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Pathogens
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Oncogenic Viruses
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Oncogenic Viruses

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 15908

Special Issue Editors

Dr. Angioletta Lasagna

E-Mail
Guest Editor
S.C. Oncologia Medica, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
Interests: cancer; vaccines; immunotherapy; viral infection; microbiome
Special Issues, Collections and Topics in MDPI journals
Dr. Irene Cassaniti

E-Mail Website
Guest Editor
Molecular Virology Unit, Department of Microbiology and Virology, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
Interests: viral infection; CMV; SARS-CoV-2; vaccines; viral infection

Special Issue Information

Dear Colleagues,

Viruses have been demonstrated to be inducers of tumorigenesis. Growing evidence has suggested links between virus, dysbiosis, and cancer, although a direct causal relationship has not yet been demonstrated for the majority of cancers. In the past, only the presence of the virus in the tumor suggested a causal relationship. The “hit-and-run” theory is an intriguing mechanism by which some viruses may trigger carcinogenesis without host genome integration. This may lead to a re-definition of the number and types of virus-induced cancers resulting in new preventive and therapeutic strategies.

This Special Issues of Pathogens aims to update the current evidence and collect the latest findings on oncogenic viruses.  Particular attention will be paid to original research articles and state-of-the-art reviews focused on viral carcinogenesis and future research directions.

All types of articles will be considered for publication, including short reports, full research articles, and reviews. 

Dr. Angioletta Lasagna
Dr. Irene Cassaniti
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. Pathogens 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 2200 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 virus
  • virome
  • viral infection
  • virus–host interactions
  • cancer
  • carcinogenesis
  • hit-and-run theory
  • vaccination

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Published Papers (5 papers)

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Research

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19 pages, 4289 KiB  
Article
Gammaherpesvirus Infection Stimulates Lung Tumor-Promoting Inflammation
by Sudurika S. Mukhopadhyay, Kenneth F. Swan, Gabriella Pridjian, Jay K. Kolls, Yan Zhuang, Qinyan Yin, Joseph A. Lasky, Erik Flemington, Cindy A. Morris, Zhen Lin and Gilbert F. Morris
Pathogens 2024, 13(9), 747; https://doi.org/10.3390/pathogens13090747 - 31 Aug 2024
Viewed by 2188
Abstract
Lung tumor-promoting environmental exposures and γherpesvirus infections are associated with Type 17 inflammation. To test the effect of γherpesvirus infection in promoting lung tumorigenesis, we infected mutant K-Ras-expressing (K-RasLA1) mice with the murine γherpesvirus MHV68 via oropharyngeal aspiration. After 7 weeks, [...] Read more.
