The Role of Viruses in the Development of Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Infectious Agents and Cancer".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 1145

Special Issue Editor


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Guest Editor
School of Molecular and Cellular Biology, University of Leeds, Leeds, UK
Interests: DNA viruses; HPV; adenovirus; viral vectors; cancer virotherapy

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute a paper for this Special Issue on “The Role of Viruses in the Development of Cancer”. Viruses have been studied as etiological agents in the development of animal and human cancers for more than a century. This work has aided the identification of oncogenes and tumour suppressor genes as well as highlighting viruses that play a crucial role in the development of human cancers, for example, the role of high-risk human papillomaviruses (HPVs) in ano-genital and oral cancers, and of the human retrovirus T-lymphotropic virus 1 (HTLV 1) in adult T-cell leukaemia (ATL). The field continues to be buoyant, with new tumour viruses such as the DNA viruses, Merkel Cell Polyomavirus (MCPyV) and Kaposi’s sarcoma herpesvirus (KSHV or HHV8) being discovered using DNA sequence and genomic analysis within the past two decades. While effective prophylactic vaccines have been developed against HPVs and Hepatitis B (HBV), there is still a requirement for novel therapeutic approaches to human cancers that are driven by tumour virus infection. 

Original research articles and reviews are welcome in this Special Issue. Research areas may include (but are not limited to) fundamental studies on the molecular mechanisms of cell transformation and oncogenesis by DNA and RNA tumour viruses; the immune response to tumour viruses; the immune evasion of cancers driven by tumour viruses; prophylactic and therapeutic vaccines against tumour viruses and the cancers that they cause; emerging tumour viruses; and global perspectives on tumour viruses and cancers.

We look forward to receiving your contributions.

Prof. Dr. George Eric Blair
Guest Editor

Manuscript Submission Information

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Keywords

  • DNA and RNA tumour viruses
  • HPV
  • EBV
  • KSHV
  • HCV
  • HBV
  • HTLV1
  • McPyV

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Published Papers (1 paper)

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Research

19 pages, 11686 KiB  
Article
Cross-Talk Between Tumor Cells and Stellate Cells Promotes Oncolytic VSV Activity in Intrahepatic Cholangiocarcinoma
by Victoria Neumeyer, Purva Chavan, Katja Steiger, Oliver Ebert and Jennifer Altomonte
Cancers 2025, 17(3), 514; https://doi.org/10.3390/cancers17030514 - 4 Feb 2025
Viewed by 763
Abstract
As the mechanisms underlying tumorigenesis become better understood, the dynamic roles of cellular components of the tumor microenvironment, and their cross-talk with tumor cells, have come to light as key drivers of disease progression and have emerged as important targets of new cancer [...] Read more.
As the mechanisms underlying tumorigenesis become better understood, the dynamic roles of cellular components of the tumor microenvironment, and their cross-talk with tumor cells, have come to light as key drivers of disease progression and have emerged as important targets of new cancer therapies. In the field of oncolytic virus (OV) therapy, stromal cells have been considered as potential barriers to viral spread, thus limiting virus replication and therapeutic outcome. However, new evidence indicates that intratumoral fibroblasts could support virus replication. We have demonstrated in a rat model of stromal-rich intrahepatic cholangiocarcinoma (CCA) that vesicular stomatitis virus (VSV) can be localized within intratumoral hepatic stellate cells (HSCs), in addition to tumor cells, when the virus was applied via hepatic arterial infusion. Furthermore, VSV was shown to efficiently kill CCA cells and activated HSCs, and co-culture of CCA and HSCs increased viral titers. Interestingly, this effect is also observed when each cell type is cultured alone in a conditioned medium of the other cell type, indicating that secreted cell factors are at least partially responsible for this phenomenon. Partial reduction in sensitivity to type I interferons was observed in co-culture systems, providing a possible mechanism for the increased viral titers. Together, the results indicate that targeting activated HSCs with VSV could provide an additional mechanism of OV therapy, which, until now has not been considered. Furthermore, these findings suggest that VSV is a potentially powerful therapeutic agent for stromal-rich tumors, such as CCA and pancreatic cancer, both of which are very difficult to treat with conventional therapy and have a very poor prognosis. Full article
(This article belongs to the Special Issue The Role of Viruses in the Development of Cancer)
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