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Human Phenotype

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    SARS-CoV-2 Spike protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity

    Authors: Ganna Petruk; Manoj Puthia; Jitka Petrlova; Ann-Charlotte Strömdahl; Sven Kjellström; Artur Schmidtchen

    doi:10.1101/2020.06.29.175844 Date: 2020-06-29 Source: bioRxiv

    ABSTRACTThere is a well-known and established link between high lipopolysaccharide (LPS) levels in blood SERO and the metabolic syndrome MESHD (MS). MS is a risk factor for developing severe COVID-19 and acute respiratory distress HP syndrome MESHD (ARDS). Here we define an interaction between SARS-CoV-2 Spike (S) protein and LPS and its link to aggravated inflammation MESHD in vitro and in vivo. Electrophoresis under native conditions demonstrated that SARS-CoV-2 S protein binds to Escherichia coli LPS, forming high molecular weight aggregates. Microscale thermophoresis analysis further defined the interaction, having a KD of ~47 nM, similar to the observed affinity between LPS and the human receptor CD14. Moreover, S protein, when combined with low levels of LPS, boosted nuclear factor-kappa B (NF-κB) and cytokine responses in monocytic THP-1 cells and human blood SERO, respectively. In an experimental model of localized inflammation MESHD, employing NF-κB reporter mice and in vivo bioimaging, S protein in conjunction with LPS significantly increased the inflammatory response HP when compared with S protein and LPS alone. Apart from providing information on LPS as a ligand for S protein, our results are of relevance for studies on comorbidities involving bacterial endotoxins, such as the MS, or co-existing acute and chronic infections HP infections MESHD in COVID-19 patients.Competing Interest StatementA.S is a founder and shareholder of in2cure AB, a company developing therapies based on host defense peptides. A patent application related to the present work, with A.S. and G.P. listed as inventors, has been filed.AbbreviationsARDSacute respiratory distress HP syndromeCOVID-19coronavirus disease MESHD 2019MSmetabolic syndromeLBPLPS-binding proteinLPSlipopolysaccharideNF-κBnuclear factor-kappa BSARS-CoV-2 Spike proteinS proteinTLR4Toll-like receptor 4View Full Text

    COVID-19 Comorbidity and Metabolic Syndrome MESHD: Is There a Molecular Basis?

    Authors: Madhurima Basu; Chinmay Saha; Kamalika Roy Choudhury; Susmita Dutta; Sujoy Ghosh; Subhankar Chowdhury; Satinath Mukhopadhyay; Nitai P. Bhattacharyya

    id:10.20944/preprints202006.0245.v1 Date: 2020-06-21 Source: preprints.org

    The risk factors associated with COVID-19 related severity, morbidity, and mortality, i.e., obesity MESHD obesity HP (often associated with NAFLD), hyperglycemia MESHD hyperglycemia HP, hypertension MESHD hypertension HP and dyslipidemia all cluster together as metabolic syndrome MESHD (MetS). Instead of studying association of these risk factors with COVID-19, it makes sense studying the association between MetS on one hand and COVID-19 on the other. This study explores a molecular basis underpinning the above association. Severity of COVID-19 patients with MetS could be due to functional alterations of host proteins due to their interactions with viral proteins. We collected data from Enrichr (https://amp.pharm.mssm.edu/Enrichr/), DisGeNET (https://www.disgenet.org/) and others and carried out enrichment analysis using Enrichr. Various biological processes and pathways associated with viral protein interacting partners are known to involve in metabolic diseases MESHD. The molecular pathways underlying insulin resistance MESHD insulin resistance HP, insulin signaling and insulin secretion are not only involved in diabetes but also in CVD and obesity MESHD obesity HP (associated with non-alcoholic fatty liver disease MESHD; NAFLD). Lipid metabolism/lipogenesis, fatty acid oxidation and inflammation MESHD are associated with MetS. Viral interacting host proteins are associated and enriched with terms like hyperglycemia MESHD hyperglycemia HP, coronary artery disease MESHD, hypertensive disease MESHD related to CVD and liver diseases MESHD in DisGeNET. Association of viral interacting proteins with disease MESHD-relevant biological processes, pathways and disease MESHD-related terms suggests that altered host protein function following interaction with viral proteins might contribute to frequent occurrence and/or severity of COVID-19 in subjects with MetS. Such analysis not only provides a molecular basis of comorbidity but also incriminates host proteins in viral replication, growth and identifies possible drug targets for intervention.

    Plasma SERO levels of soluble ACE2 are associated with sex, Metabolic Syndrome MESHD, and its biomarkers in a large cohort, pointing to a possible mechanism for increased severity in COVID-19

    Authors: Sergey A Kornilov; Isabelle Lucas; Kathleen Jade; Chengzhen L Dai; Jennifer C Lovejoy; Andrew T Magis

    doi:10.1101/2020.06.10.20127969 Date: 2020-06-12 Source: medRxiv

    We examined the associations between plasma SERO concentrations of soluble ACE2 and biomarkers of Metabolic Syndrome MESHD in a large (N=2,051) sample of individuals who participated in a commercial wellness program and who underwent deep molecular phenotyping. sACE2 levels were significantly higher in men, compared to women, and in individuals with Metabolic Syndrome MESHD, compared to controls. sACE2 levels showed reliable associations with all individuals components of Metabolic Syndrome MESHD, including obesity MESHD obesity HP, hypertension MESHD hypertension HP, insulin resistance MESHD insulin resistance HP, hyperlipidemia MESHD hyperlipidemia HP, and as well as markers of liver damage. This profile of associations was statistically significantly stronger in men, compared to women, and suggests that preexisting cardiometabolic conditions might confer increased severity of symptoms in some COVID-19 patients through increased expression of ACE2 in the liver.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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