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Biological Chemistry Jul 2017JC polyomavirus (JCPyV) is the causative agent of a fatal central nervous system demyelinating disease known as progressive multifocal leukoencephalopathy (PML). PML... (Review)
Review
JC polyomavirus (JCPyV) is the causative agent of a fatal central nervous system demyelinating disease known as progressive multifocal leukoencephalopathy (PML). PML occurs in people with underlying immunodeficiency or in individuals being treated with potent immunomodulatory therapies. JCPyV is a DNA tumor virus with a double-stranded DNA genome and encodes a well-studied oncogene, large T antigen. Its host range is highly restricted to humans and only a few cell types support lytic infection in vivo or in vitro. Its oncogenic potential in humans has not been firmly established and the international committee on oncogenic viruses lists JCPyV as possibly carcinogenic. Significant progress has been made in understanding the biology of JCPyV and here we present an overview of the field and discuss some important questions that remain unanswered.
Topics: Animals; Genomics; Humans; JC Virus; Polyomavirus Infections; Transcription, Genetic; Viral Proteins; Virus Physiological Phenomena
PubMed: 28493815
DOI: 10.1515/hsz-2016-0345 -
Clinical Microbiology and Infection :... Nov 2015Several viruses with different replication mechanisms contribute to oncogenesis by both direct and indirect mechanisms in immunosuppressed subjects after solid organ... (Review)
Review
Several viruses with different replication mechanisms contribute to oncogenesis by both direct and indirect mechanisms in immunosuppressed subjects after solid organ transplantation, after allogeneic stem cell transplantation, or with human immunodeficiency virus (HIV) infection. Epstein-Barr virus (EBV), human papillomavirus (HPV), Kaposi sarcoma herpesvirus (KSHV), human T-cell lymphotropic virus type 1 (HTLV-1) and Merkel cell polyoma virus (MCV) are the main viruses associated with the development of cancer in immunosuppressed patients. Besides being a main cause of immunodeficiency, HIV1 has a direct pro-oncogenic effect. In this review, we provide an update on the association between the condition of acquired immunodeficiency and cancer risk, specifically addressing the contributions to oncogenesis of HPV, MCV, KSHV, HTLV-1, and EBV.
Topics: Carcinogenesis; Humans; Immunocompromised Host; Neoplasms; Oncogenic Viruses; Virus Diseases
PubMed: 26197213
DOI: 10.1016/j.cmi.2015.07.009 -
International Journal of Molecular... Jun 2018Human papilloma viruses (HPVs) are a group of double-stranded DNA viruses known to be the primary cause of cervical cancer. In addition, evidence has now established... (Review)
Review
Human papilloma viruses (HPVs) are a group of double-stranded DNA viruses known to be the primary cause of cervical cancer. In addition, evidence has now established their role in non-melanoma skin cancers, head and neck cancer (HNC), and the development of other anogenital malignancies. The prevalence of HPV-related HNC, in particular oropharyngeal cancers, is rapidly increasing, foreseeing that HPV-positive oropharyngeal cancers will outnumber uterine cervical cancers in the next 15⁻20 years. Therefore, despite the successful advent of vaccines originally licensed for cervical cancer prevention, HPV burden is still very high, and a better understanding of HPV biology is urgently needed. Autophagy is the physiological cellular route that accounts for removal, degradation, and recycling of damaged organelles, proteins, and lipids in lysosomal vacuoles. In addition to this scavenger function, autophagy plays a fundamental role during viral infections and cancers and is, therefore, frequently exploited by viruses to their own benefit. Recently, a link between HPV and autophagy has clearly emerged, leading to the conceivable development of novel anti-viral strategies aimed at restraining HPV infectivity. Here, recent findings on how oncogenic HPV16 usurp autophagy are described, highlighting similarities and differences with mechanisms adopted by other oncoviruses.
