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Open AccessArticle

Downregulation of A20 Expression Increases the Immune Response and Apoptosis and Reduces Virus Production in Cells Infected by the Human Respiratory Syncytial Virus

1
Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, 28220 Madrid, Spain
2
Unidad de Bioinformática, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, 28220 Madrid, Spain
*
Author to whom correspondence should be addressed.
Alternative correspondence: [email protected]; Tel.: +34-91-822-3266; Fax: +34-91-509-7919.
Vaccines 2020, 8(1), 100; https://doi.org/10.3390/vaccines8010100
Received: 8 January 2020 / Revised: 18 February 2020 / Accepted: 19 February 2020 / Published: 24 February 2020
(This article belongs to the Special Issue Research on Innate Immunity and Inflammation)
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-κB) 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. View Full-Text
Keywords: respiratory syncytial virus; A20; ubiquitination; innate immune response; apoptosis respiratory syncytial virus; A20; ubiquitination; innate immune response; apoptosis
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Martín-Vicente, M.; González-Sanz, R.; Cuesta, I.; Monzón, S.; Resino, S.; Martínez, I. Downregulation of A20 Expression Increases the Immune Response and Apoptosis and Reduces Virus Production in Cells Infected by the Human Respiratory Syncytial Virus. Vaccines 2020, 8, 100.

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