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Viruses
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Molecular and Cellular Biology of Human Oncogenic Viruses
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Molecular and Cellular Biology of Human Oncogenic Viruses

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 5385

Special Issue Editor

Dr. Roberta Gonnella

E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena 324, 00161 Rome, Italy
Interests: herpesviruses; EBV; KSHV; virus replication; autophagy

Special Issue Information

Dear Colleagues,

The number of oncovirus-associated cancers has been increasing in recent years; it has been estimated that approximately 10% of neoplastic diseases in the world correlate with viral infections. Therefore, understanding the molecular mechanisms through which oncoviruses regulate viral and host gene expression may help in identifying potential therapeutic targets. There are currently seven recognized viruses associated with human cancer, namely EBV, KSHV, HPV, HTLV-1, HBV, HCV, and MCV. They are able to infect different cell types and can adopt similar and specific strategies to trigger the transformation of their target cells.

The aim of this Special Issue is to provide new insights into the mechanisms underlying viral oncogenesis in the attempt to identify new drugs, enabling the manipulation of the viral lytic cycle, which, in some cases, can be latent or lytic, or target the epigenetic changes and the activation of pro-oncogenic molecular pathways that oncoviruses may induce. The study of mechanisms leading to the establishment of viral infections may also provide useful information on cancer prevention, including the development of vaccines against oncoviruses.

We are looking forward to receiving your contributions.

Dr. Roberta Gonnella
Guest Editor

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

  • oncoviruses
  • antiviral drugs
  • viral oncogenesis
  • viral infection
  • oncogenic pathways
  • epigenetics

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Published Papers (5 papers)

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Research

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23 pages, 8693 KiB  
Article
DNA-Binding Activities of KSHV DNA Polymerase Processivity Factor (PF-8) Complexes
by Jennifer Kneas Travis, Megan Martin and Lindsey M. Costantini
Viruses 2025, 17(2), 190; https://doi.org/10.3390/v17020190 - 29 Jan 2025
Viewed by 319
Abstract
Kaposi’s Sarcoma Herpesvirus (KSHV) is the causative agent of several human diseases. There are few effective treatments available to treat infection and KSHV oncogenesis. Disrupting the KSHV infectious cycle would diminish the viral spread. The KSHV lytic phase and production of new virions [...] Read more.
Kaposi’s Sarcoma Herpesvirus (KSHV) is the causative agent of several human diseases. There are few effective treatments available to treat infection and KSHV oncogenesis. Disrupting the KSHV infectious cycle would diminish the viral spread. The KSHV lytic phase and production of new virions require efficient copying and packaging of the KSHV genome. KSHV encodes its own lytic DNA replication machinery, including the processivity factor (PF-8), which presents itself as an attractive target for antiviral development. We characterized PF-8 at the single molecule level using transmission electron microscopy to identify key molecular interactions that mediate viral DNA replication initiation. Our results indicate that PF-8 forms oligomeric ring structures (tetramer, hexamer, and/or dodecamer) similar to the related Epstein–Barr virus processivity factor (BMRF1). Our DNA positional mapping revealed high-frequency binding locations of PF-8 within the lytic origin of replication (OriLyt). A multi-variable analysis of PF-8 DNA-binding activity with three mutant OriLyts provides new insights into the mechanisms that PF-8 associates with viral DNA and complexes to form multi-ring-like structures. Collectively, these data enhance the mechanistic understanding of the molecular interactions (protein–protein and protein-DNA) of an essential KSHV DNA replication protein. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Human Oncogenic Viruses)
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13 pages, 3864 KiB  
Article
EZH2 Inhibition by DS3201 Triggers the Kaposi’s Sarcoma-Associated Herpesvirus Lytic Cycle and Potentiates the Effects Induced by SAHA in Primary Effusion Lymphoma Cells
by Roberta Gonnella, Flavia Collura, Vincenzo Corrado, Michele Di Crosta, Roberta Santarelli and Mara Cirone
Viruses 2024, 16(9), 1490; https://doi.org/10.3390/v16091490 - 20 Sep 2024
Cited by 1 | Viewed by 1267
Abstract
Primary Effusion Lymphoma (PEL) cells carry Kaposi’s sarcoma-associated herpesvirus (KSHV) in a latent state, except for a small number of cells in which the virus replicates to ensure its persistence into the infected host. However, the lytic cycle can be reactivated in vitro [...] Read more.
Primary Effusion Lymphoma (PEL) cells carry Kaposi’s sarcoma-associated herpesvirus (KSHV) in a latent state, except for a small number of cells in which the virus replicates to ensure its persistence into the infected host. However, the lytic cycle can be reactivated in vitro by exposing these lymphoma cells to various treatments, leading to cell lysis. To restrict viral antigen expression, KSHV induces repressive epigenetic changes, including DNA methylation and histone modifications. Among the latter, histone deacetylation and tri-methylation of Histone H3 lisyne-27 (H3K27me3) have been reported to play a role. Here, we found that the inhibition of H3K27 tri-methylation by valemetostat DS3201 (DS), a small molecule that inhibits Enhancer of Zeste Homolog 2 (EZH2) methyltransferase, induced the KSHV lytic cycle in PEL cells, and that this effect involved the activation of the wtp53–p21 axis and autophagic dysregulation. DS also potentiated the lytic cycle activation mediated by the Histone deacetylases (HDAC) inhibitor Suberoylanilide hydroxamic acid (SAHA) and reinforced its cytotoxic effect, suggesting that such a combination could be used to unbalance the latent/lytic cycle and further impair the survival of PEL cells. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Human Oncogenic Viruses)
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31 pages, 18502 KiB  
Article
Comparative Proteomic Analysis of Huh7 Cells Transfected with Sub-Saharan African Hepatitis B Virus (Sub)genotypes Reveals Potential Oncogenic Factors
by Kiyasha Padarath, Aurélie Deroubaix, Previn Naicker, Stoyan Stoychev and Anna Kramvis
Viruses 2024, 16(7), 1052; https://doi.org/10.3390/v16071052 - 29 Jun 2024
Cited by 1 | Viewed by 1449
Abstract
In sub-Saharan Africa (SSA), the (sub)genotypes A1, D3, and E of the hepatitis B virus (HBV) prevail. Individuals infected with subgenotype A1 have a 4.5-fold increased risk of HCC compared to those infected with other (sub)genotypes. The effect of (sub)genotypes on protein expression [...] Read more.
In sub-Saharan Africa (SSA), the (sub)genotypes A1, D3, and E of the hepatitis B virus (HBV) prevail. Individuals infected with subgenotype A1 have a 4.5-fold increased risk of HCC compared to those infected with other (sub)genotypes. The effect of (sub)genotypes on protein expression and host signalling has not been studied. Mass spectrometry was used to analyse the proteome of Huh7 cells transfected with replication-competent clones. Proteomic analysis revealed significantly differentially expressed proteins between SSA (sub)genotypes. Different (sub)genotypes have the propensity to dysregulate specific host signalling pathways. Subgenotype A1 resulted in dysregulation within the Ras pathway. Ras-associated protein, RhoC, was significantly upregulated in cells transfected with subgenotype A1 compared to those transfected with other (sub)genotypes, on both a proteomic (>1.5-fold) and mRNA level (p < 0.05). Two of the main cellular signalling pathways involving RHOC, MAPK and PI3K/Akt/mTOR, regulate cell growth, motility, and survival. Downstream signalling products of these pathways have been shown to increase MMP2 and MMP9 expression. An extracellular MMP2 and MMP9 ELISA revealed a non-significant increase in MMP2 and MMP9 in the cells transfected with A1 compared to the other (sub)genotypes (p < 0.05). The upregulated Ras-associated proteins have been implicated as oncoproteins in various cancers and could contribute to the increased hepatocarcinogenic potential of A1. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Human Oncogenic Viruses)
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Review