Topics: Autophagy; Female; Host-Pathogen Interactions; Humans; Papillomaviridae; Uterine Cervical Neoplasms
PubMed: 29914057
DOI: 10.3390/ijms19061775 -
Cold Spring Harbor Perspectives in... Jun 2021Early studies of transmissible tumors in chickens provided evidence that viruses such as avian leukosis virus (ALV) and Rous sarcoma virus (RSV) can cause cancer in... (Review)
Review
Early studies of transmissible tumors in chickens provided evidence that viruses such as avian leukosis virus (ALV) and Rous sarcoma virus (RSV) can cause cancer in these animals. Doubts about the relevance to human tumors and failures to replicate some early work meant the field of tumor virology followed a bumpy course. Nevertheless, viruses that can cause cancers in rodents and humans were ultimately identified, and several Nobel prizes were awarded for work in this area. In this excerpt from his forthcoming book on the history of cancer research, Joe Lipsick looks back at the early history of tumor virus research, from some of the early false starts and debates, to discovery of reverse transcriptase, and identification of human papilloma virus (HPV) as the major cause of cervical cancer.
Topics: Animals; History, 20th Century; Humans; Neoplasms; Oncogenic Viruses; Proviruses; Virology
PubMed: 34074674
DOI: 10.1101/cshperspect.a035774 -
Journal of Cellular Physiology May 2018Gastrointestinal cancers are a global public health problem, which represent a vast majority of all cancer-caused deaths in both men and women. On the other hand, viral... (Review)
Review
Gastrointestinal cancers are a global public health problem, which represent a vast majority of all cancer-caused deaths in both men and women. On the other hand, viral pathogens have been long implicated as etiological factors in the onset of certain human cancers, including gastrointestinal tumors. In this regard, Human Papilloma Virus (HPV), Epstein-Barr Virus (EBV), and John Cunningham Virus (JCV) have been more strongly suggested to be involved in gastrointestinal carcinogenesis; so that, the association of HPV with oropharyngeal and anal cancers and also the association of EBV with gastric cancer have been etiologically confirmed by epidemiological and experimental investigations. Although, the association of other viruses is less evident, but may rely on co-factors for their oncogenic roles. Therefore, to improve the prevention and treatment of these classes of cancer, their association with viral agents as potential risk factors should be investigated with care. In this respect, the present review has focused on the existing literature on the subject of viral involvement in gastrointestinal tumorgenesis, by covering and discussing various gastrointestinal cancers, corresponding viral agents and their oncogenic aspects and then summarizing evidences either supporting or rejecting a causal role of these pathogens in gastrointestinal malignancies.
Topics: Carcinogenesis; Gastrointestinal Neoplasms; Herpesvirus 4, Human; Humans; JC Virus; Papillomaviridae
PubMed: 28926109
DOI: 10.1002/jcp.26194 -
Philosophical Transactions of the Royal... Oct 2017Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune... (Review)
Review
Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune response. PRRs are localized to several different cellular compartments and are stimulated by viral proteins and nucleic acids. PRR activation initiates signal transduction events that ultimately result in an inflammatory response. Human tumour viruses, which include Kaposi's sarcoma-associated herpesvirus, Epstein-Barr virus, human papillomavirus, hepatitis C virus, hepatitis B virus, human T-cell lymphotropic virus type 1 and Merkel cell polyomavirus, are detected by several different PRRs. These viruses engage in a variety of mechanisms to evade the innate immune response, including downregulating PRRs, inhibiting PRR signalling, and disrupting the activation of transcription factors critical for mediating the inflammatory response, among others. This review will describe tumour virus PAMPs and the PRRs responsible for detecting viral infection, PRR signalling pathways, and the mechanisms by which tumour viruses evade the host innate immune system.This article is part of the themed issue 'Human oncogenic viruses'.
Topics: Humans; Immunity, Innate; Oncogenic Viruses; Pathogen-Associated Molecular Pattern Molecules; Receptors, Pattern Recognition; Signal Transduction; Tumor Virus Infections
PubMed: 28893934
DOI: 10.1098/rstb.2016.0267 -
Seminars in Oncology Apr 2015The known human tumor viruses include the DNA viruses Epstein-Barr virus (EBV), Kaposi sarcoma herpesvirus (KSHV), Merkel cell polyomavirus (MCPyV), human papillomavirus... (Review)
Review
The known human tumor viruses include the DNA viruses Epstein-Barr virus (EBV), Kaposi sarcoma herpesvirus (KSHV), Merkel cell polyomavirus (MCPyV), human papillomavirus (HPV), and hepatitis B virus (BV). RNA tumor viruses include human T-cell lymphotrophic virus type 1 (HTLV-1) and hepatitis C virus (HCV). The serological identification of antigens/antibodies in serum is a rapidly progressing field with utility for both scientists and clinicians. Serology is useful for conducting seroepidemiology studies and to inform on the pathogenesis and host immune response to a particular viral agent. Clinically, serology is useful for diagnosing current or past infection and for aiding in clinical management decisions. Serology is useful for screening blood donations for infectious agents and for monitoring the outcome of vaccination against these viruses. Serodiagnosis of human tumor viruses has improved in recent years with increased specificity and sensitivity of the assays, as well as reductions in cost and the ability to assess multiple antibody/antigens in single assays. Serodiagnosis of tumor viruses plays an important role in our understanding of the prevalence and transmission of these viruses and ultimately in the ability to develop treatments/preventions for these globally important diseases.
