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oai:repisalud.isciii.es:20.500.12105/91712025-05-29T11:20:01Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19609

00925njm 22002777a 4500 dc Martin-Vicente, Maria author Gonzalez-Sanz, Ruben author Cuesta de la Plaza, Isabel author Monzon-Fernandez, Sara author Resino, Salvador author Martinez, Isidoro author 2020-02-24 Human respiratory syncytial virus (HRSV) causes severe lower respiratory tract infections in infants, the elderly, and immunocompromised adults. Regulation of the immune response against HRSV is crucial to limiting virus replication and immunopathology. The A20/TNFAIP3 protein is a negative regulator of nuclear factor kappa B (NF-kB) and interferon regulatory factors 3/7 (IRF3/7), which are key transcription factors involved in the inflammatory/antiviral response of epithelial cells to virus infection. Here, we investigated the impact of A20 downregulation or knockout on HRSV growth and the induction of the immune response in those cells. Cellular infections in which the expression of A20 was silenced by siRNAs or eliminated by gene knockout showed increased inflammatory/antiviral response and reduced virus production. Similar results were obtained when the expression of A20-interacting proteins, such as TAX1BP1 and ABIN1, was silenced. Additionally, downregulation of A20, TAX1BP1, and ABIN1 increased cell apoptosis in HRSV-infected cells. These results show that the downregulation of A20 expression might contribute in the control of HRSV infections by potentiating the early innate immune response and increasing apoptosis in infected cells. Vaccines (Basel). 2020 Feb 24;8(1). pii: E100. 10.3390/vaccines8010100 2076-393X Vaccines 32102364 http://hdl.handle.net/20.500.12105/9171 A20 Apoptosis Innate immune response Respiratory syncytial virus Ubiquitination Downregulation of A20 Expression Increases the Immune Response and Apoptosis and Reduces Virus Production in Cells Infected by the Human Respiratory Syncytial Virus