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Novel signaling pathways regulate SARS-CoV and SARS-CoV-2 infectious disease

Cheng Division of Colorectal Surgery, Department of Surgery, Chi-Mei Medical Center|
Hui-Ping (7402359776) Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan| Chih-Yang (55700302600); Hsu PhD Program for Cancer Molecular Biology and Drug Discovery| Zhengda (56011356900); Wang Kaiser Permanente, Northern California Regional Laboratories, the Permanente Medical Group, Berkeley, CA, USA| Jia-Zhen (57217596164); Sun Emergency Department, Huashan Hospital North, Fudan University, Shanghai, China| Jui-Hsiang (23009030700); Jiang Department of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan, Taiwan| Chien-Fu (57194699916); Hung Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan| Meng-Chi (15770522900); Chen Department of Emergency Medicine, Kaohsiung Medical University Hospital| Chung-Chieh (57200333181); Yen School of Chinese Medicine for Post-Baccalaureate, I-Shou University| Nam Nhut (56781139900); Chiao NTT Institute of Hi-Technology, Nguyen Tat Thanh (NTT) University, Ho Chi Minh City, Viet Nam| Tzu-Jen (26537500800); Phan TMU Research Center of Neuroscience, Taipei Medical University, Taipei, Taiwan| Li-Chin (57211337674); Kao PhD Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes|

Medicine Số 7, năm 2021 (Tập 100, trang e24321-)

ISSN: 15365964

ISSN: 15365964

DOI: 10.1097/MD.0000000000024321

Tài liệu thuộc danh mục:

Article

English

Từ khóa: Cell Line, Tumor; Chemokines; COVID-19; Cytokines; Gene Expression Profiling; Gene Ontology; Host-Pathogen Interactions; Humans; Inflammation Mediators; Interleukin-17; Receptors, Tumor Necrosis Factor, Type II; SARS-CoV-2; Tumor Necrosis Factor-alpha; Up-Regulation; autacoid; chemokine; cytokine; interleukin 17; tumor necrosis factor; tumor necrosis factor receptor 2; biosynthesis; gene expression profiling; gene ontology; genetics; host pathogen interaction; human; immunology; metabolism; tumor cell line; upregulation
Tóm tắt tiếng anh
ABSTRACT: Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 induces severe infection, and it is responsible for a worldwide disease outbreak starting in late 2019. Currently, there are no effective medications against coronavirus. In the present study, we utilized a holistic bioinformatics approach to study gene signatures of SARS-CoV- and SARS-CoV-2-infected Calu-3 lung adenocarcinoma cells. Through the Gene Ontology platform, we determined that several cytokine genes were up-regulated after SARS-CoV-2 infection, including TNF, IL6, CSF2, IFNL1, IL-17C, CXCL10, and CXCL11. Differentially regulated pathways were detected by the Kyoto Encyclopedia of Genes and Genomes, gene ontology, and Hallmark platform, including chemokines, cytokines, cytokine receptors, cytokine metabolism, inflammation, immune responses, and cellular responses to the virus. A Venn diagram was utilized to illustrate common overlapping genes from SARS-CoV- and SARS-CoV-2-infected datasets. An Ingenuity pathway analysis discovered an enrichment of tumor necrosis factor- (TNF-) and interleukin (IL)-17-related signaling in a gene set enrichment analysis. Downstream networks were predicted by the Database for Annotation, Visualization, and Integrated Discovery platform also revealed that TNF and TNF receptor 2 signaling elicited leukocyte recruitment, activation, and survival of host cells after coronavirus infection. Our discovery provides essential evidence for transcript regulation and downstream signaling of SARS-CoV and SARS-CoV-2 infection. Copyright � 2021 the Author(s). Published by Wolters Kluwer Health, Inc.

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