Mus musculus
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PROVIDER: PRJNA248891 | ENA |
REPOSITORIES: ENA
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Project description:Papillomaviruses (PVs) are able to induce papillomas, premalignant lesions, and carcinomas in a wide variety of species. PVs are classified first based on their host and tissue tropism and then their genomic diversities. A laboratory mouse papillomavirus, MmuPV1 (formerly MusPV), naturally infects NMRI-Foxn1nu/Foxn1nu (nude; T cell deficient) mice. C57BL/6J wild-type mice were not susceptible to MmuPV1 infection; however, immunocompetent, alopecic, S/RV/Cri-ba/ba (bare) mice developed small papillomas at injection sites that regressed. NMRI-Foxn1nu and B6.Cg-Foxn1nu but not NU/J-Foxn1nu mice were susceptible to MmuPV1 infection. B6 congenic strains, but not other congenic strains carrying the same allelic mutations, that lack B- and T-cells, but not B-cells alone, were susceptible to infection, indicating that mouse strain and T-cell deficiency are critical to tumor formation. Although lesions initially observed were exophytic papillomas around the muzzle, exophytic papillomas on the tail and condylomas of the vaginal lining could be induced by experimental infections. On the dorsal skin, locally invasive, poorly differentiated tumors developed with features similar to human trichoblastomas. Transcriptome analysis revealed significant differences between the normal skin in these anatomic sites and in papillomas versus trichoblastomas. The primarily dysregulated genes involved molecular pathways associated with cancer, cellular development, cellular growth and proliferation, cell morphology, and connective tissue development and function. Surprisingly, few of the genes commonly associated with basal cell carcinoma or squamous cells carcinoma were dramatically dysregulated. To determine if there were transcriptome differences between papillomas on the tail skin compared to invasive trichoblastomas on the dorsal skin, tumors from the tail and dorsal skin from 3 B6.Cg-Foxn1nu/Foxn1nu mice and unaffected skin from the tail or contra-lateral (dorsal skin) were compared using the Affymetrix GeneChip Mouse Genome 1.0 ST Array. Concurrently, a matched study was done at the University of Louisville comparing facial (muzzle) papillomas and dorsal skin trichoblastomas to respective unaffected contralateral skin.
2014-10-28 | E-GEOD-58094 | biostudies-arrayexpress
Project description:Papillomaviruses (PVs) are able to induce papillomas, premalignant lesions, and carcinomas in a wide variety of species. PVs are classified first based on their host and tissue tropism and then their genomic diversities. A laboratory mouse papillomavirus, MmuPV1 (formerly MusPV), naturally infects NMRI-Foxn1nu/Foxn1nu (nude; T cell deficient) mice. C57BL/6J wild-type mice were not susceptible to MmuPV1 infection; however, immunocompetent, alopecic, S/RV/Cri-ba/ba (bare) mice developed small papillomas at injection sites that regressed. NMRI-Foxn1nu and B6.Cg-Foxn1nu but not NU/J-Foxn1nu mice were susceptible to MmuPV1 infection. B6 congenic strains, but not other congenic strains carrying the same allelic mutations, that lack B- and T-cells, but not B-cells alone, were susceptible to infection, indicating that mouse strain and T-cell deficiency are critical to tumor formation. Although lesions initially observed were exophytic papillomas around the muzzle, exophytic papillomas on the tail and condylomas of the vaginal lining could be induced by experimental infections. On the dorsal skin, locally invasive, poorly differentiated tumors developed with features similar to human trichoblastomas. Transcriptome analysis revealed significant differences between the normal skin in these anatomic sites and in papillomas versus trichoblastomas. The primarily dysregulated genes involved molecular pathways associated with cancer, cellular development, cellular growth and proliferation, cell morphology, and connective tissue development and function. Surprisingly, few of the genes commonly associated with basal cell carcinoma or squamous cells carcinoma were dramatically dysregulated.
2014-10-28 | GSE58094 | GEO
Project description:We sought to describe the global methylation landscape of mouse papillomavirus (MmuPV1) in the context of active and regressed MmuPV1 lesion tissue
2021-10-12 | GSE160868 | GEO
Project description:To investigate the effecs of commensal papillomavirus immunity on the homeostasis of highly mutated normal skin, spatial transcriptomics (Xenium, 10x Genomics, Pleasanton, CA) was performed on SKH-1 mouse back skin. The mice were treated with mouse papillomavirus (MmuPV1) or virus-like particles (VLP), followed by UV exposure for 25 weeks.
2024-12-11 | GSE276273 | GEO
Project description:The full transcription map of mouse papillomavirus type 1 (MmuPV1)
| PRJNA408300 | ENA
Project description:In humans, α-papillomavirus HPV-2 and γ-papillomavirus HPV-4 typically cause common warts. In rare patients, HPV-2 may cause striking “tree man” manifestations. We describe here a patient with the HPV-2-driven “tree man” phenotype, and two of his distant relatives with unusually severe HPV4-driven warts. Genetic, transcriptional, and histological analyses of the “tree man” lesions showed that they formed a multifocal benign epithelial tumor driven by a specific HPV-2 strain. Surprisingly, all three patients are homozygous for a mutation of an essential splice site in the CD28 gene, which encodes an activating surface receptor on T cells. They have no detectable CD28 on their T cells, which, with the exception of a small contingent of revertant memory CD4+ T cells, do not respond to CD28 stimulation. Their T cells express normal levels of other costimulatory molecules and CTLA-4, and respond to CD2 stimulation. T- and B-cell development, and responses to antigens are otherwise normal in these individuals. Finally, CD28-deficient mice are vulnerable to cutaneous infections with the μ-papillomavirus MmuPV1. This experiment of Nature shows that the control of HPV-2 and HPV-4 in human keratinocytes is dependent on the T-cell CD28 co-activation pathway, which seems to be otherwise largely redundant in host defense.
2021-07-31 | GSE139299 | GEO
Project description:Background. Head and neck squamous cell carcinomas (HNSCCs) represent a heterogeneous group of cancers, for which human papilloma virus (HPV) infection is an emerging risk factor. Previous studies showed promoter hypermethylation in HPV(+) oropharyngeal cancers, but only few consistent target genes have been so far described and the evidence of a functional impact on gene expression is still limited. Methods. We performed global and stratified pooled analyses of epigenome-wide data in HNSCCs based on the Illumina HumanMethylation450 bead-array data in order to identify tissue-specific components and common viral epigenetic targets in HPV-associated tumours . Results. We identified novel differentially methylated CpGs and regions associated with viral infection that are independent of the anatomic site. In particular, most hypomethylated regions were characterized by a marked loss of CpG island boundaries, which showed significant correlations with expression of neighbouring genes. Moreover, a subset of only 5 CpGs in few hypomethylated regions predicted HPV status with a high level of specificity in different cohorts. Finally, this signature was a better predictor of survival compared with HPV status determined by viral gene expression by RNA-Sequencing in the TCGA cohort. Conclusions. We identified a novel epigenetic signature of HPV infection in HNSCCs which is independent of the anatomic site, is functionally correlated with gene expression and may be leveraged for improved stratification of prognosis in HNSCCs.
2017-02-18 | GSE95036 | GEO
Project description:Dysregulation of host gene expression by mouse papillomavirus type 1 (MmuPV1) infection
| PRJNA562919 | ENA
Project description:We perfomed Targeted DNA-seq analysis using MmuPV1 infected mouse warts and uninfected control tissues for MmuPV1 integration analyses
2021-07-14 | GSE163681 | GEO