{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Huang DT"],"pubmed_abstract":["Influenza A (H7N9) is an emerging zoonotic pathogen with pandemic potential. To understand its adaptation capability, we examined the genetic changes and cellular responses following serial infections of A (H7N9) in primary human airway epithelial cells (hAECs). After 35 serial passages, six amino acid mutations were found, i.e. HA (R54G, T160A, Q226L, H3 numbering), NA (K289R, or K292R for N2 numbering), NP (V363V/I) and PB2 (L/R332R). The mutations in HA enabled A(H7N9) virus to bind with higher affinity (from 39.2% to 53.4%) to sialic acid α2,6-galactose (SAα2,6-Gal) linked receptors. A greater production of proinflammatory cytokines in hAECs was elicited at later passages together with earlier peaking at 24 hours post infection of IL-6, MIP-1α, and MCP-1 levels. Viral replication capac"],"journal":["Scientific reports"],"pagination":["11300"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5595892"],"repository":["biostudies-literature"],"pubmed_title":["Adaptation of influenza A (H7N9) virus in primary human airway epithelial cells."],"pmcid":["PMC5595892"],"pubmed_authors":["Chen JS","Huang DT","Chang LY","Chi YH","Huang LM","Li WL","Lu CY","Hsu WM","Lai MJ"],"additional_accession":[]},"is_claimable":false,"name":"Adaptation of influenza A (H7N9) virus in primary human airway epithelial cells.","description":"Influenza A (H7N9) is an emerging zoonotic pathogen with pandemic potential. To understand its adaptation capability, we examined the genetic changes and cellular responses following serial infections of A (H7N9) in primary human airway epithelial cells (hAECs). After 35 serial passages, six amino acid mutations were found, i.e. HA (R54G, T160A, Q226L, H3 numbering), NA (K289R, or K292R for N2 numbering), NP (V363V/I) and PB2 (L/R332R). The mutations in HA enabled A(H7N9) virus to bind with higher affinity (from 39.2% to 53.4%) to sialic acid α2,6-galactose (SAα2,6-Gal) linked receptors. A greater production of proinflammatory cytokines in hAECs was elicited at later passages together with earlier peaking at 24 hours post infection of IL-6, MIP-1α, and MCP-1 levels. Viral replication capac","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Sep","modification":"2025-04-22T02:36:05.837Z","creation":"2019-03-27T02:56:09Z"},"accession":"S-EPMC5595892","cross_references":{"pubmed":["28900138"],"doi":["10.1038/s41598-017-10749-5"]}}