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Tumour Virus Research Dec 2022Human tumor viruses cause various human cancers that account for at least 15% of the global cancer burden. Among the currently identified human tumor viruses, two are... (Review)
Review
Human tumor viruses cause various human cancers that account for at least 15% of the global cancer burden. Among the currently identified human tumor viruses, two are small DNA tumor viruses: human papillomaviruses (HPVs) and Merkel cell polyomavirus (MCPyV). The study of small DNA tumor viruses (adenoviruses, polyomaviruses, and papillomaviruses) has facilitated several significant biological discoveries and established some of the first animal models of virus-associated cancers. The development and use of preclinical in vivo models to study HPVs and MCPyV and their role in human cancer is the focus of this review. Important considerations in the design of animal models of small DNA tumor virus infection and disease, including host range, cell tropism, choice of virus isolates, and the ability to recapitulate human disease, are presented. The types of infection-based and transgenic model strategies that are used to study HPVs and MCPyV, including their strengths and limitations, are also discussed. An overview of the current models that exist to study HPV and MCPyV infection and neoplastic disease are highlighted. These comparative models provide valuable platforms to study various aspects of virus-associated human disease and will continue to expand knowledge of human tumor viruses and their relationship with their hosts.
Topics: Animals; Humans; Merkel cell polyomavirus; Polyomavirus Infections; Tumor Virus Infections; Neoplasms; Polyomavirus; Oncogenic Viruses
PubMed: 35636683
DOI: 10.1016/j.tvr.2022.200239 -
Molecular & Cellular Proteomics : MCP Apr 2017Oncogenic viruses are responsible for about 15% human cancers. This article explores the promise and challenges of viral proteomics in the study of the oncogenic human... (Review)
Review
Oncogenic viruses are responsible for about 15% human cancers. This article explores the promise and challenges of viral proteomics in the study of the oncogenic human DNA viruses, HPV, McPyV, EBV and KSHV. These viruses have coevolved with their hosts and cause persistent infections. Each virus encodes oncoproteins that manipulate key cellular pathways to promote viral replication and evade the host immune response. Viral proteomics can identify cellular pathways perturbed by viral infection, identify cellular proteins that are crucial for viral persistence and oncogenesis, and identify important diagnostic and therapeutic targets.
Topics: DNA Virus Infections; Host-Pathogen Interactions; Humans; Neoplasms; Oncogene Proteins; Oncogenic Viruses; Proteomics; Viral Proteins; Virus Replication
PubMed: 28104704
DOI: 10.1074/mcp.O116.065201 -
Advances in Virus Research 1972This chapter summarizes the experimental evidence bearing on the nature of virus-erythrocyte reactions characteristic of several taxonomic groups.. Such evidence is... (Review)
Review
This chapter summarizes the experimental evidence bearing on the nature of virus-erythrocyte reactions characteristic of several taxonomic groups.. Such evidence is culled from (1) the study of conditions necessary for hemagglutination; (2) the examination of specific factors affecting either the cell or the virion to enhance, alter, or abolish the reaction; and (3) the direct physicochemical analysis of cells, viruses, and “receptor analogs.” The hemadsorption phenomenon also provides evidence for virus-erythrocyte interactions, which is based on the attachment of erythrocytes to infected cells in culture having hemagglutinin at their surfaces. This phenomenon reflects the interaction between erythrocytes and viral envelope components. The major virus groups that react with erythrocytes include myxoviruses, paramyxoviruses, pseudomyxoviruses, adenoviruses, arboviruses, reoviruses, enteroviruses, and miscellaneous hemagglutinating viruse (rubella virus, coronaviruses, rhabdoviruses, and oncogenic viruses). The agglutination of erythrocytes by the direct action of viral particles was first described in connection with myxoviruses. This led directly to the discovery of viral neuraminidase—a property unique to myxoviruses and paramyxoviruses. A number of viruses unrelated to myxoviruses have since been shown to agglutinate erythrocytes of various species. The visible result of viral hemagglutination is the “pattern” formed at the bottom of a test tube or well plate by lattices of red cells lightly conjoined by viral hemagglutinin. Hemagglutination serves as a useful direct means of titering intact viral particles or hemagglutinating subunits.
