Influenza Virus Neuraminidase Engages CD83 and Promotes Pulmonary Injury.
Animals
Antigens, CD
/ genetics
Dendritic Cells
/ immunology
Female
Host-Pathogen Interactions
/ immunology
Immunity, Innate
/ immunology
Immunoglobulins
/ genetics
Influenza A Virus, H9N2 Subtype
/ enzymology
Lung Injury
/ etiology
Macrophages
/ immunology
Membrane Glycoproteins
/ genetics
Mice
Mice, Inbred C57BL
Neuraminidase
/ genetics
Orthomyxoviridae Infections
/ complications
Signal Transduction
Viral Proteins
/ genetics
Virulence
CD83 Antigen
CD83
H9N2
cytokines
dendritic cells
influenza virus
neuraminidase
Journal
Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724
Informations de publication
Date de publication:
13 01 2021
13 01 2021
Historique:
received:
10
09
2020
accepted:
30
10
2020
pubmed:
13
11
2020
medline:
16
3
2021
entrez:
12
11
2020
Statut:
epublish
Résumé
Influenza A viruses cause severe respiratory illnesses in humans and animals. Overreaction of the innate immune response to influenza virus infection results in hypercytokinemia, which is responsible for mortality and morbidity. However, the mechanism by which influenza induces hypercytokinemia is not fully understood. In this study, we established a mouse-adapted H9N2 virus, MA01, to evaluate the innate immune response to influenza in the lung. MA01 infection caused high levels of cytokine release, enhanced pulmonary injury in mice, and upregulated CD83 protein in dendritic cells and macrophages in the lung. Influenza virus neuraminidase (NA) unmasked CD83 protein and contributed to high cytokine levels. Furthermore, we provide evidence that CD83 is a sialylated glycoprotein. Neuraminidase treatment enhanced lipopolysaccharide (LPS)-stimulated NF-κB activation in RAW264.7 cells. Anti-CD83 treatment alleviated influenza virus-induced lung injury in mice. Our study indicates that influenza virus neuraminidase modulates CD83 status and contributes to the "cytokine storm," which may suggest a new approach to curb this immune injury.
Identifiants
pubmed: 33177200
pii: JVI.01753-20
doi: 10.1128/JVI.01753-20
pmc: PMC7925101
pii:
doi:
Substances chimiques
Antigens, CD
0
Immunoglobulins
0
Membrane Glycoproteins
0
Viral Proteins
0
NA protein, influenza A virus
EC 3.2.1.18
Neuraminidase
EC 3.2.1.18
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2021 American Society for Microbiology.
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