Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13731458_1.fastq.gz | Fastqsanger.gz | |||
| SRR13731458_2.fastq.gz | Fastqsanger.gz |
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Project description:Rabies is a fatal viral encephalitis caused by most or all known members of the lyssavirus genus, and no therapy is known to prevent mortality once lyssavirus has entered the human CNS. We have previously shown that a single peripheral dose of a neutralizing human monoclonal antibody (mAb) can protect mice from fatal lyssavirus infection even when delivered after CNS invasion. To determine how such therapy alters the biology of established CNS infection, mice were mock-infected or infected in the footpad with Australian bat lyssavirus expressing luciferase (ABLV-Luc) and then treated on day 5 post-infection with a single 10 mg/kg intraperitoneal dose of either the neutralizing human mAb A6 or the irrelevant-specificity control human mAb m102.4. Whole brains were harvested at day 14 post-infection and total RNA sequencing was performed. Principal component analysis separated m102.4-treated infected animals from both mock-infected controls and A6-treated infected animals, with A6-treated samples clustering closely with mock-infected controls. Infection in the presence of the control mAb induced broad upregulation of interferon-stimulated, antiviral, chemokine and inflammatory genes (e.g. Ifit1, Zbp1, Mx1, Isg15, Cxcl10, Ccl2, Ccl5, Tnf, Il12b, Cfb), whereas A6-treated animals showed few differentially expressed genes relative to mock-infected controls. Gene set enrichment analysis confirmed strong enrichment of inflammatory and antiviral pathways in m102.4-treated animals relative to both other groups. These data demonstrate that peripheral single-dose therapy with a neutralizing mAb broadly reduces expression of neuroinflammatory mediators during the acute phase of CNS-resident lyssavirus infection.
2026-09-22 | GSE347489 | GEO
Project description:Data from the VLA lyssavirus genotyping microarray. The array platform for this data is GEO accession GPL8066, and consists of 624 oligos representing two viral families. The data set itself consists of 14 arrays, 7 hybridised with RNA from mice brains infected with 7 genotypes of lyssaviruses, 1 hybridised with RNA from normal mouse brain, and 6 hybridised with RNA from coded samples consisting of infected mouse brains or control mouse brains. Keywords: Lyssavirus genotyping microarray
2009-06-09 | GSE14705 | GEO
Project description:Data from the VLA lyssavirus genotyping microarray. The array platform for this data is GEO accession GPL8066, and consists of 624 oligos representing two viral families. The data set itself consists of 14 arrays, 7 hybridised with RNA from mice brains infected with 7 genotypes of lyssaviruses, 1 hybridised with RNA from normal mouse brain, and 6 hybridised with RNA from coded samples consisting of infected mouse brains or control mouse brains. Keywords: Lyssavirus genotyping microarray Data from the VLA lyssavirus genotyping microarray. The array platform for this data is GEO accession GPL8066, and consists of 624 oligos representing two viral families. The data set itself consists of 14 arrays, 7 hybridised with RNA from mice brains infected with 7 genotypes of lyssaviruses, 1 hybridised with RNA from normal mouse brain, and 6 hybridised with RNA from coded samples consisting of infected mouse brains or control mouse brains. Statistical analysis of the data was done with DetectiV software (Watson et al., 2007). The median and array methods of normalization were used in the statistical analysis of the results. In the median method, DetectiV software calculates the mean fluorescence for each set of probes and normalised against background fluorescence of all probes, assuming that most probes are not hybridized. The array method utilizes an entire control array, e.g. RNA from a known uninfected animal, as the negative control and all probe values are divided by their respective elements from the control array.
2010-05-18 | E-GEOD-14705 | biostudies-arrayexpress
Project description:Rabies virus (RABV), the prototypical lyssavirus, suppresses neuronal ferroptosis through lipid droplet (LD) biogenesis, which is a critical immune evasion strategy we previously identified. However, the mechanistic link between LD formation and ferroptosis regulation during RABV infection remains poorly defined. Here, we report that RABV upregulates Regulator of G Protein Signaling 4 (RGS4), a ferroptosis-associated biomarker, and this induction is strictly dependent on triglyceride synthesis and subsequent LD formation. Functionally, genetic or pharmacological inhibition of RGS4 elevates ferroptosis susceptibility, thereby restricting viral replication. Mechanistically, RGS4 depletion reduces expression of the E3 ubiquitin ligase HERC2, impairing K63-linked ubiquitination of Nuclear Receptor Coactivator 4 (NCOA4) and enhancing NCOA4 stability. Stabilized NCOA4 promotes ferritinophagy, leading to degradation of ferritin heavy chain (FTH) and ultimately inducing ferroptosis. Critically, we identify that the lyssavirus matrix (M) protein directly counteracts this pathway: M protein inhibits RGS4 degradation via the Cys/N-degron system through incomplete autophagy, stabilizing RGS4 to maintain HERC2 expression, promote NCOA4 ubiquitination, and attenuate ferritinophagy. This mechanism reduces ferroptosis susceptibility and enables viral replication. Our findings unveil a novel lyssavirus-specific regulatory axis, RGS4-HERC2-NCOA4-FTH, that modulates ferroptosis, highlighting RGS4 and M protein as promising targets for antiviral therapy.
2026-09-13 | GSE345815 | GEO
Project description:VLA lyssavirus genotyping dataset
| PRJNA112087 | ENA