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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    A clinical and biological framework on the role of visceral fat tissue and leptin HGNC in SARS-CoV-2 infection MESHD related respiratory failure

    Authors: Peter van der Voort; Jill Moser; Durk F Zandstra; Anneke C Muller Kobold; Marjolein Knoester; Cornelis F Calkhoven; Inge Hamming; Matijs van Meurs

    doi:10.1101/2020.04.30.20086108 Date: 2020-05-05 Source: medRxiv

    Obesity is a risk factor for SARS-CoV-2 infected MESHD patients to develop respiratory failure MESHD. Leptin HGNC produced in visceral fat might play a role in the deterioration to mechanical ventilation. A cross sectional study was performed. The mean BMI was 31 kg/m2 (range 24.8-48.4) for the 31 SARS-CoV-2 ventilated patients and 26 kg/m2 (range 22.4-33.5) for the 8 controls. SARS-CoV-2 infected MESHD patients with a similar BMI as control patients appear to have significantly higher levels of serum leptin HGNC. The mean leptin HGNC level was 21.2 (6.0-85.2) vs 5.6 (2.4-8.2) ug/L for SARS-CoV-2 and controls respectively (p=0.0007). With these findings we designed a clinical and biological framework that explains clinical observations. The ACE2 HGNC utilization by the virus leads to local pulmonary inflammation MESHD due to ACE2 HGNC-ATII disbalance. This is enhanced by an increase in leptin HGNC production induced by SARS-CoV-2 infection MESHD of visceral fat. Leptin HGNC receptors in the lungs are now more activated to enhance local pulmonary inflammation MESHD. This adds to the pre-existent chronic inflammation MESHD in obese MESHD patients. Visceral fat, lung tissue and leptin HGNC production play an interconnecting role. This insight can lead the way to further research and treatment.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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