Innate Immune Sensing of Viruses and Its Consequences for the Central Nervous System.
C-type lectin receptors
NOD-like receptors
RIG-I-like receptors
central nervous system
cytokines
inflammasome
interferons
signaling
toll-like receptor
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
23 01 2021
23 01 2021
Historique:
received:
18
12
2020
revised:
19
01
2021
accepted:
20
01
2021
entrez:
27
1
2021
pubmed:
28
1
2021
medline:
2
3
2021
Statut:
epublish
Résumé
Viral infections remain a global public health concern and cause a severe societal and economic burden. At the organismal level, the innate immune system is essential for the detection of viruses and constitutes the first line of defense. Viral components are sensed by host pattern recognition receptors (PRRs). PRRs can be further classified based on their localization into Toll-like receptors (TLRs), C-type lectin receptors (CLR), retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), NOD-like receptors (NLRs) and cytosolic DNA sensors (CDS). TLR and RLR signaling results in production of type I interferons (IFNα and -β) and pro-inflammatory cytokines in a cell-specific manner, whereas NLR signaling leads to the production of interleukin-1 family proteins. On the other hand, CLRs are capable of sensing glycans present in viral pathogens, which can induce phagocytic, endocytic, antimicrobial, and pro- inflammatory responses. Peripheral immune sensing of viruses and the ensuing cytokine response can significantly affect the central nervous system (CNS). But viruses can also directly enter the CNS via a multitude of routes, such as the nasal epithelium, along nerve fibers connecting to the periphery and as cargo of infiltrating infected cells passing through the blood brain barrier, triggering innate immune sensing and cytokine responses directly in the CNS. Here, we review mechanisms of viral immune sensing and currently recognized consequences for the CNS of innate immune responses to viruses.
Identifiants
pubmed: 33498715
pii: v13020170
doi: 10.3390/v13020170
pmc: PMC7912342
pii:
doi:
Substances chimiques
Cytokines
0
Inflammasomes
0
Interferon Type I
0
Lectins, C-Type
0
Receptors, Pattern Recognition
0
Toll-Like Receptors
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIDA NIH HHS
ID : R01 DA052209
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH087332
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH104131
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH105330
Pays : United States
Déclaration de conflit d'intérêts
The authors declare no conflict of interest. The funders had no role in the writing of the manuscript.
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