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Nature Reviews. Microbiology Nov 2018Viral infection is a major contributor to the global cancer burden. Recent advances have revealed that seven known oncogenic viruses promote tumorigenesis through shared... (Review)
Review
Viral infection is a major contributor to the global cancer burden. Recent advances have revealed that seven known oncogenic viruses promote tumorigenesis through shared host cell targets and pathways. A comprehensive understanding of the principles of viral oncogenesis may enable the identification of unknown infectious aetiologies of cancer and the development of therapeutic or preventive strategies for virus-associated cancers. In this Review, we discuss the molecular mechanisms of viral oncogenesis in humans. We highlight recent advances in understanding how viral manipulation of host cellular signalling, DNA damage responses, immunity and microRNA targets promotes the initiation and development of cancer.
Topics: Carcinogenesis; DNA Damage; Host-Pathogen Interactions; Humans; Immunity; MicroRNAs; Neoplasms; Oncogenic Viruses; Signal Transduction; Tumor Virus Infections
PubMed: 30143749
DOI: 10.1038/s41579-018-0064-6 -
Recent Results in Cancer Research.... 2021Approximately, 1.4 million virus-induced cancers occur annually, representing roughly 10% of the worldwide cancer burden, with the majority (> 85%) occurring in the...
Approximately, 1.4 million virus-induced cancers occur annually, representing roughly 10% of the worldwide cancer burden, with the majority (> 85%) occurring in the lower- and middle-income countries. The viruses associated with the greatest number of cancer cases are human papillomaviruses (HPVs), which cause cervical cancer and several other epithelial malignancies, and hepatitis viruses HBV and HCV, which are responsible for the majority of hepatocellular cancer. Other oncoviruses include Epstein-Barr virus (EBV), Kaposi's sarcoma herpesvirus (KSHV), human T-cell leukemia virus (HTLV-I), and Merkel cell polyoma virus (MCPyV). These oncoviruses include various classes of DNA and RNA viruses and induce cancer by a variety of mechanisms. However, cancers develop in a minority of infected individuals and almost always after chronic infection of many year's duration. Identification of the oncoviruses has provided critical insights in human carcinogenesis and led to several interventions that may reduce the risk of developing the tumors they induce. These interventions include preventive vaccines against HBV and HPV, screening for persistent HPV and HCV infections, antivirals for the treatment of chronic HBV and HCV infection, and screening the blood supply for the presence of HBV and HCV. Further efforts to identify additional oncogenic viruses in human cancers and new insights into etiology and pathogenesis of virally induced cancers would likely lead to new approaches for prophylactic and therapeutic interventions.
Topics: Carcinogenesis; Carcinoma, Hepatocellular; Herpesvirus 4, Human; Humans; Neoplasms; Oncogenic Viruses; Virus Diseases
PubMed: 33200359
DOI: 10.1007/978-3-030-57362-1_1 -
International Journal of Molecular... Jan 2023Despite recent advances in oncology, cancer has remained an enormous global health burden, accounting for about 10 million deaths in 2020. A third of the cancer cases in... (Review)
Review
Despite recent advances in oncology, cancer has remained an enormous global health burden, accounting for about 10 million deaths in 2020. A third of the cancer cases in developing counties are caused by microbial infections such as human papillomavirus (HPV), Epstein-Barr Virus (EBV), and hepatitis B and C viruses. EBV, a member of the human gamma herpesvirus family, is a double-stranded DNA virus and the primary cause of infectious mononucleosis. Most EBV infections cause no long-term complications. However, it was reported that EBV infection is responsible for around 200,000 malignancies worldwide every year. Currently, there are no vaccines or antiviral drugs for the prophylaxis or treatment of EBV infection. Recently, the gut microbiota has been investigated for its pivotal roles in pathogen protection and regulating metabolic, endocrine, and immune functions. Several studies have investigated the efficacy of antiviral agents, gut microbial metabolites, and natural products against EBV infection. In this review, we aim to summarise and analyse the reported molecular mechanistic and clinical studies on the activities of gut microbial metabolites and natural medicines against carcinogenic viruses, with a particular emphasis on EBV. Gut microbial metabolites such as short-chain fatty acids were reported to activate the EBV lytic cycle, while bacteriocins, produced by strains, have shown antiviral properties. Furthermore, several natural products and dietary bioactive compounds, such as curcumin, epigallocatechin gallate, resveratrol, moronic acid, and andrographolide, have shown antiviral activity against EBV. In this review, we proposed several exciting future directions for research on carcinogenic viruses.
