Cell-type specificity and functional redundancy of RIG-I-like receptors in innate immune sensing of Coxsackievirus B3 and encephalomyocarditis virus.
Animals
DEAD Box Protein 58
/ immunology
Encephalomyocarditis virus
/ immunology
Enterovirus B, Human
/ immunology
Fibroblasts
/ immunology
Host-Pathogen Interactions
/ immunology
Immunity, Innate
Interferon Type I
/ immunology
Interferon-Induced Helicase, IFIH1
/ immunology
Macrophages
/ immunology
Mice
Mice, 129 Strain
Mice, Inbred ICR
Mice, Knockout
Signal Transduction
Virus Replication
Innate immunity
Interferon
MDA5
Macrophage
Picornavirus
RIG-I
Journal
Virology
ISSN: 1096-0341
Titre abrégé: Virology
Pays: United States
ID NLM: 0110674
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
17
10
2018
revised:
30
11
2018
accepted:
03
12
2018
pubmed:
15
12
2018
medline:
21
3
2019
entrez:
15
12
2018
Statut:
ppublish
Résumé
The contributions of RIG-I and MDA5 receptors to sensing viruses of the Picornaviridae family were investigated. The picornaviruses encephalomyocarditis virus (EMCV) and Coxsackievirus B3 (CVB3) are detected by both MDA5 and RIG-I in bone marrow derived macrophages. In macrophages from wild type mice, type I IFN is produced early after infection; IFNβ synthesis is reduced in the absence of each sensor, while IFNα production is reduced in the absence of MDA5. EMCV and CVB3 do not replicate in murine macrophages, and their detection is different in murine embryonic fibroblasts (MEFs), in which the viruses replicate to high titers. In MEFs RIG-I was essential for the expression of type I IFNs but contributes to increased yields of CVB3, while MDA5 inhibited CVB3 replication but in an IFN independent manner. These observations demonstrate functional redundancy within the innate immune response to picornaviruses.
Identifiants
pubmed: 30550976
pii: S0042-6822(18)30367-2
doi: 10.1016/j.virol.2018.12.003
pmc: PMC6401217
mid: NIHMS1516776
pii:
doi:
Substances chimiques
Interferon Type I
0
Ddx58 protein, mouse
EC 3.6.1.-
Ifih1 protein, mouse
EC 3.6.1.-
DEAD Box Protein 58
EC 3.6.4.13
Interferon-Induced Helicase, IFIH1
EC 3.6.4.13
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
7-18Subventions
Organisme : NIAID NIH HHS
ID : U19 AI083019
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI139775
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI118916
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI050754
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI127463
Pays : United States
Informations de copyright
Copyright © 2018 Elsevier Inc. All rights reserved.
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