{"id":384159,"date":"2023-12-15T16:13:11","date_gmt":"2023-12-15T21:13:11","guid":{"rendered":"https:\/\/platohealth.ai\/a-unique-pathogenic-mechanism-of-sars-cov-2-omicron-variant-selective\/"},"modified":"2023-12-17T22:30:47","modified_gmt":"2023-12-18T03:30:47","slug":"a-unique-pathogenic-mechanism-of-sars-cov-2-omicron-variant-selective","status":"publish","type":"post","link":"https:\/\/platohealth.ai\/a-unique-pathogenic-mechanism-of-sars-cov-2-omicron-variant-selective\/","title":{"rendered":"A unique pathogenic mechanism of SARS-CoV-2 omicron variant: Selective","gt_translate_keys":[{"key":"rendered","format":"text"}]},"content":{"rendered":"
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\u201cOur findings suggest that the omicron variant, in particular, leads to premature senescence in in vitro, ex vivo, and in lung tissue models.\u201d<\/em><\/p>\n

Credit: 2023 Hornung et al.<\/p>\n

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\u201cOur findings suggest that the omicron variant, in particular, leads to premature senescence in in vitro, ex vivo, and in lung tissue models.\u201d<\/em><\/p>\n

BUFFALO, NY- <\/strong>December 15<\/strong>, 2023 \u2013 <\/strong>A new research paper was published on the cover of Aging<\/u><\/em> (listed by MEDLINE\/PubMed as \u201cAging (Albany NY)\u201d and \u201cAging-US\u201d by Web of Science) Volume 15, Issue 23<\/u>, entitled, \u201cUncovering a unique pathogenic mechanism of SARS-CoV-2 omicron variant: selective induction of cellular senescence<\/u>.\u201d<\/p>\n

SARS-CoV-2 variants are constantly emerging with a variety of changes in the conformation of the spike protein, resulting in alterations of virus entry mechanisms. Solely omicron variants use the endosomal clathrin-mediated entry. <\/p>\n

In this new study, researchers Franziska Hornung, Nilay K\u00f6se-Vogel, Claude Jourdan Le Saux, Antje H\u00e4der, Lea Herrmann, Luise Schulz, Luk\u00e1\u0161 Radosa, Thurid Lauf, Tim Sandhaus, Patrick Samson, Torsten Doenst, Daniel Wittschieber, Gita Mall, Bettina L\u00f6ffler, <\/em>and Stefanie Deinhardt-Emmer<\/em> from Jena University<\/u>, Leibniz Centre for Photonics in Infection Research (LPI)<\/u>, University of California San Francisco<\/u>, Klinik f\u00fcr Herz- und Thoraxchirurgie<\/u>, and University Hospital Bonn<\/u> investigated the influence of defined altered spike formations to study their impact on premature cellular senescence.<\/p>\n

\u201cIn our study, in vitro<\/em> infections of SARS-CoV-2 variants delta (B.1.617.2) and omicron (B.1.1.529) were analyzed by using human primary small alveolar epithelial cells and human ex vivo <\/em>lung slices. We confirmed cellular senescence in human lungs of COVID-19 patients. Hence, global gene expression patterns of infected human primary alveolar epithelial cells were identified via mRNA sequencing.\u201d<\/p>\n

Solely omicron variants of SARS-CoV-2 influenced the expression of cell cycle genes, highlighted by an increased p21 expression in human primary lung cells and human ex vivo <\/em>lungs. Additionally, an upregulated senescence-associated secretory phenotype (SASP) was detected. Transcriptomic data indicate an increased gene expression of p16, and p38 in omicron-infected lung cells. Significant changes due to different SARS-CoV-2 infections in human primary alveolar epithelial cells with an overall impact on premature aging could be identified. A substantially different cellular response with an upregulation of cell cycle, inflammation- and integrin-associated pathways in omicron infected cells indicates premature cellular senescence.<\/p>\n

\u201cThis difference may be attributed to the distinct endocytic cell entry and intracellular pathways of the omicron variant when compared to the delta variant. The induction of cellular senescence in lung tissue following acute SARS-CoV-2 infection could potentially contribute to the reported cytokine storm and the development of long-COVID.\u201d<\/p>\n

Read the full study: DOI:<\/strong> https:\/\/doi.org\/10.18632\/aging.205297<\/u> <\/p>\n

Corresponding Author: <\/strong>Stefanie Deinhardt-Emmer <\/strong>\u2013 [email protected]<\/a><\/u> <\/p>\n

Keywords:<\/strong> SARS-CoV-2, variant of concern, cellular senescence, lung airway cells<\/p>\n

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About <\/strong>Aging<\/em><\/strong>:<\/strong><\/p>\n

Launched in 2009, Aging (Aging-US)<\/u><\/em> publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer\u2014and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging<\/em> go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K\/AKT\/mTOR, among others), and approaches to modulating these signaling pathways.<\/p>\n

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Journal<\/h4>\n

Aging-US<\/p>\n<\/p><\/div>\n

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DOI<\/h4>\n

10.18632\/aging.205297 <\/i><\/p>\n<\/p><\/div>\n

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Method of Research<\/h4>\n

Observational study<\/p>\n<\/p><\/div>\n

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Subject of Research<\/h4>\n

People<\/p>\n<\/p><\/div>\n

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Article Title<\/h4>\n

Uncovering a unique pathogenic mechanism of SARS-CoV-2 omicron variant: selective induction of cellular senescence<\/p>\n<\/p><\/div>\n

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Article Publication Date<\/h4>\n

12-Dec-2023<\/p>\n<\/p><\/div>\n<\/div>\n<\/div>\n<\/div>\n