Topics: Adenoviridae; Animals; Arboviruses; Butanols; Cell Membrane; Chickens; Enterovirus; Erythrocytes; Haplorhini; Hemadsorption; Hemagglutination; Humans; Oncogenic Viruses; Orthomyxoviridae; Paramyxoviridae; Rats; Reoviridae; Rubella virus; Viruses
PubMed: 4348510
DOI: 10.1016/s0065-3527(08)60746-0 -
International Journal of Molecular... Oct 2017Matricellular proteins differ from other classical extracellular matrix proteins; for instance, they are transiently expressed as soluble proteins rather than being... (Review)
Review
Matricellular proteins differ from other classical extracellular matrix proteins; for instance, they are transiently expressed as soluble proteins rather than being constitutively expressed in pathological conditions, such as acute viral infections. Accumulating studies have revealed that matricellular proteins, including osteopontin and tenascin-C, both of which interact with integrin heterodimers, are involved in inflammatory diseases, autoimmune disorders, and cancers. The concentrations of these matricellular proteins are elevated in the plasma of patients with certain types of cancers, indicating that they play important roles in oncogenesis. Chronic viral infections are associated with certain cancers, which are distinct from non-viral cancers. Viral oncogenes play critical roles in the development and progression of such cancers. It is vital to investigate the mechanisms of tumorigenesis and, particularly, the mechanism by which viral proteins induce tumor progression. Viral proteins have been shown to influence not only the viral-infected cancer cells, but also the stromal cells and matricellular proteins that constitute the extracellular matrix that surrounds tumor tissues. In this review, we summarize the recent progress on the involvement of matricellular proteins in oncogenic virus-induced cancers to elucidate the mechanism of oncogenesis and consider the possible role of matricellular proteins as therapeutic targets in virus-induced cancers.
Topics: Animals; Extracellular Matrix; Humans; Neoplasms; Oncogenic Viruses; Osteopontin; Tenascin; Tumor Virus Infections
PubMed: 29065446
DOI: 10.3390/ijms18102198 -
International Journal of Molecular... May 2023Globally, viral infections substantially contribute to cancer development. Oncogenic viruses are taxonomically heterogeneous and drive cancers using diverse strategies,... (Review)
Review
Globally, viral infections substantially contribute to cancer development. Oncogenic viruses are taxonomically heterogeneous and drive cancers using diverse strategies, including epigenomic dysregulation. Here, we discuss how oncogenic viruses disrupt epigenetic homeostasis to drive cancer and focus on how virally mediated dysregulation of host and viral epigenomes impacts the hallmarks of cancer. To illustrate the relationship between epigenetics and viral life cycles, we describe how epigenetic changes facilitate the human papillomavirus (HPV) life cycle and how changes to this process can spur malignancy. We also highlight the clinical impact of virally mediated epigenetic changes on cancer diagnosis, prognosis, and treatment.
Topics: Humans; Oncogenic Viruses; Epigenome; Neoplasms; Epigenesis, Genetic; Viruses; DNA Methylation
PubMed: 37298494
DOI: 10.3390/ijms24119543 -
Molecular Cancer Therapeutics Jan 2012Oncogenic viruses represent a significant public health burden in light of the multitude of malignancies that result from chronic or spontaneous viral infection and... (Review)
Review
Oncogenic viruses represent a significant public health burden in light of the multitude of malignancies that result from chronic or spontaneous viral infection and transformation. Although many of the molecular signaling pathways that underlie virus-mediated cellular transformation are known, the impact of these viruses on metabolic signaling and phenotype within proliferating tumor cells is less well understood. Whether the interaction of oncogenic viruses with metabolic signaling pathways involves enhanced glucose uptake and glycolysis (both hallmark features of transformed cells) or dysregulation of molecular pathways that regulate oxidative stress, viruses are adept at facilitating tumor expansion. Through their effects on cell proliferation pathways, such as the PI3K and MAPK pathways, the cell cycle regulatory proteins p53 and ATM, and the cell stress response proteins HIF-1α and AMPK, viruses exert control over critical metabolic signaling cascades. Additionally, oncogenic viruses modulate the tumor metabolomic profile through direct and indirect interactions with glucose transporters, such as GLUT1, and specific glycolytic enzymes, including pyruvate kinase, glucose 6-phosphate dehydrogenase, and hexokinase. Through these pathways, oncogenic viruses alter the phenotypic characteristics and energy-use methods of transformed cells; therefore, it may be possible to develop novel antiglycolytic therapies to target these dysregulated pathways in virus-derived malignancies.
