Virus research | 2021

Impact of human rhinoviruses on gene expression in pediatric patients with severe acute respiratory infection.

 
 
 
 
 
 
 
 

Abstract


Human rhinovirus (HRV) is one of the most common viruses, causing mild to severe respiratory tract infections in children and adults. Moreover, it can lead to patients hospitalization. Nowadays, evaluation of gene expression alterations in host cells due to viral respiratory infections considered essential to understand the viral effects on cells.\n\n\nOBJECTIVE\nIn this study, we aimed to find important differentially expressed genes (DEGs) related to rhinitis and asthma exacerbation stimulated with Poly (I: C) and then to validate their expression in clinical samples of children how were less than 5 years old, hospitalized with severe acute respiratory infection (SARI) due to HRV infection in comparison with healthy cases.\n\n\nMETHODS\nEight candidate genes involved in immunity, viral defense, inflammation, P53 pathway, and viral release processes were selected based on the analysis of a gene expression data set (GSE51392) and gene enrichment analysis. Then quantitative real-time PCR on cDNAs was performed for selected genes. The results were analyzed by Livak method and visualized by GraphPad prism software (8.4.3).\n\n\nRESULT\nCXCL10, CMPK2, RSAD2, SERPINA3, TNFAIP6, CXCL14, IVNS1AB, and ZMAT3 were selected based on the enrichment and topological analysis of the constructed protein-protein interaction (PPI) network. Laboratory validation by real-time PCR showed CXCL10, CMPK2, RSAD2, SERPINA3, and TNFAIP6 (belonged to immunity, inflammatory responses and viral defense) were up-regulated, whereas CXCL14 (related to immunity) and IVNS1AB, ZMAT3 (associated to Influenza and P53 pathway) were down-regulated.\n\n\nCONCLUSION\nOur results showed, that in children less than 5 years old affected by HRV and hospitalized with SARI, the inflammatory responses, antiviral defense, and type 1 interferon-signaling pathway have significantly affected by viral infection.

Volume None
Pages \n 198408\n
DOI 10.1016/j.virusres.2021.198408
Language English
Journal Virus research

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