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Viral Immunology Mar 2017Nucleic acid recognition by toll-like receptor 9 (TLR9) initiates signaling pathways that regulate the production of proinflammatory cytokines or type I interferons, as... (Review)
Review
Nucleic acid recognition by toll-like receptor 9 (TLR9) initiates signaling pathways that regulate the production of proinflammatory cytokines or type I interferons, as well as many other molecules required to initialize the immune response. The use of synthetic oligodeoxynucleotides (ODNs) has been crucial to emulate the recognition of DNA sequences by TLR9. Furthermore, ODN administration to mice has shown to confer protection against a wide range of viral, bacterial, and parasitic pathogens. In contrast, oncogenic DNA viruses like hepatitis B virus, Epstein-Barr virus, and human papilloma virus inhibit TLR9 expression, thus contributing to the establishment of chronic viral infections. In this review, we will focus on TLR9 signals initiated by ODN recognition, on the inhibition of TLR9 expression mediated by DNA oncogenic viruses, and on TLR9 expression as a relevant event in the progression to cancer, considering other functions of this receptor, aside from viral recognition.
Topics: Animals; Carcinogenesis; Host-Pathogen Interactions; Humans; Neoplasms; Oncogenic Viruses; Toll-Like Receptor 9
PubMed: 28151089
DOI: 10.1089/vim.2016.0103 -
Med (New York, N.Y.) Jun 2023The majority of oncogenic viruses are capable of integrating into the host genome, posing significant challenges to clinical control. Recent conceptual and technological...
The majority of oncogenic viruses are capable of integrating into the host genome, posing significant challenges to clinical control. Recent conceptual and technological advances, however, offer promising clinical applications. Here, we summarize the advances in our understanding of oncogenic viral integration, their clinical relevance, and the future perspectives.
Topics: Oncogenic Viruses; Genome; Virus Integration
PubMed: 37301195
DOI: 10.1016/j.medj.2023.04.007 -
Cancer Letters Apr 2011Cell fusion is fundamental to the development and physiology of multicellular organisms, such as fertilization, placentation, development of skeletal muscle and bone.... (Review)
Review
Cell fusion is fundamental to the development and physiology of multicellular organisms, such as fertilization, placentation, development of skeletal muscle and bone. Oncogenic virus-mediated cell fusion, however, may lead to chromosomal instability (CIN) by various mechanisms when tumor suppressor p53 is deregulated and produce oncogenic aneuploid cells. It is worth noting that all human oncogenic viruses, including human papillomavirus (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), human herpesviruses-8/Kaposi sarcoma herpesvirus (HHV-8/KSHV) and human T-cell lymphotropic virus type 1 (HTLV-1), are capable of both inducing cell fusion and inhibiting the functions of p53 as well as pRb. Although it is now not clear whether a link between virus-mediated cell fusion and cancer established in experimental systems also exists in humans, the fact that the observation of tetraploid cells is more frequent in virus-positive than virus-negative premalignant lesions supports this link. Additionally, there are now no available vaccines against most oncogenic viruses except for HBV and HPV. Given these, developing fusion inhibitors is beneficial to cancer prevention and therapy of virus-associated cancers via inhibiting virus entry, spread and oncogenic role.
Topics: Animals; Cell Fusion; Disease Progression; Humans; Neoplasms; Oncogenic Viruses
PubMed: 21306823
DOI: 10.1016/j.canlet.2010.12.021 -
Microbial Pathogenesis Oct 2023Cancer is a serious public health problem globally. Many human cancers are induced by viruses. Understanding of the mechanisms by which oncogenic (tumorigenic) viruses... (Review)
Review
Cancer is a serious public health problem globally. Many human cancers are induced by viruses. Understanding of the mechanisms by which oncogenic (tumorigenic) viruses induce cancer is essential in the prevention and control of cancer. This review covers comprehensive characteristics and molecular mechanisms of the main virus-attributed cancers caused by human papillomavirus, hepatitis B virus, hepatitis C virus, Epstein-Barr virus, human herpesvirus type 8, human T-cell lymphotropic virus, human polyomaviruses, Merkel cell polyomavirus, and HIV. Oncogenic viruses employ biological processes to replicate and avoid detection by host cell immune systems. Tumorigenic infectious agents activate oncogenes in a variety of ways, allowing the pathogen to block host tumour suppressor proteins, inhibit apoptosis, enhance cell proliferation, and promote invasion of host cells. Furthermore, this review assesses many pathways of viruses linked to cancer, including host cellular communication perturbation, DNA damage mechanisms, immunity, and microRNA targets that promote the beginning and progression of cancer. The current cancer prevention is primarily focused on non-communicable diseases, but infection-attributable cancer also needs attention to significantly reduce the rising cancer burden and related deaths.
Topics: Humans; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Neoplasms; Oncogenic Viruses; Hepacivirus
PubMed: 37557930
DOI: 10.1016/j.micpath.2023.106292 -
Progress in Experimental Tumor Research 1964
Review
Topics: Animals; Antigens; Cricetinae; DNA; DNA, Viral; Guinea Pigs; Haplorhini; Mice; Neoplasms; Neoplasms, Experimental; Oncogenic Viruses; Rabbits; Rats; Simian virus 40; Tissue Culture Techniques; Virus Cultivation
PubMed: 14150246
DOI: 10.1159/000385971 -
Journal of Virological Methods Dec 2014Avian oncogenic viruses include the avian leukosis virus (ALV), reticuloendotheliosis virus (REV) and Marek's disease virus (MDV). Multiple oncogenic viral infections...
