lncRNA EDAL restricts rabies lyssavirus replication in a cell-specific and infection route-dependent manner.
J Gen Virol
; 103(3)2022 03.
Article
en En
| MEDLINE
| ID: mdl-35234607
ABSTRACT
Rabies, caused by rabies lyssavirus (RABV), is a fatal disease among humans and almost all warm-blooded animals. Our previous study showed that the long non-coding RNA (lncRNA) EZH2 degradation-associated lncRNA (EDAL) effectively inhibits RABV infection both in vitro and in vivo by degrading EZH2 and promoting the transcription of an antiviral gene, Pcp4l1. Herein, we found that recombinant RABV expressing EDAL (rRABV-EDAL) restricts RABV replication in primary granule neurons but not in primary cortical neurons or astrocytes. Further study revealed that EDAL induced EZH2 protein degradation and thereby decreased trimethylation of lysine 27 on the histone 3 (H3K27me3) level in granule neuron cells but not in cortical neurons or astrocytes. Furthermore, rRABV-EDAL infection induces more Pcp4l1 mRNA transcription in granule neurons, while there are almost no obvious changes in cortical neurons or astrocytes. Consistently, compared with the parent virus RABV, reduced pathogenicity of rRABV-EDAL was observed in mice post-intranasal infection but not intramuscular infection. These results suggest that the lncRNA EDAL restricts RABV replication in a cell-specific and infection route-dependent manner.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Rabia
/
Virus de la Rabia
/
Lyssavirus
/
ARN Largo no Codificante
Límite:
Animals
Idioma:
En
Revista:
J Gen Virol
Año:
2022
Tipo del documento:
Article