Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851705 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19792334_1.fastq.gz | Fastqsanger.gz | |||
| SRR19792334_2.fastq.gz | Fastqsanger.gz | |||
| SRR19792335_1.fastq.gz | Fastqsanger.gz | |||
| SRR19792335_2.fastq.gz | Fastqsanger.gz | |||
| SRR25824394_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 14 |
Similar Datasets
Project description:Following acute infection, herpes simplex virus type 1 (HSV-1) establishes life-long latency in neurons. Although sensory neurons in trigeminal ganglia (TG) are primary sites for latency, brainstem is also an important site for latency. For example, the principal sensory nucleus of the spinal trigeminal tract (Pr5) receives afferent inputs from TG and harbors latent HSV-1. The locus coeruleus (LC), is indirectly linked to Pr5. The latency associated transcript (LAT) locus is the only viral gene abundantly expressed during latency, and LAT mediates establishment and maintenance of latency. Previous studies revealed senescent cells inflammation were detected in Pr5 and LC of aged mice and young mice latently infected with HSV-1 indicating HSV-1 influences senescence and inflammation during latency. To expand our understanding of how HSV-1 influences senescence and inflammation in Pr5 and LC, NanoString studies in mice latently infected with wild-type HSV-1 and a LAT-null mutant (dLAT2903) were compared to age matched uninfected C57Bl/6 male and female mice. Cellular genes that regulate neuron differentiation, axonal projection, and pro-inflammatory mediators were more prevalent in mice latently infected with wild-type (wt) HSV-1 and dLAT2903 versus uninfected mice. Thus, HSV-1 latency in Pr5 and LC is not a static process.
2026-06-03 | GSE326523 | GEO
Project description:Comparison of the effect of ocular surface desiccation and the lack of adaptive immunity (T and B cells) on gene expression in the trigeminal ganglia. Eight-week-old female mice of both strains were either operated on day 1 (either bilateral extraorbital lacrimal gland excision or sham surgery) and allowed to develop a dry eye state until day 10, when they were euthanized and the trigeminal ganglia were excised for RNA extraction. The two trigeminal ganglia of each mouse were pooled in one sample. There were 12 samples in total (2 x 2 design, 2 strains, 2 treatments).
2024-04-01 | E-MTAB-13945 | biostudies-arrayexpress
Project description:Herpes simplex virus type 1 (HSV-1) is a 152 Kb double stranded DNA alpha-herpesvirus, which establishes long life latent infection in sensory neurons. Most of our knowledge regarding HSV-1 latency comes from in vivo studies using small animal models, mainly rodents and rabbits, which are not naturally infected by HSV-1. Furthermore, these animal models do not fully recapitulate the species specific effects of human HSV-1 infection. Human cellular models utilize trigeminal ganglia removed from cadavers or, alternatively, neuron-like cells derived from cancerous cell lines that do not fully reflect effects on normal human neurons. This limitation poses the need to develop an in vitromodel to investigate molecular details of the mechanisms underlying quiescence and reactivation in human neurons. Induced pluripotent stem (iPS) celltechnologies offer an unprecedented opportunity to generate unlimited supplies of neurons and the facility to manipulate such cells in vitro. In this study, we developed an in vitro HSV-1 infection model in human iPS-derived neurons, which displays the main hallmarks of latency defined in animal models and in humans. Our results show for the first time that: i) persistent infection cannot be established in neural progenitor cells (NPCs); ii) the ability of HSV-1 to establish persistent infection is extended to glutamatergic neurons, and not limited to sensory neurons; iii) in neuronal cultures persistently infected with HSV-1, viral genome is localized at the nuclear periphery; iv) HSV-1 acute infection reduces RNA editing at the GluRB site. These results highlight the importance of iPS-based platforms to elucidate unknown aspects of HSV-1 quiescence in human neurons. NPCs were 70-80% confluence
2014-05-02 | E-GEOD-46042 | biostudies-arrayexpress