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22 pages, 972 KiB  
Review
Regulation of Granzymes A and B by High-Risk HPV: Impact on Immune Evasion and Carcinogenesis
by Mashego Nathan Maleka, Zukile Mbita and Vivian Morafo
Viruses 2025, 17(2), 221; https://doi.org/10.3390/v17020221 - 3 Feb 2025
Abstract
The number of new cancer cases is soaring, and currently, there are 440.5 per 100,000 new cases reported every year. A quarter of these are related to human papillomavirus (HPV) infections, particularly types 16 and 18. These include oropharyngeal, anal, vaginal, and penile [...] Read more.
The number of new cancer cases is soaring, and currently, there are 440.5 per 100,000 new cases reported every year. A quarter of these are related to human papillomavirus (HPV) infections, particularly types 16 and 18. These include oropharyngeal, anal, vaginal, and penile cancers. A critical aspect of their oncogenic potential lies in their ability to manipulate host immune responses, facilitating immune evasion and carcinogenesis. High-risk HPVs target key immune components like granzymes A and B and MHC-I, which are crucial for the elimination of virus-infected and transformed cells, thereby weakening immune surveillance. Evidence suggests that high-risk HPVs downregulate the expression of tumor suppressors, such as p53 and pRB, and the activity of these immune components, weakening CTL and NK cell responses, thus enabling persistent infection and carcinogenesis. We discuss the implications of granzyme and MHC-I dysregulation for immune evasion, tumor progression, and potential therapeutic strategies. This review further explores the regulation of granzyme A, B, and MHC-I by high-risk HPVs, focusing on how viral oncoproteins, E6 and E7, interfere with granzyme-mediated cytotoxicity and antigen presentation. The complex interplay between high-risk HPVs, granzyme A, granzyme B, and MHC-I may provide insights into novel approaches for targeting HPV-associated cancers. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Human Oncogenic Viruses)
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21 pages, 1556 KiB  
Review
Oncoviral Infections and Small Extracellular Vesicles
by Łukasz Ważny, Theresa L. Whiteside and Monika Pietrowska
Viruses 2024, 16(8), 1291; https://doi.org/10.3390/v16081291 - 13 Aug 2024
Cited by 1 | Viewed by 1800
Abstract
Small extracellular vesicles (sEV) are small membrane-bound nanovesicles with a size range below 200 nm that are released by all types of cells. sEV carry a diverse cargo of proteins, lipids, glycans, and nucleic acids that mimic the content of producer cells. sEV [...] Read more.
Small extracellular vesicles (sEV) are small membrane-bound nanovesicles with a size range below 200 nm that are released by all types of cells. sEV carry a diverse cargo of proteins, lipids, glycans, and nucleic acids that mimic the content of producer cells. sEV mediate intercellular communication and play a key role in a broad variety of physiological and pathological conditions. Recently, numerous reports have emerged examining the role of sEV in viral infections. A significant number of similarities in the sEV biogenesis pathways and the replication cycles of viruses suggest that sEV might influence the course of viral infections in diverse ways. Besides directly modulating virus propagation by transporting the viral cargo (complete virions, proteins, RNA, and DNA), sEV can also modify the host antiviral response and increase the susceptibility of cells to infection. The network of mutual interactions is particularly complex in the case of oncogenic viruses, deserving special consideration because of its significance in cancer progression. This review summarizes the current knowledge of interactions between sEV and oncogenic viruses, focusing on sEV abilities to modulate the carcinogenic properties of oncoviruses. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Human Oncogenic Viruses)
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