Regulation of innate immune responses by rabies virus.
apotosis
autophagy
infectious disease and host defense
innate immunity and inflammation
rabies virus
Journal
Animal models and experimental medicine
ISSN: 2576-2095
Titre abrégé: Animal Model Exp Med
Pays: United States
ID NLM: 101726292
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
15
07
2022
accepted:
31
08
2022
pubmed:
24
9
2022
medline:
1
11
2022
entrez:
23
9
2022
Statut:
ppublish
Résumé
Rabies virus (RABV) is an infectious and neurotropic pathogen that causes rabies and infects humans and almost all warm-blooded animals, posing a great threat to people and public safety. It is well known that innate immunity is the critical first line of host defense against viral infection. It monitors the invading pathogens by recognizing the pathogen-associated molecular patterns and danger-associated molecular patterns through pattern-recognition receptors, leading to the production of type I interferons (IFNα/β), inflammatory cytokines, and chemokines, or the activation of autophagy or apoptosis to inhibit virus replication. In the case of RABV, the innate immune response is usually triggered when the skin or muscle is bitten or scratched. However, RABV has evolved many ways to escape or even hijack innate immune response to complete its own replication and eventually invades the central nervous system (CNS). Once RABV reaches the CNS, it cannot be wiped out by the immune system or any drugs. Therefore, a better understanding of the interplay between RABV and innate immunity is necessary to develop effective strategies to combat its infection. Here, we review the innate immune responses induced by RABV and illustrate the antagonism mechanisms of RABV to provide new insights for the control of rabies.
Identifiants
pubmed: 36138548
doi: 10.1002/ame2.12273
pmc: PMC9610147
doi:
Substances chimiques
Cytokines
0
Chemokines
0
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
418-429Informations de copyright
© 2022 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences.
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