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© Thomas Wollert
Publication : Journal of leukocyte biology

Influenza A virus PB1-F2 protein: An ambivalent innate immune modulator and virulence factor.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of leukocyte biology - 01 May 2020

Cheung PH, Lee TT, Chan CP, Jin DY,

Link to Pubmed [PMID] – 32323899

Link to DOI – 10.1002/JLB.4MR0320-206R

J Leukoc Biol 2020 05; 107(5): 763-771

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.

https://pubmed.ncbi.nlm.nih.gov/32323899