to chronic kidney disease (CKD). Inflammation, characterized by complex crosstalk between intrinsic renal cells and immune cells, is critical in maladaptive kidney repair. In this review, we summarize the progress of studies on COVID-19-induced AKI and the interactions between immune cells and intrinsic renal cells involved in the process of maladaptive kidney repair. We also discuss inflammation-related pathways as potential therapeutic targets.

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Relationship between betacoronaviruses and the endocrine system: a new key to understand the COVID-19 pandemic—A comprehensive review

Piticchio

Moli

Tumino

et al. 2021

J Endocrinol Invest

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Background A new harmful respiratory disease, called COVID-19 emerged in China in December 2019 due to the infection of a novel coronavirus, called SARS-Coronavirus 2 (SARS-CoV-2), which belongs to the betacoronavirus genus, including SARS-CoV-1 and MERS-CoV. SARS-CoV-2 shares almost 80% of the genome with SARS-CoV-1 and 50% with MERS-CoV. Moreover, SARS-CoV-2 proteins share a high degree of homology (approximately 95%) with SARS-CoV-1 proteins. Hence, the mechanisms of SARS-Cov-1 and SARS-Cov-2 infection are similar and occur via binding to ACE2 protein, which is widely distributed in the human body, with a predominant expression in endocrine tissues including testis, thyroid, adrenal and pituitary. Purpose On the basis of expression pattern of the ACE2 protein among different tissues, similarity between SARS-Cov-1 and SARS-Cov-2 and the pathophysiology of COVID-19 disease, we aimed at discussing, after almost one-year pandemic, about the relationships between COVID-19 infection and the endocrine system. First, we discussed the potential effect of hormones on the susceptibility to COVID-19 infection; second, we examined the evidences regarding the effect of COVID-19 on the endocrine system. When data were available, a comparative discussion between SARS and COVID-19 effects was also performed. Methods A comprehensive literature search within Pubmed was performed. This review has been conducted according to the PRISMA statements. Results Among 450, 100 articles were selected. Tissue and vascular damages have been shown on thyroid, adrenal, testis and pituitary glands, with multiple alterations of endocrine function. Conclusion Hormones may affect patient susceptibility to COVID-19 infection but evidences regarding therapeutic implication of these findings are still missing. SARS and COVID-19 may affect endocrine glands and their dense vascularization, impairing endocrine system function. A possible damage of endocrine system in COVID-19 patients should be investigated in both COVID-19 acute phase and recovery to identify both early and late endocrine complications that may be important for patient’s prognosis and well-being after COVID-19 infection.

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Decontamination of SARS-CoV-2 and other RNA viruses from N95 level meltblown polypropylene fabric using heat under different humidities

Cited by 6 publications

References 31 publications

Targeting of the CD80/86 proinflammatory axis as a therapeutic strategy to prevent severe COVID-19

Targeting of the CD80/86 proinflammatory axis as a therapeutic strategy to prevent severe COVID-19

Immune Response in COVID-19-associated Acute Kidney Injury and Maladaptive Kidney Repair

Relationship between betacoronaviruses and the endocrine system: a new key to understand the COVID-19 pandemic—A comprehensive review

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