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Pathogens
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Oncoviruses and Molecular Mechanisms of Viral Carcinogenesis
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Oncoviruses and Molecular Mechanisms of Viral Carcinogenesis

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1658

Special Issue Editors

Prof. Dr. Jaqueline Carvalho De Oliveira

E-Mail Website
Guest Editor
Department of Genetics, Federal University of Paraná (UFPR), Centro Politécnico, Jardim das Américas, Curitiba 81530-000, PR, Brazil
Interests: gene regulation; non-coding RNAs; cancer pathways; molecular biomarkers
Prof. Dr. Patrícia Savio De Araujo-Souza

E-Mail Website
Guest Editor
Department of Genetics, Federal University of Paraná (UFPR), Centro Politécnico, Jardim das Américas, Curitiba 81530-000, PR, Brazil
Interests: viral-associated cancers; tumor immunology; molecular biology of cancer; immunogenetics

Special Issue Information

Dear Colleagues,

Viral infections are associated with 15–20% of all human cancers, playing a critical role in carcinogenesis in different sites. The leading causal role of specific viruses with certain cancer types are well documented, such as human papillomavirus (HPV) with cervical cancer, hepatitis B/C virus (HBV and HCV) with hepatocarcinoma and Epstein–Barr virus (EBV) with Burkitt lymphoma. Other viruses contributing to human cancers are human T-lymphotropic virus 1 (HTLV1) and Merkel cell polyomavirus (MCV). Human immunodeficiency virus (HIV), which causes acquired immune deficiency syndrome (AIDS), also increases the risk of several types of cancer, such as Kaposi's sarcoma (caused by human herpes virus 8 (HHV-8, also known as Kaposi's sarcoma herpes virus, KSHV)).

Detailed molecular mechanisms of viral carcinogenesis emerged from recent advances in virology and oncology research. Omics analysis disclosed new possibilities in host–pathogen interactions according to cell/tissue type. However, there are potential new mechanisms influencing carcinogenesis and immune evasion to be explored, as well as some unsolved questions. A deep understanding of these mechanisms may contribute to developing therapeutic or preventive strategies for virus-associated cancers.

Thus, it is expected that this Special Issue will shed attractive and stimulating new light on various aspects of the molecular mechanisms of viral carcinogenesis related to oncoviruses.

Prof. Dr. Jaqueline Carvalho De Oliveira
Prof. Dr. Patrícia Savio De Araujo-Souza
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 2700 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

  • cancer
  • oncoviruses
  • HCV
  • HBV
  • HPV
  • HHV-8/KSHV
  • HTLV1
  • EBV
  • carcinogenesis
  • molecular markers
  • cell biology
  • apoptosis
  • proliferation
  • cell cycle
  • immune evasion

Published Papers (2 papers)

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Research

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12 pages, 553 KiB  
Article
APOBEC3A/B Polymorphism Is Not Associated with Human Papillomavirus Infection and Cervical Carcinogenesis
by Eliza Pizarro Castilha, Rafaela Roberta de Jaime Curti, Janaina Nicolau de Oliveira, Glauco Akelinghton Freire Vitiello, Roberta Losi Guembarovski, José d’Oliveira Couto-Filho and Karen Brajão de Oliveira
Pathogens 2023, 12(5), 636; https://doi.org/10.3390/pathogens12050636 - 23 Apr 2023
Cited by 1 | Viewed by 1050
Abstract
The persistence of a high-risk Human papillomavirus (HPV-HR) infection of the cervix results in different manifestations of lesions depending on the immunologic capacity of the host. Variations in apolipoprotein B mRNA editing enzyme catalytic polypeptide (APOBEC)-like genes, such as the APOBEC3A/B deletion hybrid [...] Read more.
The persistence of a high-risk Human papillomavirus (HPV-HR) infection of the cervix results in different manifestations of lesions depending on the immunologic capacity of the host. Variations in apolipoprotein B mRNA editing enzyme catalytic polypeptide (APOBEC)-like genes, such as the APOBEC3A/B deletion hybrid polymorphism (A3A/B), may contribute to cervical malignancy in the presence of HPV. The aim of this study was to investigate the association between the A3A/B polymorphism and HPV infection and the development of cervical intraepithelial lesions and cervical cancer in Brazilian women. The study enrolled 369 women, who were categorized according to the presence of infection and subdivided according to the degree of intraepithelial lesion and cervical cancer. APOBEC3A/B was genotyped by allele-specific polymerase chain reaction (PCR). As for the A3A/B polymorphism, the distribution of genotypes was similar between groups and among the analyzed subgroups. There were no significant differences in the presence of infection or development of lesions, even after exclusion of confounding factors. This is the first study to show that the A3A/B polymorphism is not associated with HPV infection and the development of intraepithelial lesions and cervical cancer in Brazilian women. Full article
(This article belongs to the Special Issue Oncoviruses and Molecular Mechanisms of Viral Carcinogenesis)
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Review

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20 pages, 1888 KiB  
Review
Hepatitis Delta Virus and Hepatocellular Carcinoma
by Daniele Lombardo, Maria Stella Franzè, Giuseppe Caminiti and Teresa Pollicino
Pathogens 2024, 13(5), 362; https://doi.org/10.3390/pathogens13050362 - 27 Apr 2024
Viewed by 238
Abstract
The hepatitis D virus (HDV) is a compact, enveloped, circular RNA virus that relies on hepatitis B virus (HBV) envelope proteins to initiate a primary infection in hepatocytes, assemble, and secrete new virions. Globally, HDV infection affects an estimated 12 million to 72 [...] Read more.
The hepatitis D virus (HDV) is a compact, enveloped, circular RNA virus that relies on hepatitis B virus (HBV) envelope proteins to initiate a primary infection in hepatocytes, assemble, and secrete new virions. Globally, HDV infection affects an estimated 12 million to 72 million people, carrying a significantly elevated risk of developing cirrhosis, liver failure, and hepatocellular carcinoma (HCC) compared to an HBV mono-infection. Furthermore, HDV-associated HCC often manifests at a younger age and exhibits more aggressive characteristics. The intricate mechanisms driving the synergistic carcinogenicity of the HDV and HBV are not fully elucidated but are believed to involve chronic inflammation, immune dysregulation, and the direct oncogenic effects of the HDV. Indeed, recent data highlight that the molecular profile of HCC associated with HDV is unique and distinct from that of HBV-induced HCC. However, the question of whether the HDV is an oncogenic virus remains unanswered. In this review, we comprehensively examined several crucial aspects of the HDV, encompassing its epidemiology, molecular biology, immunology, and the associated risks of liver disease progression and HCC development. Full article
(This article belongs to the Special Issue Oncoviruses and Molecular Mechanisms of Viral Carcinogenesis)
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