Viruses and Cancer: From Cellular Mechanism to Therapeutic Aspects

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 4769

Special Issue Editors


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Guest Editor
Department of Microbiology and Immunology, Penn State Cancer Institute, 400 University Drive, Hershey, PA 17033, USA
Interests: merkel cell polyomavirus; merkel cell carcinoma; oncogenic viruses; immune evasion; DNA replication; virus latency; ubiquitin-protein ligases; oncogene; protein degradation; p53; cell cycle

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Guest Editor
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Interests: human gammaherpesvirus 8; oncogenic viruses; t-lymphocytes; interferon regulatory factors; mitophagy; autophagy; apoptosis; NF-kB; ubiquitination; cytokines; virus-host interactions

Special Issue Information

Dear Colleagues, 

Viruses cause a wide spectrum of clinical diseases; several have even been shown to be capable of causing cancers in humans. Additional events and host factors, such as an immunosuppressive tumor microenvironment, oncogenic mutations accumulated with age, and host genetic predisposition, are also predicted to play a role in viral diseases. A comprehensive understanding of viral oncogenesis and the molecular mechanisms of host responses may enable the identification of unknown infectious cancer etiologies; thus, enhancing our knowledge of this area holds much promise for the development of more effective and tolerable strategies for virus-associated cancers. 

This Special Issue of Cells aims to bring together the latest key findings on host responses during virus infection leading to viral oncogenesis and discuss new diagnostic and therapeutic ideas and applications.  Research areas of interest include (but are not limited to) the following topics:

  • Host cell responses: cellular and molecular mechanisms;
  • Virus–host interaction;
  • Host immunity and viral evasion mechanisms;
  • Viral oncogenesis;
  • Metabolic reprogramming;
  • Therapeutic approaches. 

Original research articles and reviews are both welcome. We look forward to receiving your contributions. 

Dr. Hyun Jin Kwun
Dr. Young Bong Choi
Guest Editors

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Keywords

  • virus-induced cancer
  • host stress responses
  • DNA damage response
  • virus–host interactions
  • autophagy
  • cellular innate immunity
  • cell metabolism
  • immune evasion mechanisms
  • inflammation
  • therapeutic approach

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Published Papers (2 papers)

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Research

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20 pages, 6066 KiB  
Article
Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs the Urea Cycle
by Natalia F. Zakirova, Olga A. Khomich, Olga A. Smirnova, Jennifer Molle, Sarah Duponchel, Dmitry V. Yanvarev, Vladimir T. Valuev-Elliston, Lea Monnier, Boyan Grigorov, Olga N. Ivanova, Inna L. Karpenko, Mikhail V. Golikov, Cedric Bovet, Barbara Rindlisbacher, Alex R. Khomutov, Sergey N. Kochetkov, Birke Bartosch and Alexander V. Ivanov
Cells 2024, 13(12), 1036; https://doi.org/10.3390/cells13121036 - 14 Jun 2024
Cited by 1 | Viewed by 1199
Abstract
Hepatitis C virus (HCV) is an oncogenic virus that causes chronic liver disease in more than 80% of patients. During the last decade, efficient direct-acting antivirals were introduced into clinical practice. However, clearance of the virus does not reduce the risk of end-stage [...] Read more.
Hepatitis C virus (HCV) is an oncogenic virus that causes chronic liver disease in more than 80% of patients. During the last decade, efficient direct-acting antivirals were introduced into clinical practice. However, clearance of the virus does not reduce the risk of end-stage liver diseases to the level observed in patients who have never been infected. So, investigation of HCV pathogenesis is still warranted. Virus-induced changes in cell metabolism contribute to the development of HCV-associated liver pathologies. Here, we studied the impact of the virus on the metabolism of polyamines and proline as well as on the urea cycle, which plays a crucial role in liver function. It was found that HCV strongly suppresses the expression of arginase, a key enzyme of the urea cycle, leading to the accumulation of arginine, and up-regulates proline oxidase with a concomitant decrease in proline concentrations. The addition of exogenous proline moderately suppressed viral replication. HCV up-regulated transcription but suppressed protein levels of polyamine-metabolizing enzymes. This resulted in a decrease in polyamine content in infected cells. Finally, compounds targeting polyamine metabolism demonstrated pronounced antiviral activity, pointing to spermine and spermidine as compounds affecting HCV replication. These data expand our understanding of HCV’s imprint on cell metabolism. Full article
(This article belongs to the Special Issue Viruses and Cancer: From Cellular Mechanism to Therapeutic Aspects)
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Review

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13 pages, 846 KiB  
Review
The Role of RNA Sensors in Regulating Innate Immunity to Gammaherpesviral Infections
by Huirong Zhang, Praneet K. Sandhu and Blossom Damania
Cells 2023, 12(12), 1650; https://doi.org/10.3390/cells12121650 - 17 Jun 2023
Cited by 1 | Viewed by 2765
Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV) and the Epstein–Barr virus (EBV) are double-stranded DNA oncogenic gammaherpesviruses. These two viruses are associated with multiple human malignancies, including both B and T cell lymphomas, as well as epithelial- and endothelial-derived cancers. KSHV and EBV establish a life-long [...] Read more.
Kaposi’s sarcoma-associated herpesvirus (KSHV) and the Epstein–Barr virus (EBV) are double-stranded DNA oncogenic gammaherpesviruses. These two viruses are associated with multiple human malignancies, including both B and T cell lymphomas, as well as epithelial- and endothelial-derived cancers. KSHV and EBV establish a life-long latent infection in the human host with intermittent periods of lytic replication. Infection with these viruses induce the expression of both viral and host RNA transcripts and activates several RNA sensors including RIG-I-like receptors (RLRs), Toll-like receptors (TLRs), protein kinase R (PKR) and adenosine deaminases acting on RNA (ADAR1). Activation of these RNA sensors induces the innate immune response to antagonize the virus. To counteract this, KSHV and EBV utilize both viral and cellular proteins to block the innate immune pathways and facilitate their own infection. In this review, we summarize how gammaherpesviral infections activate RNA sensors and induce their downstream signaling cascade, as well as how these viruses evade the antiviral signaling pathways to successfully establish latent infection and undergo lytic reactivation. Full article
(This article belongs to the Special Issue Viruses and Cancer: From Cellular Mechanism to Therapeutic Aspects)
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