Hyperimmune convalescent plasma therapy can downregulate inflammatory and proteolytic storms in Covid-19

The pandemic spread of a novel coronavirus – SARS coronavirus-2 (SARS-CoV-2) as a cause of acute respiratory illness, named Covid-19, is placing the healthcare systems of many countries under unprecedented stress. Global economies are also spiraling towards a recession in fear of this new life-threatening disease. Vaccines that prevent SARS-CoV-2 infection and therapeutics that reduces

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Lymphopenia, neutrophilia and cytokines in severe Covid-19 patients

The dynamic changes of lymphocyte subsets, neutrophils and cytokines profiles of patients with novel coronavirus disease (COVID-19) and their correlation with the disease severity has been studied in a paper recently published on EBioMedicine https://doi.org/10.1016/j.ebiom.2020.102763. Of the 40 COVID-19 patients enrolled, 13 severe cases showed significant and sustained decreases in lymphocyte counts, but increases in

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Early Indicators: Investigational convalescent plasma is safe for patients with COVID-19

The first safety study communications overview, Early Safety Indicators of COVID-19 Convalescent Plasma in 5,000 Patients, for the national expanded access program for convalescent plasma has been published https://www.medrxiv.org/content/10.1101/2020.05.12.20099879v1 The report tells us: Mayo Clinic and collaborators reported safety data on the first 5,000 hospitalized patients transfused with investigational convalescent plasma as part of the

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Face masks essential in combating spread of SARS-CoV-2 aerosols and droplets

SARS-CoV-2 spread occurs through the transmission of droplets and aerosols from infected people through speaking, breathing, coughing, and sneezing. Wearing masks can reduce the airborne transmission of the novel coronavirus, a new study finds. The research is published in the journal Science. The team of researchers at the University of California San Diego and the National Sun Yat-sen

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Neutrophil Extracellular Traps are involved in Severe COVID-19 proteolytic storm

Neutrophil released NETs to control microbial/viral infections, could serve as a therapeutic target in coronavirus infections. In March this year, Dr. Knight and Kanthy of Michigan University observed a striking similarity between an autoimmune disease known as antiphospholipid syndrome (APS) and COVID-19. Both conditions appeared to involve blood clots in arteries, veins, and the microvasculature.

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Proteomic and Metabolomic Characterization of COVID-19 Patient Sera

Early detection and effective treatment of severe COVID-19 patients remain major challenges. In this paper, published on Cell, has been performed proteomic and metabolomic profiling of sera from 46 COVID-19 and 53 control individuals and then trained a machine learning model using proteomic and metabolomic measurements from a training cohort of 18 non-severe and 13

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Type I and Type III Interferons – Induction, Signaling, Evasion, and Application to Combat COVID-19

In this review, published in Cell Host & Microbe, it’s described the recent progress in understanding of both type I and type III IFN-mediated innate antiviral responses against human coronaviruses and discussed the potential use of IFNs as a treatment strategy for COVID-19. Type I and type III IFNs establish the cellular state of viral

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SARS-CoV-2 strategically mimics proteolytic activation 2 of human epithelial sodium channel α-subunit (ENaC-α)

Molecular mimicry is an evolutionary strategy adopted by viruses to exploit the host cellular machinery. This paper reports that SARS-CoV-2 has evolved a unique S1/S2 cleavage site, absent in any previous coronavirus sequenced, resulting in striking mimicry of an identical FURIN-cleavable peptide on the human epithelial sodium channel α-subunit (ENaC-α). Genetic alteration of ENaC-α causes

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In Covid-19 neutrophils induce an imbalanced “proteolytic storm”, fighted by human plasma transfusion proteolytic cascades balancing.

In a recent Comment published on EBioMedicine entitled “COVID-19 as a STING disorder with delayed oversecretion of Interferon-beta”, Berthelot and Lioté suggests that SARS-CoV-2 firstly inhibits interferon release but the NETs self-DNA induces delayed activation of STING with“cytokine storm”, causing the combination of interstitial lung disease and inflammatory vasculopathy. The assumption that SARS-CoV-2 had no

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