Eurosurv. Excess cases of influenza-like illnesses synchronous with coronavirus disease (COVID-19) epidemic, France, March 2020
Today, 12:09 PM
Excess cases of influenza-like illnesses synchronous with coronavirus disease (COVID-19) epidemic, France, March 2020
Pierre-Yves Boëlle1, Cécile Souty1, Titouan Launay1, Caroline Guerrisi1, Clément Turbelin1, Sylvie Behillil5, Vincent Enouf5, Chiara Poletto2, Bruno Lina8,9, Sylvie van der Werf4,5,6,7, Daniel Lévy-Bruhl3, Vittoria Colizza2, Thomas Hanslik1, Thierry Blanchon1
Several French regions where coronavirus disease (COVID-19) has been reported currently show a renewed increase in ILI cases in the general practice-based Sentinelles network. We computed the number of excess cases by region from 24 February to 8 March 2020 and found a correlation with the number of reported COVID-19 cases so far. The data suggest larger circulation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the French population than apparent from confirmed cases.
https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.14.2000326#html_fulltext
Reposting, sorry... Some Vitamin D research:
Biochem Pharmacol - Vitamin D attenuates lung injury via stimulating epithelial repair, reducing epithelial cell apoptosis and inhibits TGF-B induced epithelial to mesenchymal transition.
Today, 11:18 AM
Biochem Pharmacol. 2020 Apr 3:113955. doi: 10.1016/j.bcp.2020.113955. [Epub ahead of print]
Vitamin D attenuates lung injury via stimulating epithelial repair, reducing epithelial cell apoptosis and inhibits TGF-B induced epithelial to mesenchymal transition.
Zheng S1, Yang J2, Hu X3, Li M4, Wang Q5, Dancer RCA6, Parekh D7, Gao-Smith F8, Thickett DR9, Jin S10.Author information
Abstract
Vitamin D regulates cell proliferation, inhibits cytokines release at sites of inflammation and reduces inflammatory responses. In this study, the aim was to investigate whether exogenous vitamin D attenuates LPS-induced lung injury via modulating epithelial cell proliferation, migration, apoptosis and epithelial mesenchymal transition (EMT). Murine and in vitro primary type II alveolar epithelial cell work were included in this study. In vivo, mice were mildly vitamin D deficient, 0.1, 1.5, 10mg/kg 1,25(OH)2-vitamin D3 or 25(OH)-vitamin D3 was administrated by means of an intra-gastric injection for 14 days pre-intra-tracheal (IT) LPS, which remarkedly promoted alveolar epithelial type II cells proliferation, inhibited ATII cells apoptosis and inhibited EMT, with the outcome of attenuated LPS-induced lung injury. In vitro, vitamin D stimulated epithelial cell scratch wound repair, reduced primary ATII cells apoptosis as well. Vitamin D promoted primary human ATII cells proliferation through the PI3K/AKT signaling pathway and activation of vitamin D receptor (VDR). Moreover, vitamin D inhibited EMT in response to TGF-B;, which was vitamin D receptor dependent. In conclusion, vitamin D attenuates lung injury via stimulating ATII cells proliferation and migration, reducing epithelial cell apoptosis and inhibits TGF-B; induced EMT. Together, these results suggest that vitamin D has therapeutic potential for the resolution of ARDS.
Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.
KEYWORDS:
acute respiratory distress syndrome; alveolar type II cells; epithelial to mesenchymal transition; vitamin D; wound repair and apoptosis
PMID: 32251673 DOI: 10.1016/j.bcp.2020.113955
https://www.ncbi.nlm.nih.gov/pubmed/32251673
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Nutrients: Evidence that Vitamin D Supplementation Could Reduce Risk of Influenza and COVID-19 Infections and Deaths
Today, 11:15 AM
Nutrients. 2020 Apr 2;12(4). pii: E988. doi: 10.3390/nu12040988.
Evidence that Vitamin D Supplementation Could Reduce Risk of Influenza and COVID-19 Infections and Deaths.
Grant WB1, Lahore H2, McDonnell SL3, Baggerly CA3, French CB3, Aliano JL3, Bhattoa HP4.Author information
Abstract
The world is in the grip of the COVID-19 pandemic. Public health measures that can reduce the risk of infection and death in addition to quarantines are desperately needed. This article reviews the roles of vitamin D in reducing the risk of respiratory tract infections, knowledge about the epidemiology of influenza and COVID-19, and how vitamin D supplementation might be a useful measure to reduce risk. Through several mechanisms, vitamin D can reduce risk of infections. Those mechanisms include inducing cathelicidins and defensins that can lower viral replication rates and reducing concentrations of pro-inflammatory cytokines that produce the inflammation that injures the lining of the lungs, leading to pneumonia, as well as increasing concentrations of anti-inflammatory cytokines. Several observational studies and clinical trials reported that vitamin D supplementation reduced the risk of influenza, whereas others did not. Evidence supporting the role of vitamin D in reducing risk of COVID-19 includes that the outbreak occurred in winter, a time when 25-hydroxyvitamin D (25(OH)D) concentrations are lowest; that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome; and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration. To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d. The goal should be to raise 25(OH)D concentrations above 40-60 ng/mL (100-150 nmol/L). For treatment of people who become infected with COVID-19, higher vitamin D3 doses might be useful. Randomized controlled trials and large population studies should be conducted to evaluate these recommendations.
KEYWORDS:
COVID-19; UVB; acute respiratory distress syndrome (ARDS); ascorbic acid; cathelicidin; coronavirus; cytokine storm; influenza; observational; pneumonia; prevention; respiratory tract infection; solar radiation; treatment; vitamin C; vitamin D
PMID: 32252338 DOI: 10.3390/nu12040988
https://www.ncbi.nlm.nih.gov/pubmed/32252338