Recognition of copy-back defective interfering rabies virus genomes by RIG-I triggers efficient immune response against vaccine strains
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ABSTRACT:
PROVIDER: PRJNA803174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17872228.fastq.gz | Fastqsanger.gz | |||
| SRR17872229.fastq.gz | Fastqsanger.gz | |||
| SRR17872230.fastq.gz | Fastqsanger.gz | |||
| SRR17872231.fastq.gz | Fastqsanger.gz | |||
| SRR17872232.fastq.gz | Fastqsanger.gz |
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Project description:Rabies is an ancient infectious disease but still lacking efficient therapeutic approach despite of vaccine. In this study, we have identified a novel cytoplasmic lncRNA, namely rabies virus related lncRNA 1(RVRL1), whose expression in neuronal cells is up-regulated upon the infection of the causative agent of rabies, the neurotropic virus rabies virus (RABV). RVRL1 effectively inhibits RABV infection both in neuronal cells and in a mouse model. RVRL1 binds to EZH2 and disrupts the PRC2 complex, which is consistent with the inverse relationship between RVRL1 expression and the cellular H3K27me3 level. RVRL1 expression positively regulates the expression of PCP4L1 encoding a 10 kD peptide, which is shown to inhibit RABV replication. These findings highlight a novel mechanism for lncRNAs to upregulate the expression of antiviral genes, and define two potential anti-rabies reagents including an antiviral lncRNA and an antiviral peptide.
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