Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    NETs By-products and Extracellular DNA May Play a Key Role in COVID-19 MESHD Pathogenesis: Incidence on Patient Monitoring and Therapy

    Authors: Alain Thierry; Benoit ROCH

    id:10.20944/preprints202004.0238.v1 Date: 2020-04-15 Source:

    Neutrophils play an important role as the first line of innate immune defense. One function of neutrophils, called neutrophil extracellular traps (NETs), has been discovered recently. NETs are extensive fibrous structures released extracellularly from activated neutrophils in response to infection. They are composed of cytosolic protein assembled on a scaffold of released chromatin. These structures suppress the dissemination of micro-organisms in blood by trapping them mechanically, and by exploiting coagulant function to segregate them within the circulation. In addition, NET components (DNA, histone, and granule proteins) also contribute to the triggering of an inflammatory process. NET function, however, can be regarded as a double-edged sword. On one hand, NET formation is an efficient strategy for neutralizing invading micro-organisms. On the other hand, NET can be harmful to the host, as its exposed by-products that are toxic to endothelial cells and parenchymal tissue. We present here the analogous biological and physiological features of the harmful positive amplification loop between inflammation MESHD and tissue damage induced by NETosis dysregulation and Coronavirus Disease MESHD-2019 ( COVID-19 MESHD) pathogenesis. Considering the rapid evolution of this disease symptoms and its lethality, we hypothesize that COVID-19 MESHD progresses under an amplifier loop, leading to an massive, uncontrolled inflammation process MESHD. We also describe the correlations of COVID-19 MESHD symptoms and biological features with those consecutive to uncontrolled NET formation causing various sterile or infectious diseases MESHD. General clinical conditions, and numerous pathological and biological features, are analogous with NETs deleterious effects. We postulate that Severe Acute Respiratory Syndrome-Coronavirus MESHD 2 (SARS-CoV2) induces a disproportionate virus-induced NET release, and that this plays a key role in COVID-19 MESHD pathogenesis. While neutrophils are the principal starting point for extracellular and circulating DNA release, targeting NETs rather than neutrophils themselves may stand for an effective strategy. This paper offers an in-depth review of NET formation, function and pathogenic dysregulation, as well as of current and future therapies to control NET unbalance. As such, it enables us also to suggest new therapeutic strategies to fight COVID-19 MESHD. In combination with or independent of the latest tested approaches, we propose that, in the short term, deoxyribonuclease I HGNC ( DNase-1 HGNC) treatment should be evaluated; we also advocate a significant increase in research on the development of toll-like receptors (TLR) and C-type Lectin like receptors (CLEC) inhibitors, and on anti-IL26 therapies.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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