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Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [RNA-Seq]

ABSTRACT: Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [RNA-Seq]

PROVIDER: PRJNA952559 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24086064.fastq.gz	Fastqsanger.gz
	SRR24086065.fastq.gz	Fastqsanger.gz
	SRR24086066.fastq.gz	Fastqsanger.gz
	SRR24086067.fastq.gz	Fastqsanger.gz
	SRR24086068.fastq.gz	Fastqsanger.gz

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Similar Datasets

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [ChIP-Seq]

Project description:Merkel cell polyomavirus (MCPyV) is linked to Merkel cell carcinoma (MCC), a rare and aggressive skin cancer. This study investigated the influence of MCPyV T antigens on the host genome using transcriptomics and epigenomics. Results revealed a role for the small Tumor (sT) antigen in subverting type I interferon response and immune evasion, contributing to persistent infection and tumor progression. These findings enhance our understanding of MCPyV pathogenesis and may inform new therapeutic strategies.

2024-04-04 | GSE230758 | GEO

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [RNA-Seq]

2024-04-04 | GSE229019 | GEO

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling

Project description:Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling

| PRJNA962521 | ENA

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [ChIP-Seq]

Project description:Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling [ChIP-Seq]

| PRJNA962520 | ENA

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling.

Project description:Merkel cell polyomavirus (MCPyV) is the causative agent of the majority of Merkel cell carcinomas (MCC). The virus has limited coding capacity, with its early viral proteins, large T (LT) and small T (sT), being multifunctional and contributing to infection and transformation. A fundamental difference in early viral gene expression between infection and MCPyV-driven tumorigenesis is the expression of a truncated LT (LTtr) in the tumor. In contrast, sT is expressed in both conditions and contributes significantly to oncogenesis. Here, we identified novel functions of early viral proteins by performing genome-wide transcriptome and chromatin studies in primary human fibroblasts. Due to current limitations in infection and tumorigenesis models, we mimic these conditions by ectopically expressing sT, LT or LTtr, individually or in combination, at different time points. In addition to its known function in cell cycle and inflammation modulation, we reveal a fundamentally new function of sT. We show that sT regulates the type I interferon (IFN) response downstream of the type I interferon receptor (IFNAR) by interfering with the interferon-stimulated gene factor 3 (ISGF3)-induced interferon-stimulated gene (ISG) response. Expression of sT leads to a reduction in the expression of interferon regulatory factor 9 (IRF9) which is a central component of the ISGF3 complex. We further show that this function of sT is conserved in BKPyV. We provide a first mechanistic understanding of which early viral proteins trigger and control the type I IFN response, which may influence MCPyV infection, persistence and, during MCC progression, regulation of the tumor microenvironment.

| S-EPMC11333005 | biostudies-literature

Characterization of human Merkel cells and their response to Merkel cell polyomavirus

Project description:Merkel cells are epidermal mechanoreceptor cells responsible for the perception of gentle touch. Merkel cell carcinoma (MCC) is a rare and highly aggressive skin cancer. Although MCC histologically resembles Merkel cells, the cell of origin for MCC is unknown. MCC frequently contains integrated Merkel cell polyomavirus (MCPyV), a small DNA tumor virus with widespread prevalence. Whether MCPyV can transform Merkel cells is unknown. Here, we describe the isolation and long-term expansion of human Merkel cells from neonatal foreskin. We validated the expression of several Merkel cell-related factors by RNASeq, and assessed the ultrastructure by electron microscopy. Culture of Merkel cell preparations on an artificial basement membrane promoted the formation of structures containing both Merkel and non-Merkel cell populations. To determine whether Merkel cells were susceptible to transformation, we expressed tumor-derived MCPyV T antigens and additional oncogenes. We were unable to demonstrate tumorigenesis in immunodeficient mice, but were able to detect T antigen expression from excised cells weeks after implantation. These results highlight that foreskin-isolated Merkel cells can be propagated extensively, sustain expression of MCPyV T antigens, but are not susceptible to transformation by MCPyV, suggesting that Merkel cells from non-glabrous skin may not be a cell of origin for MCC.

2017-04-01 | GSE79657 | GEO

Dynamics of host response to Merkel cell polyomavirus oncogenes

Project description:Merkel cell polyomavirus (MCPyV) small tumor antigen (ST), truncated large tumor antigen (TLT), early region (ER), and GFP control inducible vectors were introduced into IMR90 human lung embryonic fibrobrasts. After induction, cells were extracted and sequenced in triplicate every 4 hours for the first 24 hours, then every 8 hours until 48 hours. The purpose of this experiment was to identify the dynamic host response to MCPyV oncogenes, using both differential expression analysis and transcriptional network reconstruction, and to provide a systems-level understanding of the initial steps toward Merkel cell carcinoma.

2023-11-06 | GSE130639 | GEO

Comparative Transcriptional Profiling of human Merkel cells and Merkel Cell Carcinoma

Project description:Merkel cell carcinoma is supposed to be derived from Merkel cells after infection by Merkel cell polyomavirus (MCV) and other poorly known events. A transcriptional profiling with cDNA microarrays was performed on cells from MCV+ Merkel cell carcinomas and isolated normal Merkel cells. This microarray revealed numerous significantly upregulated genes and down-regulated genes. The extensive list of genes identified in these experiments provides a large body of potentially valuable information of Merkel cell carcinoma carcinogenesis and could represent a source of potential targets for cancer therapy. Two-conditions experiment, MCV vs Normal Merkel Cell. Biological replicates : 4 MCV (Cy5), 1 control = pool of Normal Merkel cells from 3 liftings

2014-01-01 | E-GEOD-50434 | biostudies-arrayexpress

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-04 | GSE230760 | GEO

Host response to Merkel cell polyomavirus oncogenes in neonatal human dermal fibroblast

Project description:Merkel cell polyomavirus (MCPyV) early region (ER) and vector control inducible vectors were introduced into neonatal human dermal fibroblasts (nHDFs). Total RNA was then extracted and sequenced in triplicate at 0, 48 and 96 hours post-induction with doxycycline treatment. The purpose of this experiment was to identify the host response to MCPyV ER at the transcriptomic level, using both differential expression analysis and transcriptional network reconstruction. Together with our previous IMR90 model, we aim to systematically understand the initial steps toward Merkel cell carcinoma in different potential precursor cell types.

2024-12-16 | GSE278335 | GEO

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