Avian oncogenic viruses include the avian leukosis virus (ALV), reticuloendotheliosis virus (REV) and Marek's disease virus (MDV). Multiple oncogenic viral infections are frequently seen, with even Marek's disease vaccines reported to be contaminated with ALV and REV. The gross lesions caused by avian oncogenic viruses often overlap, making differentiation diagnosis based on histopathology difficult. The objective of this study is to develop a rapid approach to simultaneously differentiate, subgroup and pathotype the avian oncogenic viruses. The oligonucleotide microarray was employed in this study. Particular DNA sequences were recognized using specific hybridization between the DNA target and probe on the microarray, followed with colorimetric development through enzyme reaction. With 10 designed probes, ALV-A, ALV-E, ALV-J, REV, MDV pathogenic and vaccine strains were clearly discriminated on the microarray with the naked eyes. The detection limit was 27 copy numbers, which was 10-100 times lower than multiplex PCR. Of 102 field samples screened using the oligonucleotide microarray, 32 samples were positive for ALV-E, 17 samples were positive for ALV-J, 6 samples were positive for REV, 4 samples were positive for MDV, 7 samples were positive for both ALV-A and ALV-E, 5 samples were positive for ALV-A, ALV-E and ALV-J, one sample was positive for both ALV-J and MDV, and 3 samples were positive for both REV and MDV. The oligonucleotide microarray, an easy-to-use, high-specificity, high-sensitivity and extendable assay, presents a potent technique for rapid differential diagnosis of avian oncogenic viruses and the detection of multiple avian oncogenic viral infections under field conditions.
Topics: Animals; Avian Leukosis; Avian Leukosis Virus; Chickens; Diagnosis, Differential; Limit of Detection; Mardivirus; Marek Disease; Multiplex Polymerase Chain Reaction; Oligonucleotide Array Sequence Analysis; Oncogenic Viruses; Poultry Diseases; Reticuloendotheliosis virus; Time Factors; Tumor Virus Infections
PubMed: 25286179
DOI: 10.1016/j.jviromet.2014.09.019 -
Emerging Infectious Diseases May 2014
Topics: Cell Transformation, Viral; History, 20th Century; Humans; Oncogenic Viruses; Research
PubMed: 24751102
DOI: 10.3201/eid2005.131876 -
The Journal of Pathology Sep 1981
Review
Topics: Adenoviridae; Animals; Avian Sarcoma Viruses; Cats; Cattle; Cell Transformation, Neoplastic; Cell Transformation, Viral; Cricetinae; DNA Replication; DNA, Viral; Dogs; Guinea Pigs; Haplorhini; Herpesviridae; Herpesvirus 4, Human; Humans; Mice; Neoplasms; Oncogenic Viruses; Papillomaviridae; Polyomaviridae; Rabbits; Rats; Retroviridae; Virus Replication
PubMed: 6271940
DOI: 10.1002/path.1711350105 -
Advances in Cancer Research 1969
Review
Topics: Adenoviridae; Animals; Avian Sarcoma Viruses; Cell Transformation, Neoplastic; Cricetinae; DNA Viruses; Haplorhini; Helper Viruses; Humans; Hybridization, Genetic; Mice; Neoplasm Transplantation; Oncogenic Viruses; Polyomavirus; RNA Viruses; Rats; Sarcoma, Experimental; Simian virus 40; Virus Replication
PubMed: 4310052
DOI: 10.1016/s0065-230x(08)60330-9 -
Current Opinion in Immunology Oct 2021Oncoviruses are viruses that can cause tumors. Seven viruses are currently recognized as oncogenic in humans: Epstein Barr virus (EBV), Kaposi sarcoma-associated... (Review)
Review
Oncoviruses are viruses that can cause tumors. Seven viruses are currently recognized as oncogenic in humans: Epstein Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV, also known as HHV8), human papillomaviruses (HPVs), hepatitis B virus (HBV), hepatitis C virus (HCV), human T-lymphotropic virus-1 (HTLV-1), and Merkel cell polyomavirus (MCPyV). The clinical phenotypes resulting from infection with these oncoviruses range from asymptomatic infection to invasive cancers. Patients with inborn errors of immunity (IEI) are prone to the development of infectious diseases caused by a narrow or broad spectrum of pathogens, including oncoviruses in some cases. Studies of patients with IEI have deepened our understanding of the non-redundant mechanisms underlying the control of EBV, HHV8 and HPV infections. The human genetic factors conferring predisposition to oncogenic HBV, HCV, HTLV-1 and MCPyV manifestations remain elusive. We briefly review here what is currently known about the IEI conferring predisposition to severe infection with oncoviruses.
Topics: Autoimmunity; Biomarkers; Genetic Predisposition to Disease; Genetic Variation; Host-Pathogen Interactions; Humans; Immunity; Mutation; Oncogenic Viruses; Phenotype; Species Specificity; Tumor Virus Infections
PubMed: 34364035
DOI: 10.1016/j.coi.2021.06.017