Topics: Antibodies, Viral; Humans; Neoplasms; Oncogenic Viruses; Serologic Tests
PubMed: 25843726
DOI: 10.1053/j.seminoncol.2014.12.024 -
Reviews in Medical Virology Nov 2019Seven oncogenic viruses are known for tumorigenesis and contribute to 12% of all human cancers. The oncogenic factors, the target tissue, and pathology of cancer vary... (Review)
Review
Seven oncogenic viruses are known for tumorigenesis and contribute to 12% of all human cancers. The oncogenic factors, the target tissue, and pathology of cancer vary among these viruses with several mechanisms proposed for the initiation and development of cancer. Aneuploidy in cells is associated with anomalies in chromosome number that can be a hallmark of cancer, a disease defined by expanded proliferative potential. In this review, we summarize the different mechanisms of aneuploidy and furthermore discuss recent findings of the role of viral oncoproteins in inducing cellular aneuploidy that might facilitate tumorigenesis. Improved understanding of viral oncogenesis may help to find new strategies for controlling virus-associated cancers.
Topics: Aneuploidy; Animals; Cell Transformation, Viral; Humans; Neoplasms; Oncogenic Viruses; Tumor Virus Infections
PubMed: 31407416
DOI: 10.1002/rmv.2076 -
Pharmacological Research Aug 2021Chemoresistance is often referred to as a major leading reason for cancer therapy failure, causing cancer relapse and further metastasis. As a result, an urgent need has... (Review)
Review
Chemoresistance is often referred to as a major leading reason for cancer therapy failure, causing cancer relapse and further metastasis. As a result, an urgent need has been raised to reach a full comprehension of chemoresistance-associated molecular pathways, thereby designing new therapy methods. Many of metastatic tumor masses are found to be related with a viral cause. Although combined therapy is perceived as the model role therapy in such cases, chemoresistant features, which is more common in viral carcinogenesis, often get into way of this kind of therapy, minimizing the chance of survival. Some investigations indicate that the infecting virus dominates other leading factors, i.e., genetic alternations and tumor microenvironment, in development of cancer cell chemoresistance. Herein, we have gathered the available evidence on the mechanisms under which oncogenic viruses cause drug-resistance in chemotherapy.
Topics: Animals; Antineoplastic Agents; Cell Transformation, Viral; Drug Resistance, Viral; Gene Expression Regulation, Neoplastic; Host-Pathogen Interactions; Humans; Neoplasms; Oncogenic Viruses; Signal Transduction; Tumor Microenvironment
PubMed: 34119621
DOI: 10.1016/j.phrs.2021.105730 -
Infection, Genetics and Evolution :... Apr 2020Polyomaviruses (PyVs) are small DNA viruses that infect several species, including mammals, birds and fishes. Their study gained momentum after the report of previously... (Review)
Review
Polyomaviruses (PyVs) are small DNA viruses that infect several species, including mammals, birds and fishes. Their study gained momentum after the report of previously unidentified viral species in the past decade, and especially, since the description of the first polyomavirus clearly oncogenic for humans. The aim of this work was to review the most relevant aspects of the evolution and molecular epidemiology of polyomaviruses, allowing to reveal general evolutionary patterns and to identify some unaddressed issues and future challenges. The main points analysed included: 1) the species and genera assignation criteria; 2) the hypotheses, mechanisms and timescale of the ancient and recent evolutionary history of polyomaviruses; and 3) the molecular epidemiology of human viruses, with special attention to JC, BK and Merkel cell polyomaviruses.
Topics: Animals; Evolution, Molecular; Humans; Phylogeny; Polyomavirus; Polyomavirus Infections; Tumor Virus Infections
PubMed: 31870972
DOI: 10.1016/j.meegid.2019.104150