Mice with type I interferon signaling deficiency are prone to epilepsy upon HSV-1 infection.
Virol Sin
; 39(2): 251-263, 2024 Apr.
Article
en En
| MEDLINE
| ID: mdl-38219860
ABSTRACT
Viral encephalitis continues to be a significant public health concern. In our previous study, we discovered a lower expression of antiviral factors, such as IFN-ß, STING and IFI16, in the brain tissues of patients with Rasmussen's encephalitis (RE), a rare chronic neurological disorder often occurred in children, characterized by unihemispheric brain atrophy. Furthermore, a higher cumulative viral score of human herpes viruses (HHVs) was also found to have a significant positive correlation with the unihemispheric atrophy in RE. Type I IFNs (IFN-I) signaling is essential for innate anti-infection response by binding to IFN-α/ß receptor (IFNAR). In this study, we infected WT mice and IFNAR-deficient A6 mice with herpes simplex virus 1 (HSV-1) via periocular injection to investigate the relationship between IFN-I signaling and HHVs-induced brain lesions. While all mice exhibited typical viral encephalitis lesions in their brains, HSV-induced epilepsy was only observed in A6 mice. The gene expression matrix, functional enrichment analysis and protein-protein interaction network revealed four gene models that were positively related with HSV-induced epilepsy. Additionally, ten key genes with the highest scores were identified. Taken together, these findings indicate that intact IFN-I signaling can effectively limit HHVs induced neural symptoms and brain lesions, thereby confirming the positive correlation between IFN-I signaling repression and brain atrophy in RE and other HHVs encephalitis.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Interferón Tipo I
/
Herpesvirus Humano 1
/
Epilepsia
/
Herpes Simple
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Virol Sin
/
Virol. sin. (Online)
/
Virologica sinica (Online)
Asunto de la revista:
VIROLOGIA
Año:
2024
Tipo del documento:
Article
País de afiliación:
China