Topics: Humans; Herpesvirus 4, Human; Epstein-Barr Virus Infections; Gastrointestinal Microbiome; Carcinogens; Neoplasms; Antiviral Agents; Carcinogenesis
PubMed: 36675232
DOI: 10.3390/ijms24021716 -
Cancer Treatment and Research 2019Malignancies were one of the earliest recognized manifestations that led to the description of the acquired immune deficiency syndrome (AIDS). The majority of cancers... (Review)
Review
Malignancies were one of the earliest recognized manifestations that led to the description of the acquired immune deficiency syndrome (AIDS). The majority of cancers in AIDS patients are associated with coinfection with oncogenic viruses, such as Epstein-Barr virus, human herpesvirus 8, and human papillomavirus, with resulting malignancies occurring secondary to diminished immune surveillance against viruses and virus-infected tumor cells. Over 50% of AIDS lymphomas are associated with Epstein-Barr virus (EBV) and/or HHV8 infection. HHV8-associated diseases include Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease (MCD). EBV is associated with several malignancies, including Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). Coinfection with HIV and HPV is associated with an increased risk of various squamous cell carcinomas of epithelial tissues. HAART has significantly impacted the incidence, management, and prognosis of AIDS-related malignancies. In addition to changing the natural history of HIV infection in regard to incidence and survival, HAART has dramatically decreased the incidence of certain virally mediated HIV-associated malignancies such as KS and primary CNS lymphoma. The beneficial effects of HAART on these tumors are attributed to drug-mediated HIV suppression and immune reconstitution. However, HAART has had a less favorable impact on EBV- and HPV-related malignancies. This chapter presents an overview of HIV-associated malignancies mediated by HHV-8, EBV, and HPV, and reviews the effect of HAART on the epidemiology, presentation, treatment, and outcomes of these cancers.
Topics: Acquired Immunodeficiency Syndrome; Antiretroviral Therapy, Highly Active; Coinfection; HIV Infections; Herpesviridae Infections; Herpesvirus 4, Human; Herpesvirus 8, Human; Humans; Neoplasms; Oncogenic Viruses; Papillomaviridae; Papillomavirus Infections; Sarcoma, Kaposi; Tumor Virus Infections
PubMed: 30523619
DOI: 10.1007/978-3-030-03502-0_1 -
Virologica Sinica Apr 2015
Topics: Host-Pathogen Interactions; Humans; Neoplasms; Oncogenic Viruses
PubMed: 25924992
DOI: 10.1007/s12250-015-3599-y -
Journal of Cancer 2018Enhanced glycolysis under normoxic conditions is known as aerobic glycolysis or the Warburg effect and is a hallmark of many tumors. Viral infection may also induce... (Review)
Review
Enhanced glycolysis under normoxic conditions is known as aerobic glycolysis or the Warburg effect and is a hallmark of many tumors. Viral infection may also induce aerobic glycolysis as it is required for replication and survival. Tumor viruses inducing aerobic glycolysis and lactate production during latent infection suggest a potential role of virus-induced glycolysis in tumorigenesis. Virus or virus-encoded proteins regulate glucose uptake and lactate export, increase the activity of glycolytic enzymes, and modulate glucose metabolic signals. Accumulating evidence suggests that virus-induced glycolysis may facilitate cell growth, transformation, migration, and invasion, but its significance in tumorigenesis remains unclear. We summarize the effects of oncogenic viruses on the metabolic shift to aerobic glycolysis and discuss the possible association of this metabolic reprogramming with tumor development and progression.
PubMed: 30405839
DOI: 10.7150/jca.27279 -
Biomedicines Mar 2022With the advent of combination antiretroviral therapy (cART), overall survival has been improved, and the incidence of acquired immunodeficiency syndrome (AIDS)-defining... (Review)
Review
With the advent of combination antiretroviral therapy (cART), overall survival has been improved, and the incidence of acquired immunodeficiency syndrome (AIDS)-defining cancers has also been remarkably reduced. However, non-AIDS-defining cancers among human immunodeficiency virus-1 (HIV-1)-associated malignancies have increased significantly so that cancer is the leading cause of death in people living with HIV in certain highly developed countries, such as France. However, it is currently unknown how HIV-1 infection raises oncogenic virus-mediated cancer risks in the HIV-1 and oncogenic virus co-infected patients, and thus elucidation of the molecular mechanisms for how HIV-1 expedites the oncogenic viruses-triggered tumorigenesis in the co-infected hosts is imperative for developing therapeutics to cure or impede the carcinogenesis. Hence, this review is focused on HIV-1 and oncogenic virus co-infection-mediated molecular processes in the acceleration of non-AIDS-defining cancers.