Lung tumor-promoting environmental exposures and γherpesvirus infections are associated with Type 17 inflammation. To test the effect of γherpesvirus infection in promoting lung tumorigenesis, we infected mutant K-Ras-expressing (K-RasLA1) mice with the murine γherpesvirus MHV68 via oropharyngeal aspiration. After 7 weeks, the infected mice displayed a more than 2-fold increase in lung tumors relative to their K-RasLA1 uninfected littermates. Assessment of cytokines in the lung revealed that expression of Type 17 cytokines (Il-6, Cxcl1, Csf3) peaked at day 7 post-infection. These observations correlated with the post-infection appearance of known immune mediators of tumor promotion via IL-17A in the lungs of tumor-bearing mice. Surprisingly, Cd84, an immune cell marker mRNA, did not increase in MHV68-infected wild-type mice lacking lung tumors. Csf3 and Cxcl1 protein levels increased more in the lungs of infected K-RasLA1 mice relative to infected wild-type littermates. Flow cytometric and transcriptomic analyses indicated that the infected K-RasLA1 mice had increased Ly6Gdim/Ly6Chi immune cells in the lung relative to levels seen in uninfected control K-RasLA1 mice. Selective methylation of adenosines (m6A modification) in immune-cell-enriched mRNAs appeared to correlate with inflammatory infiltrates in the lung. These observations implicate γherpesvirus infection in lung tumor promotion and selective accumulation of immune cells in the lung that appears to be associated with m6A modification of mRNAs in those cells. Full article
(This article belongs to the Special Issue Oncogenic Viruses)
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14 pages, 322 KiB  
Article
Detection and Genotyping of Human Papillomavirus (HPV16/18), Epstein–Barr Virus (EBV), and Human Cytomegalovirus (HCMV) in Endometrial Endometroid and Ovarian Cancers
by Beniamin Oskar Grabarek, Piotr Ossowski, Justyna Czarniecka, Mateusz Ożóg, Justyna Prucnal, Ireneusz Dziuba, Aleksander Ostenda, Konrad Dziobek, Dariusz Boroń, Wojciech Peszek, Piotr Kras, Szymon Januszyk, Maciej Dąbala, Tomasz Kasela and Marcin Opławski
Pathogens 2023, 12(3), 397; https://doi.org/10.3390/pathogens12030397 - 1 Mar 2023
Cited by 5 | Viewed by 2886
Abstract
The purpose of this study was to evaluate the relationship between human papillomavirus (HPV16/18), Epstein–Barr virus (EBV), and human cytomegalovirus (HCMV) infections and the occurrence of ovarian cancer in 48 women, of whom 36 underwent surgery and chemotherapy (group A), 12 in whom [...] Read more.
The purpose of this study was to evaluate the relationship between human papillomavirus (HPV16/18), Epstein–Barr virus (EBV), and human cytomegalovirus (HCMV) infections and the occurrence of ovarian cancer in 48 women, of whom 36 underwent surgery and chemotherapy (group A), 12 in whom surgery was sufficient (group B), and 60 with endometroid endometrial cancer stage G1-G3 (group C), compared to patients in whom the uterus and its appendages were removed for nononcological reasons (control group). The detection of HPV, EBV, and HCMV in tumor tissue and normal tissue was performed using the real-time polymerase chain reaction (RT-PCR) technique. A statistically significantly higher risk of endometrial cancer was noted in patients infected only with HCMV (OR > 1; p < 0.05). In contrast, a significantly higher risk of ovarian cancer in group A was associated with HPV16, HPV18, and EBV (OR > 1; p < 0.05); a significantly higher risk of ovarian cancer in group B was associated with HPV18 and HMCV (OR > 1; p < 0.05). The obtained results suggest that HCMV infection is associated with the development of a stage of ovarian cancer when treatment can be completed with surgery alone. Meanwhile, EBV appears to be responsible for the development of ovarian cancer in more advanced stages. Full article
(This article belongs to the Special Issue Oncogenic Viruses)

