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44 results for “Polyomavirus”
A more accurate risk biomarkers recognition for Progressive Multifocal Leukoencephalopathy (PML) caused by Polyomavirus JC in patients with multiple sclerosis during treatment with disease-modifying therapies (DMTs): an ongoing clinical challenge.
<p>The therapeutic scenario for the treatment of MS has recently been characterized by a veritable revolution, which has included the introduction, for the first time, of drug treatment guidelines and the entry, in the therapeutic landscape of the last decade, of numerous new drugs that, in varying but significantly relevant ways, have proven capable of modifying the course of the disease (Disease-Modifying Therapies - DMTs). <br> While the arsenal of available drugs has resulted in advances in efficacy and selectivity, it has also exposed them to the danger of side effects, potentially serious and in some cases even fatal. Among the most important side effects, complications of infectious origin, characterized by cases of viral infection/reactivation, as in the case of JCPyV, the etiologic agent of PML, are the most represented. This study, based on the follow-up of MS patients treated with different DMTs, contributes to implementing the data in the literature regarding a greater understanding of the risks related to the administration of these drugs and more appropriate monitoring of MS treatment. The risk of JCPyV reactivation with Fingolimod and Dimethyl fumarate is lower than the risk of viral reactivation associated with natalizumab.<br> In light of the data obtained, it is possible to conclude that, in the case of natalizumab, testing for JC viruria would seem to be more useful in identifying those patients with a JCPyV-specific humoral response that is not yet detectable. In addition, our results, draw attention to the importance of analyzing the NCCR rearrangements of JCPyV. Indeed, the particular rearrangements found in plasma and PBMCs of patients with RRMS treated with natalizumab could represent an alert of neuroinvasiveness in order to detect early those patients with a higher risk of developing PML. In the case of dimethyl fumarate, it seems likely that monitoring of lymphopenia would identify a higher risk group of patients in whom alternative therapy should be sought. Prolonged lymphopenia, with absolute lymphocyte counts less than 750 lymphocytes/mL, might be the major risk factor for PML although, a greater risk might lie in the loss of CD8+ cells that are crucial for JCPyV control.<br> For fingolimod, this strategy cannot be applied because the number of circulating lymphocytes decreases while the actual lymphocyte function appears largely normal therefore, monitoring viruria and viremia along with identification of the neurotrophic variant of the virus seems a more exploitable means for risk stratification.</p> <p>In conclusion, the results of this study can be considered directly transferable to the National Health System in that, both the monitoring of JCPyV reactivation by viruria and the sequence analysis of viral NCCR and host immune set-up could play the role of translatable biomarkers in clinical practice in order to assess the risk of PML onset. In addition to improving risk stratification of this disease, these biomarkers of viral reactivation and pathogenicity could facilitate timely diagnosis, optimizing the use of health care resources and contributing to the reduction of direct and indirect costs of MS disease.</p> <p>Prezioso Carla was supported by the Italian Ministry of Health (Starting Grant: SG-2018-12366194).</p>
The Transcriptome Architecture of Polyomaviruses
<p>Processed data and code sufficient to reproduce findings from <strong>The Transcriptome Architecture of Polyomaviruses</strong>.</p>
T cell deficiency precipitates antibody evasion and emergence of neurovirulent polyomavirus
<p>JC polyomavirus (JCPyV) causes progressive multifocal leukoencephalopathy (PML), a life-threatening brain disease in immunocompromised patients. Inherited and acquired T cell deficiencies are associated with PML. The incidence of PML is increasing with the introduction of new immunomodulatory agents, several of which target T cells or B cells. PML patients often carry mutations in the JCPyV VP1 capsid protein, which confer resistance to neutralizing VP1 antibodies (Ab). Polyomaviruses (PyV) are tightly species-specific; the absence of tractable animal models has handicapped understanding of PyV pathogenesis. Using mouse polyomavirus (MuPyV), we found that T cell deficiency during persistent infection, in the setting of monospecific VP1 Ab, was required for outgrowth of VP1 Ab-escape viral variants. CD4 T cells were primarily responsible for limiting polyomavirus infection in the kidney, a major reservoir of persistent infection by both JCPyV and MuPyV, and checking emergence of these mutant viruses. T cells also provided a second line of defense by controlling the outgrowth of VP1 mutant viruses that evaded Ab neutralization. A virus with two capsid mutations, one conferring Ab-escape yet impaired infectivity and a second compensatory mutation, yielded a highly neurovirulent variant. These findings link T cell deficiency and evolution of Ab-escape polyomavirus VP1 variants with neuropathogenicity.</p>