PubMed: 35453518
DOI: 10.3390/biomedicines10040768 -
Critical Reviews in Oncogenesis 2019Epstein-Barr virus (EBV) seroprevalence is extremely high worldwide. This member of the herpesvirus family is considered to be a human carcinogen, implicated in lymphoid... (Review)
Review
Epstein-Barr virus (EBV) seroprevalence is extremely high worldwide. This member of the herpesvirus family is considered to be a human carcinogen, implicated in lymphoid and epithelial malignancies. Because of its characteristics, EBV has been investigated in thyroid specimens, especially in autoimmune and neoplastic lesions. However, the role of EBV in thyroid diseases is still unclear. Reports on its presence in thyroid cancer (TC) vary drastically according to population and applied methodology. This review presents the history of EBV and TC, aiming to better understand the role of this oncogenic virus in thyroid tumorigenesis. We hope to assist researchers, and we discuss possible approaches to better understand the role of EBV in TC.
Topics: Epstein-Barr Virus Infections; Herpesvirus 4, Human; Humans; Thyroid Neoplasms
PubMed: 32421991
DOI: 10.1615/CritRevOncog.2019031618 -
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 -
International Journal of Molecular... Apr 2023Some viruses are known to be associated with the onset of specific cancers. These microorganisms, oncogenic viruses or oncoviruses, can convert normal cells into cancer... (Review)
Review
Some viruses are known to be associated with the onset of specific cancers. These microorganisms, oncogenic viruses or oncoviruses, can convert normal cells into cancer cells by modulating the central metabolic pathways or hampering genomic integrity mechanisms, consequently inhibiting the apoptotic machinery and/or enhancing cell proliferation. Seven oncogenic viruses are known to promote tumorigenesis in humans: human papillomavirus (HPV), hepatitis B and C viruses (HBV, HCV), Epstein-Barr virus (EBV), human T-cell leukemia virus 1 (HTLV-1), Kaposi sarcoma-associated herpesvirus (KSHV), and Merkel cell polyomavirus (MCPyV). Recent research indicates that SARS-CoV-2 infection and COVID-19 progression may predispose recovered patients to cancer onset and accelerate cancer development. This hypothesis is based on the growing evidence regarding the ability of SARS-CoV-2 to modulate oncogenic pathways, promoting chronic low-grade inflammation and causing tissue damage. Herein, we summarize the main relationships known to date between virus infection and cancer, providing a summary of the proposed biochemical mechanisms behind the cellular transformation. Mechanistically, DNA viruses (such as HPV, HBV, EBV, and MCPyV) encode their virus oncogenes. In contrast, RNA viruses (like HCV, HTLV-1) may encode oncogenes or trigger host oncogenes through cis-/-trans activation leading to different types of cancer. As for SARS-CoV-2, its role as an oncogenic virus seems to occur through the inhibition of oncosuppressors or controlling the metabolic and autophagy pathways in the infected cells. However, these effects could be significant in particular scenarios like those linked to severe COVID-19 or long COVID. On the other hand, looking at the SARS-CoV-2─cancer relationship from an opposite perspective, oncolytic effects and anti-tumor immune response were triggered by SARS-CoV-2 infection in some cases. In summary, our work aims to recall comprehensive attention from the scientific community to elucidate the effects of SARS-CoV-2 and, more in general, β-coronavirus infection on cancer susceptibility for cancer prevention or supporting therapeutic approaches.
Topics: Humans; SARS-CoV-2; Epstein-Barr Virus Infections; Papillomavirus Infections; Post-Acute COVID-19 Syndrome; Herpesvirus 4, Human; COVID-19; Neoplasms; Oncogenic Viruses; Cell Transformation, Neoplastic; Hepatitis C
PubMed: 37175509
DOI: 10.3390/ijms24097803