Review

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13 pages, 1021 KiB  
Review
Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link
by Abdelbasset Amara, Saoussen Trabelsi, Abdul Hai, Syeda Huma H. Zaidi, Farah Siddiqui and Sami Alsaeed
Pathogens 2024, 13(12), 1070; https://doi.org/10.3390/pathogens13121070 - 6 Dec 2024
Viewed by 4401
Abstract
The COVID-19 infection caused by SARS-CoV-2 in late 2019 posed unprecedented global health challenges of massive proportions. The persistent effects of COVID-19 have become a subject of significant concern amongst the medical and scientific community. This article aims to explore the probability of [...] Read more.
The COVID-19 infection caused by SARS-CoV-2 in late 2019 posed unprecedented global health challenges of massive proportions. The persistent effects of COVID-19 have become a subject of significant concern amongst the medical and scientific community. This article aims to explore the probability of a link between the COVID-19 infection and the risk of lung cancer development. First, this article reports that SARS-CoV-2 induces severe inflammatory response and cellular stress, potentially leading to tumorigenesis through common pathways between SARS-CoV-2 infection and cancer. These pathways include the JAK/STAT3 pathway which is activated after the initiation of cytokine storm following SARS-CoV-2 infection. This pathway is involved in cellular proliferation, differentiation, and immune homeostasis. The JAK/STAT3 pathway is also hyperactivated in lung cancer which serves as a link thereof. It predisposes patients to lung cancer through myriad molecular mechanisms such as DNA damage, genomic instability, and cell cycle dysregulation. Another probable pathway to tumorigenesis is based on the possibility of an oncogenic nature of SARS-CoV-2 through hijacking the p53 protein, leading to cell oxidative stress and interfering with the DNA repair mechanisms. Finally, this article highlights the overexpression of the SLC22A18 gene in lung cancer. This gene can be overexpressed by the ZEB1 transcription factor, which was found to be highly expressed during COVID-19 infection. Full article
(This article belongs to the Special Issue Oncogenic Viruses)
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13 pages, 1352 KiB  
Review
Immune Modulation by Epstein–Barr Virus Lytic Cycle: Relevance and Implication in Oncogenesis
by Nevena Todorović, Maria Raffaella Ambrosio and Amedeo Amedei
Pathogens 2024, 13(10), 876; https://doi.org/10.3390/pathogens13100876 - 8 Oct 2024
Viewed by 2781
Abstract
EBV infects more than 90% of people globally, causing lifelong infection. The phases of the EBV life cycle encompass primary infection, latency, and subsequent reactivation or lytic phase. The primary infection usually happens without noticeable symptoms, commonly in early life stages. If it [...] Read more.
EBV infects more than 90% of people globally, causing lifelong infection. The phases of the EBV life cycle encompass primary infection, latency, and subsequent reactivation or lytic phase. The primary infection usually happens without noticeable symptoms, commonly in early life stages. If it manifests after childhood, it could culminate in infectious mononucleosis. Regarding potential late consequences, EBV is associated with multiple sclerosis, rheumatoid arthritis, chronic active EBV infection, lymphomas, and carcinomas. Previous reports that the lytic phase plays a negligible or merely secondary role in the oncogenesis of EBV-related tumors are steadily losing credibility. The right mechanisms through which the lytic cycle contributes to carcinogenesis are still unclear, but it is now recognized that lytic genes are expressed to some degree in different cancer-type cells, implicating their role here. The lytic infection is a persistent aspect of virus activity, continuously stimulating the immune system. EBV shows different strategies to modulate and avoid the immune system, which is thought to be a key factor in its ability to cause cancer. So, the principal goal of our review is to explore the EBV’s lytic phase contribution to oncogenesis. Full article
(This article belongs to the Special Issue Oncogenic Viruses)
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17 pages, 2380 KiB  
Review
Unlocking the Potential: Epstein-Barr Virus (EBV) in Gastric Cancer and Future Treatment Prospects, a Literature Review
by Salvatore Corallo, Angioletta Lasagna, Beatrice Filippi, Domiziana Alaimo, Anna Tortorella, Francesco Serra, Alessandro Vanoli and Paolo Pedrazzoli
Pathogens 2024, 13(9), 728; https://doi.org/10.3390/pathogens13090728 - 28 Aug 2024
Cited by 1 | Viewed by 2923
Abstract
Gastric cancer (GC) is a complex disease with various etiologies. While Helicobacter pylori infection is still one of the leading risk factors for GC, increasing evidence suggests a link between GC and other infective agents such as Epstein Bar Virus (EBV). EBV-associated gastric [...] Read more.
Gastric cancer (GC) is a complex disease with various etiologies. While Helicobacter pylori infection is still one of the leading risk factors for GC, increasing evidence suggests a link between GC and other infective agents such as Epstein Bar Virus (EBV). EBV-associated gastric cancer (EBVaGC) is now recognized as a distinct subgroup of GC, and the complex interactions between the virus and gastric mucosa may influence its development. A recent integrative analysis of the genome and proteome of GC tissues by The Cancer Genome Atlas project has identified EBVaGC as a specific subtype characterized by PIK3CA and ARID1A mutations, extensive DNA hyper-methylation, and activation of immune signaling pathways. These molecular characteristics are markers of the unique molecular profile of this subset of GC and are potential targets for therapy. This review aims to provide an overview of the current knowledge on EBVaGC. It will focus on the epidemiology, clinic-pathological features, and genetic characteristics of EBVaGC. Additionally, it will discuss recent data indicating the potential use of EBV infection as a predictive biomarker of response to chemotherapy and immune checkpoint inhibitors. The review also delves into potential therapeutic approaches for EBVaGC, including targeted therapies and adoptive immunotherapy, highlighting the promising potential of EBV as a therapeutic target. Full article
(This article belongs to the Special Issue Oncogenic Viruses)
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