T cell deficiency precipitates antibody evasion and emergence of neurovirulent polyomavirus
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Human genomics of the humoral immune response against polyomaviruses
<p>Meta-analyses results of the manuscript "Human genomics of the humoral immune response against polyomaviruses".</p>
Murine polyomavirus DNA transitions through spatially distinct nuclear replication subdomains during infection
<p>The replication of small DNA viruses requires both host DNA replication and repair factors that are often recruited to subnuclear domains termed viral replication centers (VRCs). Aside from serving as a spatial focus for viral replication, little is known about these dynamic areas in the nucleus. We investigated the organization and function of VRCs during murine polyomavirus (MuPyV) infection using 3D structured illumination microscopy (3D-SIM). We localized MuPyV replication center components, such as the viral large T-antigen (LT) and the cellular replication protein A (RPA), to spatially distinct subdomains within VRCs. We found that viral DNA (vDNA) trafficked sequentially through these subdomains post-synthesis, suggesting their distinct functional roles in vDNA processing. Additionally, we observed disruption of VRC organization and vDNA trafficking during mutant MuPyV infections or inhibition of DNA synthesis. These results reveal a dynamic organization of VRC components that coordinates virus replication.</p>
Single-cell analysis reveals host S phase drives large T antigen expression during BK polyomavirus infection
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Study To Evaluate The Safety, Tolerability And Immunogenicity Of 4 mg Of ITI-3000 In Patients With Polyomavirus-Positive Merkel Cell Carcinoma (MCC)
ClinicalTrials.gov study NCT05422781. IPD Sharing: NO. Countries: 1. Publications: 1.
Adoptive Cellular Immunotherapy for Progressive Multifocal Leukoencephalopathy With Ex Vivo Generated Polyomavirus-Specific T-Cells
ClinicalTrials.gov study NCT02694783. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Impact of Immunosuppressive Regimens on Polyomavirus-related Transplant Nephropathy
ClinicalTrials.gov study NCT00160966. IPD Sharing: YES. Countries: 1. Publications: 23.
A Trial to Treat Polyomavirus Infections (BKPyV) in Kidney and Simultaneous Kidney Pancreas Transplant Recipients
ClinicalTrials.gov study NCT05325008. IPD Sharing: NO. Countries: 1. Publications: 1.
Murine polyomavirus DNA transitions through spatially distinct nuclear replication subdomains during infection
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B cells specific for polyomavirus-derived oncoprotein are predictive of Merkel cell carcinoma progression
GEO Series GSE301498. Homo sapiens. 5 samples. Type: Other.
Normal human urothelial cells infected with BK polyomavirus (BKPyV) in the presence or absence of interferon gamma (IFNg)
GEO Series GSE174244. Homo sapiens. 26 samples. Type: Expression profiling by high throughput sequencing.
Cellular Transcriptional Responses to Merkel cell polyomavirus T antigens
GEO Series GSE68503. Homo sapiens. 12 samples. Type: Expression profiling by array.
Peripheral blood transcriptomic profiles of rejection and polyomavirus-associated nephropathy after kidney transplantation
GEO Series GSE175718. Homo sapiens. 384 samples. Type: Expression profiling by high throughput sequencing.
Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [ChIP-Seq]
GEO Series GSE230758. Homo sapiens. 20 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Merkel Cell Polyomavirus Encodes Circular RNAs (circRNAs) Enabling a Dynamic circRNA/microRNA/mRNA Regulatory Network
GEO Series GSE162627. Rattus norvegicus; Homo sapiens. 4 samples. Type: Other.
Merkel cell polyomavirus pan-T antigen knockdown reduces cancer cell stemness and promotes neural differentiation independent of RB1
GEO Series GSE254170. Homo sapiens. 3 samples. Type: Expression profiling by high throughput sequencing.
microRNA expression patterns related to merkel cell polyomavirus infection in human merkel cell carcinoma
GEO Series GSE43699. Homo sapiens. 16 samples. Type: Non-coding RNA profiling by array.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
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OpenNeuro
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