Influenza A virus PB1-F2 protein: An ambivalent innate immune modulator and virulence factor.
avian influenza virus
inflammasome
inflammation
influenza A virus
innate antiviral response
type I IFNs
Journal
Journal of leukocyte biology
ISSN: 1938-3673
Titre abrégé: J Leukoc Biol
Pays: England
ID NLM: 8405628
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
15
12
2019
revised:
23
03
2020
accepted:
24
03
2020
pubmed:
24
4
2020
medline:
5
11
2020
entrez:
24
4
2020
Statut:
ppublish
Résumé
Influenza 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.
Identifiants
pubmed: 32323899
doi: 10.1002/JLB.4MR0320-206R
doi:
Substances chimiques
PB1-F2 protein, Influenza A virus
0
Viral Proteins
0
Virulence Factors
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
763-771Informations de copyright
©2020 Society for Leukocyte Biology.
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