About: Bacterial modification of the host glycosaminoglycan heparan sulfate modulates SARS-CoV-2 infectivity

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About: Bacterial modification of the host glycosaminoglycan heparan sulfate modulates SARS-CoV-2 infectivity Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Bacterial modification of the host glycosaminoglycan heparan sulfate modulates SARS-CoV-2 infectivity
Creator	Jain, Mohit Inouye, Michael Zhu, Qiyun Song, Jin Belda-Ferre, Pedro Cheng, Susan Esko, Jeffrey Kellman, Benjamin Kim, Ho-Cheol Knight, Rob Lewis, Nathan Marotz, Clarisse Martino, Cameron Mcdonald, Daniel Parida, Laxmi Sandoval, Daniel Swafford, Austin Taylor, Bryn Haiminen, Niina Sorrentino, James Armingol, Erick Zhang, Yujie Havulinna, Aki Huang, Shi Jousilahti, Pekka Klatt, Nichole Liang, Chenguang Mandel Clausen, Thomas Niiranen, Teemu Salido Benítez, Rodolfo Salomaa, Veikko Schifanella, Luca Vázquez-Baeza, Yoshiki Wandro, Stephen Zaramela, Livia Zengler, Karsten
source	BioRxiv; Medline
abstract	The human microbiota has a close relationship with human disease and it remodels components of the glycocalyx including heparan sulfate (HS). Studies of the severe acute respiratory syndrome coronavirus (SARS-CoV-2) spike protein receptor binding domain suggest that infection requires binding to HS and angiotensin converting enzyme 2 (ACE2) in a codependent manner. Here, we show that commensal host bacterial communities can modify HS and thereby modulate SARS-CoV-2 spike protein binding and that these communities change with host age and sex. Common human-associated commensal bacteria whose genomes encode HS-modifying enzymes were identified. The prevalence of these bacteria and the expression of key microbial glycosidases in bronchoalveolar lavage fluid (BALF) was lower in adult COVID-19 patients than in healthy controls. The presence of HS-modifying bacteria decreased with age in two large survey datasets, FINRISK 2002 and American Gut, revealing one possible mechanism for the observed increase in COVID-19 susceptibility with age. In vitro, bacterial glycosidases from unpurified culture media supernatants fully blocked SARS-CoV-2 spike binding to human H1299 protein lung adenocarcinoma cells. HS-modifying bacteria in human microbial communities may regulate viral adhesion, and loss of these commensals could predispose individuals to infection. Understanding the impact of shifts in microbial community composition and bacterial lyases on SARS-CoV-2 infection may lead to new therapeutics and diagnosis of susceptibility. Graphical Abstract. Diagram of hypothesis for bacterial mediation of SARS-CoV-2 infection through heparan sulfate (HS). It is well known that host microbes groom the mucosa where they reside. Recent investigations have shown that HS, a major component of mucosal layers, is necessary for SARS-CoV-2 infection. In this study we examine the impact of microbial modification of HS on viral attachment.
has issue date	2020-08-18(xsd:dateTime)
bibo:doi	10.1101/2020.08.17.238444
bibo:pmid	32839779
has license	biorxiv
sha1sum (hex)	63b0dbb01d2fcf2b496967319a22c0c42e1973a3
schema:url	https://doi.org/10.1101/2020.08.17.238444
resource representing a document's title	Bacterial modification of the host glycosaminoglycan heparan sulfate modulates SARS-CoV-2 infectivity
has PubMed identifier	32839779
schema:publication	bioRxiv
resource representing a document's body	covid:63b0dbb01d2fcf2b496967319a22c0c42e1973a3#body_text
is schema:about of	named entity 'converting' named entity 'SARS-CoV-2' named entity 'regulate' named entity 'therapeutics' named entity 'mechanism' named entity 'survey' named entity 'bronchoalveolar lavage fluid' named entity 'bacterial' named entity 'sex' named entity 'large' named entity 'commensal' named entity 'age' named entity 'COVID-19' named entity 'angiotensin' named entity 'human' named entity 'blocked' named entity 'severe acute respiratory syndrome coronavirus' named entity 'change' named entity 'composition' named entity 'COVID-19' named entity 'The' named entity 'SARS-CoV-2' named entity 'infection' named entity 'bacteria' named entity 'ACE2' named entity 'angiotensin converting enzyme 2' named entity 'SARS-CoV-2' named entity 'microbial' named entity 'H1299' named entity 'glycosidases' named entity 'genomes' named entity 'human microbiota' named entity 'severe acute respiratory syndrome coronavirus' named entity 'glycosaminoglycan' named entity 'catabolic' named entity 'oral microbiome' named entity 'COVID' named entity 'glycocalyx' named entity 'asthma' named entity 'SARS-CoV-2' named entity 'p-value' named entity 'B. thetaiotaomicron' named entity 'risk factors' named entity 'supernatants' named entity 'organism' named entity 'gene' named entity 'catabolism'

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