Topics: Cell Cycle; Cell Proliferation; Glucose; Glycolysis; Humans; Metabolic Networks and Pathways; Neoplasms; Oncogenic Viruses; Signal Transduction; Stress, Physiological
PubMed: 22234809
DOI: 10.1158/1535-7163.MCT-11-0517 -
FEMS Immunology and Medical Microbiology Dec 1999Patients with AIDS are at risk of lymphoma and Kaposi's sarcoma. These tumours are associated with the gamma herpesviruses, Epstein-Barr virus (EBV) and human... (Review)
Review
Patients with AIDS are at risk of lymphoma and Kaposi's sarcoma. These tumours are associated with the gamma herpesviruses, Epstein-Barr virus (EBV) and human herpesvirus 8 (HHV-8), although a proportion of AIDS lymphomas lacks both viruses. EBV and HHV-8 are latent in the tumour cells, with genes that play a direct role in driving cell proliferation. Human immunodeficiency virus, in contrast, while being the greatest risk factor for lymphoma and Kaposi's sarcoma, acts indirectly, mainly by causing immune suppression, as immunosuppressed transplant patients are at risk for the same types of tumour.
Topics: Acquired Immunodeficiency Syndrome; Animals; Humans; Male; Neoplasms; Oncogenic Viruses; Virus Diseases
PubMed: 10575133
DOI: 10.1111/j.1574-695X.1999.tb01393.x -
Frontiers in Cellular and Infection... 2021Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are two oncogenic human γ-herpesviruses that are each associated with 1-2% of human tumors.... (Review)
Review
Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are two oncogenic human γ-herpesviruses that are each associated with 1-2% of human tumors. They encode bona fide oncogenes that they express during latent infection to amplify their host cells and themselves within these. In contrast, lytic virus particle producing infection has been considered to destroy host cells and might be even induced to therapeutically eliminate EBV and KSHV associated tumors. However, it has become apparent in recent years that early lytic replication supports tumorigenesis by these two human oncogenic viruses. This review will discuss the evidence for this paradigm change and how lytic gene products might condition the microenvironment to facilitate EBV and KSHV associated tumorigenesis.
Topics: Epstein-Barr Virus Infections; Herpesvirus 4, Human; Herpesvirus 8, Human; Humans; Oncogenes; Virus Replication
PubMed: 33842383
DOI: 10.3389/fcimb.2021.605258 -
International Journal of Molecular... Aug 2021The tumor viruses human T-lymphotropic virus 1 (HTLV-1), hepatitis C virus (HCV), Merkel cell polyomavirus (MCPyV), high-risk human papillomaviruses (HR-HPVs),... (Review)
Review
The tumor viruses human T-lymphotropic virus 1 (HTLV-1), hepatitis C virus (HCV), Merkel cell polyomavirus (MCPyV), high-risk human papillomaviruses (HR-HPVs), Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpes virus (KSHV) and hepatitis B virus (HBV) account for approximately 15% of all human cancers. Although the oncoproteins of these tumor viruses display no sequence similarity to one another, they use the same mechanisms to convey cancer hallmarks on the infected cell. Perturbed gene expression is one of the underlying mechanisms to induce cancer hallmarks. Epigenetic processes, including DNA methylation, histone modification and chromatin remodeling, microRNA, long noncoding RNA, and circular RNA affect gene expression without introducing changes in the DNA sequence. Increasing evidence demonstrates that oncoviruses cause epigenetic modifications, which play a pivotal role in carcinogenesis. In this review, recent advances in the role of host cell epigenetic changes in virus-induced cancers are summarized.
Topics: Animals; DNA Methylation; Epigenomics; Humans; Neoplasms; Oncogenic Viruses; Tumor Virus Infections
PubMed: 34361112
DOI: 10.3390/ijms22158346 -
PLoS Pathogens Jan 2017
Review
Topics: Host-Pathogen Interactions; Humans; Neoplasms; Oncogenic Viruses; Symbiosis; Tumor Virus Infections
PubMed: 28103305
DOI: 10.1371/journal.ppat.1006078