BST2 inhibits infection of influenza A virus by promoting apoptosis of infected cells

Autor: Se Ho Park, Hye Ri Kang, Eunbi Yi, Moon Jung Song, Jinsoo Oh
Rok vydání: 2019
Předmět:
X-Box Binding Protein 1
0301 basic medicine
Biophysics
Apoptosis
Protein Serine-Threonine Kinases
Endoplasmic Reticulum
GPI-Linked Proteins
Virus Replication
medicine.disease_cause
Biochemistry
Virus
Madin Darby Canine Kidney Cells
03 medical and health sciences
Dogs
Influenza A Virus
H1N1 Subtype
0302 clinical medicine
Viral envelope
Antigens
CD
Chlorocebus aethiops
Endoribonucleases
Influenza A virus
medicine
Animals
Humans
Vero Cells
Molecular Biology
Cytopathic effect
biology
Caspase 3
Chemistry
Cytochrome c
Wild type
Cytochromes c
Cell Biology
Endoplasmic Reticulum Stress
Caspase 9
Immunity
Innate
Cell biology
HEK293 Cells
030104 developmental biology
Gene Expression Regulation
030220 oncology & carcinogenesis
Host-Pathogen Interactions
biology.protein
Unfolded protein response
Poly(ADP-ribose) Polymerases
Signal Transduction
Zdroj: Biochemical and Biophysical Research Communications. 509:414-420
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2018.12.110
Popis: BST2 is an antiviral factor that inhibits the release of enveloped virus at the plasma membrane via an unusual topology in which its N-terminal is in the cytosol while its C-terminal is anchored by glycophosphatidylinositol (GPI). BST2-deficient cells showed substantially higher release of virions than wild type cells. Influenza-infected BST2-deficient cells showed greatly reduced cytopathic effect (CPE) than wild type cells despite their generally robust virus production. This finding prompted us to determine whether BST2 was involved in the apoptotic process of virus-infected host cells. Our results revealed that BST2 might be involved in IRE1α-mediated ER stress pathway by increasing spliced form XBP-1. Consequently, levels of cytochrome C, caspase-3, caspase-9, and PARP as representative molecules of apoptosis were significantly increased in wild type cells than those in BST2-deficient cells. These results suggest that BST2 might participate in innate host defense by augmenting ER-stress-induced apoptotic signaling to inhibit the replication and spread of virus.
Databáze: OpenAIRE
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