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Viruses
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Viral Oncogenes
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Viral Oncogenes

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 2634

Special Issue Editors

Dr. Francesca Caccuri

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, Section of Microbiology, University of Brescia Medical School, Brescia, Italy
Interests: HIV; human respiratory viruses; vaccines; gene therapy; viral oncology; cell/host interaction; endothelial cell dysfunction; cancer microenvironment
Special Issues, Collections and Topics in MDPI journals
Dr. Antonella Bugatti

E-Mail Website
Guest Editor
Section of Microbiology, Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy
Interests: respiratory viral infection, antiviral, vaccine
Special Issues, Collections and Topics in MDPI journals
Dr. Alberto Zani

E-Mail Website
Guest Editor
Section of Microbiology, Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy
Interests: SARS-CoV-2; HIV-1; viral proteins

Special Issue Information

Dear Colleagues,

We are pleased to announce a call for submissions for a Special Issue focusing on the topic of "Viral Oncogenes ".

Human viral oncogenesis is a complex phenomenon and a major contributor to the global cancer burden. Certain viruses have been shown to be vital in the development of various cancers by integrating viral DNA into the host genome and activating viral oncogenes, leading to uncontrolled cell proliferation, evasion of apoptosis, and genomic instability. Oncogenic viruses include the Human Papillomavirus (HPV), Hepatitis B and C Viruses (HBV and HCV), Epstein–Barr Virus (EBV), and Human T-Cell Leukemia Virus (HTLV-1), which are all linked to the development of a myriad of human cancers. A comprehensive understanding of the principles of viral oncogenesis may enable the identification of unknown infectious etiologies of cancer and the development of therapeutic or preventive strategies for virus-associated cancers.

This Special Issue will examine the wide range of viral strategies related to oncogenesis, as well as how oncogenic viruses interact with host cellular components and affect cancer pathogenesis. By elucidating the complex connection between viruses and cancer, this Special Issue will improve our knowledge of oncogenic mechanisms and open the door to novel approaches to both antiviral and anticancer treatments.

We invite you to share your most insightful primary research work, reviews, and hypotheses on this important topic. All submitted articles will undergo a rigorous peer review process to ensure that they are of the highest scientific quality and are relevant to the field. We encourage contributions from researchers, clinicians, and experts in this field.

Should you have any questions, require further information, or need any assistance, please do not hesitate to reach out to us. We are here to support and facilitate your participation in this Special Issue.

Thank you for your attention regarding this matter; we look forward to receiving your valuable contributions.

Dr. Francesca Caccuri
Dr. Antonella Bugatti
Dr. Alberto Zani
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oncogenic viruses
  • viral oncogenesis
  • human oncoviruses, virus–host interactions
  • antiviral agents
  • anticancer strategies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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11 pages, 1090 KiB  
Article
The Differential Expression of the JAK/STAT Pathway in Breast Cancer Cells Transfected with Human Papillomavirus Oncogenes
by Stephanie Loureiro Leão, Gabriel Rômulo Parente da Silva, Daffany Luana dos Santos, Bianca de França São Marcos, Pedro Henrique Bezerra Fontes, Beatriz Eda de Oliveira Isídio, Isabelle Silva Simões, Elisa Fotin Genn Barros, David Beltrán Lussón, Joelson Germano Crispim, Lígia Rosa Sales Leal, Anna Jéssica Duarte Silva, Vanessa Emanuelle Pereira Santos and Antonio Carlos de Freitas
Viruses 2025, 17(7), 880; https://doi.org/10.3390/v17070880 - 23 Jun 2025
Viewed by 443
Abstract
Breast cancer is among the most prevalent and deadly types of cancer worldwide. Viral infections have been investigated as contributing factors in breast carcinogenesis, including infections by high-risk genotypes of human papillomavirus (HPV). Although viral DNA has been detected in breast tumors, the [...] Read more.
Breast cancer is among the most prevalent and deadly types of cancer worldwide. Viral infections have been investigated as contributing factors in breast carcinogenesis, including infections by high-risk genotypes of human papillomavirus (HPV). Although viral DNA has been detected in breast tumors, the role of HPV activity in this type of cancer remains poorly understood. HPV oncogenes interact with various host genes, including those involved in the JAK/STAT signaling pathway. This pathway is associated with the regulation of gene expression related to the tumor microenvironment, and understanding how HPV oncogenes interact with JAK/STAT components may provide insights into the relationship between the virus and breast cancer development. In this study, we assessed the differential expression of the JAK/STAT pathway in MDA-MB-231 cells individually transfected with the E5, E6, and E7 oncogenes of HPV16. The results revealed downregulation of STAT4 in the presence of the E5, E6, and E7 oncogenes. Notably, cells transfected with E5 alone exhibited upregulation of JAK2, STAT3, and STAT6, whereas transfection with E6 and E7 resulted in their downregulation. These findings highlight the underexplored role of the E5 oncogene in contrast to the more extensively studied E6 and E7. Our results support the hypothesis that HPV oncogenes actively modulate the expression of genes involved in the tumor microenvironment in breast cancer. Full article
(This article belongs to the Special Issue Viral Oncogenes)
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Review

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33 pages, 4537 KiB  
Review
The Use of Intrinsic Disorder and Phosphorylation by Oncogenic Viral Proteins to Dysregulate the Host Cell Cycle Through Interaction with pRb
by Heidi Kast-Woelbern, Sarah K. Martinho, Kayla T. Julio, Audrey M. Vazzana, Abbey E. Mandagie and Ariane L. Jansma
Viruses 2025, 17(6), 835; https://doi.org/10.3390/v17060835 - 10 Jun 2025
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Abstract
Approximately 15% of cancers worldwide are caused by oncogenic viruses. These infectious agents utilize multiple strategies to dysregulate their host cells as a means of viral reproduction. While this typically involves a small number of viral oncoproteins known to interact with a myriad [...] Read more.
Approximately 15% of cancers worldwide are caused by oncogenic viruses. These infectious agents utilize multiple strategies to dysregulate their host cells as a means of viral reproduction. While this typically involves a small number of viral oncoproteins known to interact with a myriad of host cell proteins, direct binding with the tumor suppressor retinoblastoma protein (pRb) as a means to dysregulate the cell cycle appears to be a common mechanism among most known oncogenic viruses. This review evaluates the shared structural themes of binding motif, intrinsic disorder, and viral oncoprotein phosphorylation, utilized by eight different oncogenic viruses for the subjugation of pRb. Cancer caused by oncogenic viruses represents one of the few potentially preventable forms of cancer. The more we understand the common strategies used by these infectious agents, the better equipped we will be to further optimize vaccination and therapeutic strategies to fight them. Full article
(This article belongs to the Special Issue Viral Oncogenes)
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