"The development of an advanced immune system to fight off microbial pathogens is a considerable part of the evolutionary success of multicellular organisms. Yet, like most success stories there is always a flip side. New evidence from investigators at the University of Colorado (CU) Cancer Center shows how the action of various immunity-based enzymes can spill over onto the host genome when trying to fight off various viral pathogens—ultimately leading to cancer-causing DNA mutations. Findings from the new study were published recently in Viruses, in an article entitled “Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression.”"
Showing posts with label papillomavirus. Show all posts
Showing posts with label papillomavirus. Show all posts
Our own treacherous immune genes can cause cancer after viral infection - Medical News Today
HPV (human papillomavirus) infection is widely known to induce cancer.
Many of the mutations that cause this virally-induced cancer are caused
by a family of genes that normally combats viral infections, finds new
UCL research.
This raises the possibility of developing drugs to regulate the activity
of these genes to prevent HPV-associated cancers from developing and
reduce the ability of existing cancers to evolve resistance to
treatments.
The research, published in Cell Reports, shows for the first
time that genes from the 'APOBEC' family, which help to fight off viral
infection, actually cause mutations that lead to HPV-associated cancer.
This research was funded by the Rosetrees Trust, a charity dedicated to
supporting pioneering medical research, with additional funding from the
Debbie Fund and Cancer Research UK.
From:-
APOBEC-Mediated Cytosine Deamination Links PIK3CA Helical Domain Mutations to Human Papillomavirus-Driven Tumor Development
Many of the mutations that cause this virally-induced cancer are caused
by a family of genes that normally combats viral infections, finds new
UCL research.
This raises the possibility of developing drugs to regulate the activity
of these genes to prevent HPV-associated cancers from developing and
reduce the ability of existing cancers to evolve resistance to
treatments.
The research, published in Cell Reports, shows for the first
time that genes from the 'APOBEC' family, which help to fight off viral
infection, actually cause mutations that lead to HPV-associated cancer.
This research was funded by the Rosetrees Trust, a charity dedicated to
supporting pioneering medical research, with additional funding from the
Debbie Fund and Cancer Research UK.
From:-
APOBEC-Mediated Cytosine Deamination Links PIK3CA Helical Domain Mutations to Human Papillomavirus-Driven Tumor Development
microRNAs are biomarkers of oncogenic human papillomavirus infections
Cellular and viral microRNAs (miRNAs) are the transcriptional products of RNA polymerase II and are regulated by transcriptional factors for their differential expression. The altered expression of miRNAs in many cancer types has been explored as a marker for possible diagnosis and therapy. We report in this study that oncogenic human papillomaviruses (HPVs) induce aberrant expression of many cellular miRNAs and that HPV18 infection produces no detectable viral miRNA. Thirteen abundant host miRNAs were specifically regulated by HPV16 and HPV18 in organotypic raft cultures of foreskin and vaginal keratinocytes as determined by miRNA array in combination with small RNA sequencing. The increase of miR-16, miR-25, miR-92a, and miR-378 and the decrease of miR-22, miR-27a, miR-29a, and miR-100 could be attributed to viral oncoprotein E6, E7, or both, all of which are known to target many cellular transcription factors. The examination of 158 cervical specimens, including 38 normal, 52 cervical intraepithelial neoplasia (CIN), and 68 cervical cancer (CC) tissues, for the expression of these eight miRNAs showed a remarkable increase of miR-25, miR-92a, and miR-378 with lesion progression but no obvious change of miR-22, miR-29a, and miR-100 among the HPV-infected tissues. Further analyses indicate that an expression ratio ≥1.5 of miR-25/92a group over miR-22/29a group could serve as a cutoff value to distinguish normal cervix from CIN and from CIN to CC.
Integrated virus-host methylome analysis in head and neck squamous cell carcinoma.
One in six cancers worldwide is caused by infection and human papillomavirus (HPV) is one of the main culprits. To better understand the dynamics of HPV integration and its effect on both the viral and host methylomes, we conducted whole-genome DNA methylation analysis using MeDIP-seq of HPV+ and HPV- head and neck squamous cell carcinoma (HNSCC). We determined the viral subtype to be HPV-16 in all cases and show that HPV-16 integrates into the host genome at multiple random sites and that this process predominantly involves the transcriptional repressor gene (E2) in the viral genome. Comparative analysis identified 453 (FDR ≤ 0.01) differentially methylated regions (DMRs) in the HPV+ host methylome. Bioinformatics characterization of these DMRs confirmed the previously reported cadherin genes to be affected but also revealed new targets for HPV-mediated methylation changes at regions not covered by array-based platforms, including the recently identified super-enhancers.
Genome-wide siRNA screen identifies the retromer as a cellular entry factor for human papillomavirus
Despite major advances in our understanding of many aspects of human papillomavirus (HPV) biology, HPV entry is poorly understood. To identify cellular genes required for HPV entry, we conducted a genome-wide screen for siRNAs that inhibited infection of HeLa cells by HPV16 pseudovirus. Many retrograde transport factors were required for efficient infection, including multiple subunits of the retromer, which initiates retrograde transport from the endosome to the trans-Golgi network (TGN). The retromer has not been previously implicated in virus entry. Furthermore, HPV16 capsid proteins arrive in the TGN/Golgi in a retromer-dependent fashion during entry, and incoming HPV proteins form a stable complex with retromer subunits. We propose that HPV16 directly engages the retromer at the early or late endosome and traffics to the TGN/Golgi via the retrograde pathway during cell entry. These results provide important insights into HPV entry, identify numerous potential antiviral targets, and suggest that the role of the retromer in infection by other viruses should be assessed.
Some types of papilloma virus might prevent cervical cancer
Certain types of papilloma virus might actually prevent cervical cancer, according to a new study by researchers from The University of Manchester.
Scientists find cancer-causing virus in the brain, potential connection to epilepsy
Researchers at Shriner's Hospital Pediatric Research Center at the Temple University School of Medicine, and the University of Pennsylvania have evidence linking the human papillomavirus 16 (HPV16) – the most common cause of cervical cancer – to a common form of childhood epilepsy. They have shown for the first time that HPV16 may be present in the human brain, and found that when they added a viral protein to the brains of fetal mice, the mice all demonstrated the same developmental problems in the cerebral cortex associated with this type of epilepsy, called focal cortical dysplasia type IIB (FCDIIB). The findings suggest that the virus could play a role in the development of epilepsy.
Read more at: http://medicalxpress.com/news/2013-01-scientists-cancer-causing-virus-brain-potential.html#jCp
Read more at: http://medicalxpress.com/news/2013-01-scientists-cancer-causing-virus-brain-potential.html#jCp
Two viruses link to prostate cancer: High-risk human papilloma virus found with Epstein Barr virus
Two common viruses known to be associated with human cancers are both present -- and may even be collaborating with each other -- in most male prostate cancers, a new study suggests. The human papilloma virus (HPV) and Epstein Barr virus (EBV) were present in more than half of the malignant cancers, as well as in a high proportion of benign and normal prostate samples.
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