Gene expression profiling in the pathogenesis of Visna-Maedi viral disease
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ABSTRACT:
PROVIDER: PRJNA419757 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs) are short endogenous, single-stranded, non-coding small RNA molecules of about 22 nucleotides in length. They regulate gene expression post-transcriptionally by silencing mRNA molecules and they regulate many physiological processes. Visna-Maedi virus (VMV) is a lentivirus that causes Visna-Maedi disease (VM) in sheep characterised by pneumonia, mastitis, arthritis and encephalitis; and affects cells of the monocyte/macrophage lineage. So far, there are no studies in the role of miRNAs in this viral disease. Using RNAseq technology and bioinformatics analysis the expression of miRNAs in different phases of the disease were studied. A total of 212 miRNAs were found, of which 46 were conserved sequences found for the first time in sheep and 12 were completely novel. Differential expression analysis showed changes in several miRNAs comparing uninfected and seropositive groups, but did not detect significant differences between seropositive asymptomatic and diseased sheep. The high increase in expression of oar-miR-21 agrees with the increase of the same miRNA detected in other viral diseases. In addition, the target prediction of dysregulated miRNAs revealed that they control genes involved in proliferation-related signalling pathways like PI3K-Akt, AMPK and ErbB.
2018-12-19 | GSE115415 | GEO
Project description:To test if LEDGF/p75 influences distribution of Maedi-visna virus (MVV) integration sites, we infected sheep CPT3, LKO1 (PSIP1-null), LHKO1 and LHKO2 (PSIP1/HDGFL2-null) cells with MVV-derived vector. Genomic DNA was isolated from infected cells, and chromosomal junctions at integrated U5 vDNA ends were amplified using linker-mediated PCR, sequenced using Illumina technology and mapped to sheep genome.
2022-02-06 | GSE196041 | GEO
Project description:To test if LEDGF/p75 influences distribution of Maedi-visna virus (MVV) integration sites, we infected human HEK293T, LKO (PSIP1-null), and LHKO (PSIP1/HDGFL2-null) cells with MVV-derived vector. Genomic DNA was isolated from infected cells, and chromosomal junctions at integrated U5 vDNA ends were amplified using linker-mediated PCR, sequenced using Illumina technology and mapped to human genome.
2022-02-06 | GSE196040 | GEO
Project description:A study was designed to further define the viral landscape within Sjogren's Syndrome (pSS) affected salivary gland tissue to identify potential viral-mediated triggers in the pathogenesis of this autoimmune disease. Viral Probes for Vertebrate Infecting Viral Families
2017-05-01 | E-GEOD-77599 | biostudies-arrayexpress
Project description:Kyasanur Forest disease virus (KFDV) and the closely related Alkhurma hemorrhagic disease virus (AHFV) are emerging flaviviruses that cause severe viral hemorrhagic fevers in humans. Increasing geographical expansion and case numbers, particularly of KFDV in southwest India, class these viruses as a public health threat. Viral pathogenesis is not well understood and additional vaccines and antivirals are needed to effectively counter the impact of these viruses. However, current animal models for KFDV do not accurately reproduce viral tissue tropism or clinical outcomes observed in humans. Here, we show pigtailed macaques (Macaca nemestrina) infected with KFDV or AHFV develop viremia that peaks 2 to 4 days following inoculation. Over the course of infection, animals developed lymphocytopenia, thrombocytopenia, and elevated liver enzymes. Infected animals exhibited hallmark signs of human disease characterized by a flushed appearance, piloerection, dehydration, loss of appetite, weakness, and hemorrhagic signs such as epistaxis. Virus was commonly present in the gastrointestinal tract, consistent with human disease caused by KFDV and AHFV where gastrointestinal symptoms (hemorrhage, vomiting, diarrhea) are common. This work characterizes a nonhuman primate model for KFDV and AHFV that closely resembles human disease for further utilization in understanding host immunity and development of antiviral countermeasures.
2021-10-22 | GSE185797 | GEO
Project description:Puri2010 - Mathematical Modeling for the
Pathogenesis of Alzheimer's Disease
Puri2010 - Mathematical Modeling for the Pathogenesis of
Alzheimer's Disease
Encoded non-curated model. Issues:
- Confusing replacement of
α16
when t = 3 years
- Confusing 4th rate equation
This model is described in the article:
Mathematical modeling for
the pathogenesis of Alzheimer's disease.
Puri IK, Li L.
PLoS ONE 2010; 5(12): e15176
Abstract:
Despite extensive research, the pathogenesis of
neurodegenerative Alzheimer's disease (AD) still eludes our
comprehension. This is largely due to complex and dynamic
cross-talks that occur among multiple cell types throughout the
aging process. We present a mathematical model that helps
define critical components of AD pathogenesis based on
differential rate equations that represent the known
cross-talks involving microglia, astroglia, neurons, and
amyloid-? (A?). We demonstrate that the inflammatory activation
of microglia serves as a key node for progressive
neurodegeneration. Our analysis reveals that targeting
microglia may hold potential promise in the prevention and
treatment of AD.
This model is hosted on
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and identified by:
MODEL1409240001.
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To the extent possible under law, all copyright and related or
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Public Domain Dedication for more information.
2015-04-15 | MODEL1409240001 | BioModels
Project description:A study was designed to further define the viral landscape within Sjogren's Syndrome (pSS) affected salivary gland tissue to identify potential viral-mediated triggers in the pathogenesis of this autoimmune disease.
2017-05-01 | GSE77599 | GEO