An outbreak of coronavirus infections in Washington State that began at the end of February was likely sparked by a traveler who entered the state in mid-February, rather than by an infected person who flew from Wuhan, China, to Seattle in mid-January, as was previously thought. The data point to Germany and Italy outbreaks starting independently by
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.
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
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
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
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
In this new paper, published on medXriv https://doi.org/10.1101/2020.05.20.2010223 the outcomes of thirty-nine hospitalized patients with severe to life-threatening COVID-19 who received convalescent plasma transfusion were compared against a cohort of retrospectively matched controls. Plasma recipients were selected based on supplemental oxygen needs at the time of enrollment and the time elapsed since the onset of
In a paper just published on Preprints, REGENHEALTHSOLUTIONS Research Team shows that, in Covid-19 critically ill patients, serine proteases released by recruited neutrophils are responsible for endothelitis, NETosis, platelet activation, ULVWF multimers release, thrombi formation and MOF for viral sepsis. Based on Chinese CDCP report on COVID-19, 14% of patients presented severe disease and 5%
There has been a surge in cases of an inflammatory syndrome in children, believed to be linked to covid-19, following an alert to doctors in the UK at the end of April. The syndrome, which in the UK is referred to as the “paediatric inflammatory multisystem syndrome which is temporarily associated with SARS-CoV-2,” has also
The Smithsonian Science Education Center, in collaboration with the World Health Organization (WHO) and the InterAcademy Partnership (IAP)—a partnership of 140 national academies of science, engineering and medicine—has developed “COVID-19! How can I protect myself and others?,” a new rapid-response guide for youth ages 8–17. The guide, which is based on the UN Sustainable Development Goals,