Project description:Herpes simplex virus type 1 (HSV-1) is a 152 Kb double stranded DNA alpha-herpesvirus, which establishes long life latent infection in sensory neurons. Most of our knowledge regarding HSV-1 latency comes from in vivo studies using small animal models, mainly rodents and rabbits, which are not naturally infected by HSV-1. Furthermore, these animal models do not fully recapitulate the species specific effects of human HSV-1 infection. Human cellular models utilize trigeminal ganglia removed from cadavers or, alternatively, neuron-like cells derived from cancerous cell lines that do not fully reflect effects on normal human neurons. This limitation poses the need to develop an in vitro model to investigate molecular details of the mechanisms underlying latency and reactivation in human neurons. Induced pluripotent stem (iPS) cell technologies offer an unprecedented opportunity to generate unlimited supplies of neurons and the facility to manipulate such cells in vitro. In this study, we developed an in vitro HSV-1 infection model in human iPS-derived neural progenitor cells (NPCs) and neurons, which displays the main hallmarks of latency defined in animal models and in humans. Induced pluripotent stem (iPS) cells were generated from human skin biopsy samples
2014-05-02 | E-GEOD-46041 | biostudies-arrayexpress
Project description:The uni- and bilateral excision models allow comparison of the combined effects of ocular desiccation and neuroinflammation on trigeminal gene expression vs the isolated effects of neuroinflammation propagated from the other side. Also, the transient receptor potential vanilloid 1 (Trpv1)-deficient mice allow the assessment of the role of this channel. In the unilateral excision model, only the left trigeminal ganglia were analyzed, which were contralateral to the desiccated eyes (right eyes) secondary to excision of the right-side extraorbital lacrimal glands, as the left-side lacrimal glands were left untouched. Eight-week-old female mice of both strains were either operated on day 1 (either bilateral or unilateral -right-side- extraorbital lacrimal gland excision or sham surgery) and allowed to develop a dry eye state until day 10, when they were euthanized and the trigeminal ganglia were excised for RNA extraction. The two trigeminal ganglia of each mouse were pooled in one sample for the bilateral excision or sham groups whereas only the left trigeminal ganglion of each mouse was harvested for the contralateral (unilateral) group. There were 18 samples in total (2 x 3 design, 2 strains, 3 treatments) including 3 replicates/group.
2025-07-01 | E-MTAB-15193 | biostudies-arrayexpress
Project description:SARS-CoV-2, the virus responsible for COVID-19, infects both human airway epithelial cells and trigeminal ganglia. We assessed the consequences of SARS-CoV-2 infection on gene expression in Calu-3 cells and in primary Mus musculus trigeminal ganglia cells (mmTG). Here, we provide datasets that include raw reads and mapped reads for the following: 1) mock infected mmTG 48 hrs post infection; 2) SARS-CoV-2 infected mmTG 48 hrs post infection; 3) mock infected Calu-3 cells 24 hrs post infection; 4) SARS-CoV-2 infected Calu-3 cells 24 hrs post infection; 5) mock infected Calu-3 cells 48 hrs post infection; 6) SARS-CoV-2 infected Calu-3 cells 48 hrs post infection.
2024-01-08 | GSE252056 | GEO
Project description:Herpes simplex virus type 1 (HSV-1) is a 152 Kb double stranded DNA alpha-herpesvirus, which establishes long life latent infection in sensory neurons. Most of our knowledge regarding HSV-1 latency comes from in vivo studies using small animal models, mainly rodents and rabbits, which are not naturally infected by HSV-1. Furthermore, these animal models do not fully recapitulate the species specific effects of human HSV-1 infection. Human cellular models utilize trigeminal ganglia removed from cadavers or, alternatively, neuron-like cells derived from cancerous cell lines that do not fully reflect effects on normal human neurons. This limitation poses the need to develop an in vitromodel to investigate molecular details of the mechanisms underlying quiescence and reactivation in human neurons. Induced pluripotent stem (iPS) celltechnologies offer an unprecedented opportunity to generate unlimited supplies of neurons and the facility to manipulate such cells in vitro. In this study, we developed an in vitro HSV-1 infection model in human iPS-derived neurons, which displays the main hallmarks of latency defined in animal models and in humans. Our results show for the first time that: i) persistent infection cannot be established in neural progenitor cells (NPCs); ii) the ability of HSV-1 to establish persistent infection is extended to glutamatergic neurons, and not limited to sensory neurons; iii) in neuronal cultures persistently infected with HSV-1, viral genome is localized at the nuclear periphery; iv) HSV-1 acute infection reduces RNA editing at the GluRB site. These results highlight the importance of iPS-based platforms to elucidate unknown aspects of HSV-1 quiescence in human neurons.
2014-05-02 | GSE46042 | GEO
Project description:Sensory neurons were extracted from the dorsal root or trigeminal ganglia of AdvGFP transgenic mice and their molecular profile analysed via RNA-seq.
2017-10-11 | GSE100175 | GEO