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Article: Influenza A virus PB1‐F2 protein: An ambivalent innate immune modulator and virulence factor

TitleInfluenza A virus PB1‐F2 protein: An ambivalent innate immune modulator and virulence factor
Authors
Keywordsinfluenza A virus
innate antiviral response
type I IFNs
inflammation
inflammasome
Issue Date2020
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at https://jlb.onlinelibrary.wiley.com/journal/19383673
Citation
Journal of Leukocyte Biology, 2020, v. 107 n. 5, p. 763-771 How to Cite?
AbstractInfluenza A virus (IAV) causes not only seasonal respiratory illness, but also outbreaks of more severe disease and pandemics when novel strains emerge as a result of reassortment or interspecies transmission. PB1‐F2 is an IAV protein expressed from the second open reading frame of PB1 gene. Small as it is, PB1‐F2 is a critical virulence factor. Multiple key amino acid residues and motifs of PB1‐F2 have been shown to influence the virulence of IAV in a strain‐ and host‐specific manner, plausibly through the induction of apoptotic cell death, modulation of type I IFN response, activation of inflammasome, and facilitation of secondary bacterial infection. However, the exact role of PB1‐F2 in IAV pathogenesis remains unexplained. Through reanalysis of the current literature, we redefine PB1‐F2 as an ambivalent innate immune modulator that determines IAV infection outcome through induction of immune cell death, differential modulation of early‐ and late‐type I IFN response, and promotion of pathogenic inflammation. PB1‐F2 functions both intracellularly and extracellularly. Further investigations of the mechanistic details of PB1‐F2 action will shed new light on immunopathogenesis of IAV infection.
Persistent Identifierhttp://hdl.handle.net/10722/288398
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.521
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheung, PHH-
dc.contributor.authorLee, TWT-
dc.contributor.authorChan, CP-
dc.contributor.authorJin, DY-
dc.date.accessioned2020-10-05T12:12:18Z-
dc.date.available2020-10-05T12:12:18Z-
dc.date.issued2020-
dc.identifier.citationJournal of Leukocyte Biology, 2020, v. 107 n. 5, p. 763-771-
dc.identifier.issn0741-5400-
dc.identifier.urihttp://hdl.handle.net/10722/288398-
dc.description.abstractInfluenza A virus (IAV) causes not only seasonal respiratory illness, but also outbreaks of more severe disease and pandemics when novel strains emerge as a result of reassortment or interspecies transmission. PB1‐F2 is an IAV protein expressed from the second open reading frame of PB1 gene. Small as it is, PB1‐F2 is a critical virulence factor. Multiple key amino acid residues and motifs of PB1‐F2 have been shown to influence the virulence of IAV in a strain‐ and host‐specific manner, plausibly through the induction of apoptotic cell death, modulation of type I IFN response, activation of inflammasome, and facilitation of secondary bacterial infection. However, the exact role of PB1‐F2 in IAV pathogenesis remains unexplained. Through reanalysis of the current literature, we redefine PB1‐F2 as an ambivalent innate immune modulator that determines IAV infection outcome through induction of immune cell death, differential modulation of early‐ and late‐type I IFN response, and promotion of pathogenic inflammation. PB1‐F2 functions both intracellularly and extracellularly. Further investigations of the mechanistic details of PB1‐F2 action will shed new light on immunopathogenesis of IAV infection.-
dc.languageeng-
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at https://jlb.onlinelibrary.wiley.com/journal/19383673-
dc.relation.ispartofJournal of Leukocyte Biology-
dc.rightsThis is the peer reviewed version of the following article: Journal of Leukocyte Biology, 2020, v. 107 n. 5, p. 763-771, which has been published in final form at https://doi.org/10.1002/JLB.4MR0320-206R. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectinfluenza A virus-
dc.subjectinnate antiviral response-
dc.subjecttype I IFNs-
dc.subjectinflammation-
dc.subjectinflammasome-
dc.titleInfluenza A virus PB1‐F2 protein: An ambivalent innate immune modulator and virulence factor-
dc.typeArticle-
dc.identifier.emailCheung, PHH: hinson01@connect.hku.hk-
dc.identifier.emailChan, CP: chancp10@hku.hk-
dc.identifier.emailJin, DY: dyjin@hku.hk-
dc.identifier.authorityChan, CP=rp02031-
dc.identifier.authorityJin, DY=rp00452-
dc.description.naturepostprint-
dc.identifier.doi10.1002/JLB.4MR0320-206R-
dc.identifier.pmid32323899-
dc.identifier.scopuseid_2-s2.0-85083801960-
dc.identifier.hkuros315278-
dc.identifier.volume107-
dc.identifier.issue5-
dc.identifier.spage763-
dc.identifier.epage771-
dc.identifier.isiWOS:000527792800001-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl0741-5400-

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