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Viruses
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Understanding the Oncogenesis of Human Herpesviruses through Their Critical Comparisons
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Understanding the Oncogenesis of Human Herpesviruses through Their Critical Comparisons

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

Deadline for manuscript submissions: 25 April 2025 | Viewed by 2459

Special Issue Editors

Dr. Ya-Fang Chiu

E-Mail Website
Guest Editor
School of Medicine, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
Interests: oncogenic viruses
Prof. Dr. Bill Sugden

E-Mail Website
Guest Editor
McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53705, USA
Interests: EBV-associated tumors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Two human herpesviruses, Epstein–Barr virus (EBV) and Kaposi’s sarcoma herpesvirus (KSHV), cause lymphomas, carcinomas, and sarcomas in people. These viruses were discovered in 1964 and 1994 and have been studied intensively since then. We are assembling, under the auspices of Viruses, a collection of reviews to address these studies creatively. We propose to compare and contrast how these two tumor viruses together contribute to oncogenesis. We plan for each review to cover a given topic for both EBV and KSHV, a creative combination, which is yet to be carried out systematically.

We envision three topics to consider the facets of the life-cycles of EBV and KSHV that underpin their normal infections in people. These topics provide a background for considering the rare events that lead to tumorigenesis. These are as follows:

  1. What are the latent reservoirs of EBV and KSHV?
  2. How do EBV and KSHV persist in vivo and avoid their productive infections killing cells that may evolve into tumors?
  3. How do EBV and KSHV benefit from their plasmid replicons?

With these topics as a foundation, we envision five more to describe oncogenesis mediated by EBV and KSHV. They include the following:

  1. How do cells infected with EBV and KSHV escape being killed by their host's immune responses?
  2. How do EBV and KSHV suppress tumor suppressors?
  3. How do EBV and KSHV mediate lymphomagenesis in BL, DLBCL, and PEL?
  4. How do EBV and KSHV mediate the development of carcinomas and sarcomas?
  5. How will vaccines protect against herpesvirus oncogenesis?

We expect that these eight topics will illuminate the oncogenesis of both EBV and KSHV by comparing and contrasting their life-cycles and their transforming properties. Scientists or teams with expertise in both of these human tumor viruses might consider contributing to this ensemble, reflecting 90 years of combined research on EBV and KSHV. 

Dr. Ya-Fang Chiu
Prof. Dr. Bill Sugden
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.

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Published Papers (2 papers)

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Review

16 pages, 720 KiB  
Review
How Epstein Barr Virus Causes Lymphomas
by Ya-Fang Chiu, Khongpon Ponlachantra and Bill Sugden
Viruses 2024, 16(11), 1744; https://doi.org/10.3390/v16111744 - 6 Nov 2024
Viewed by 668
Abstract
Since Epstein–Barr Virus (EBV) was isolated 60 years ago, it has been studied clinically, epidemiologically, immunologically, and molecularly in the ensuing years. These combined studies allow a broad mechanistic understanding of how this ubiquitous human pathogen which infects more than 90% of adults [...] Read more.
Since Epstein–Barr Virus (EBV) was isolated 60 years ago, it has been studied clinically, epidemiologically, immunologically, and molecularly in the ensuing years. These combined studies allow a broad mechanistic understanding of how this ubiquitous human pathogen which infects more than 90% of adults can rarely cause multiple types of lymphomas. We survey these findings to provide a coherent description of its oncogenesis. Full article
(This article belongs to the Special Issue Understanding the Oncogenesis of Human Herpesviruses through Their Critical Comparisons)
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16 pages, 1085 KiB  
Review
Ubiquitin-Mediated Effects on Oncogenesis during EBV and KSHV Infection
by Rachel Mund and Christopher B. Whitehurst
Viruses 2024, 16(10), 1523; https://doi.org/10.3390/v16101523 - 26 Sep 2024
Viewed by 872
Abstract
The Herpesviridae include the Epstein–Barr Virus (EBV) and the Kaposi Sarcoma-associated Herpesvirus (KSHV), both of which are oncogenic gamma-herpesviruses. These viruses manipulate host cellular mechanisms, including through ubiquitin-mediated pathways, to promote viral replication and oncogenesis. Ubiquitin, a regulatory protein which tags substrates for [...] Read more.
The Herpesviridae include the Epstein–Barr Virus (EBV) and the Kaposi Sarcoma-associated Herpesvirus (KSHV), both of which are oncogenic gamma-herpesviruses. These viruses manipulate host cellular mechanisms, including through ubiquitin-mediated pathways, to promote viral replication and oncogenesis. Ubiquitin, a regulatory protein which tags substrates for degradation or alters their function, is manipulated by both EBV and KSHV to facilitate viral persistence and cancer development. EBV infects approximately 90% of the global population and is implicated in malignancies including Burkitt lymphoma (BL), Hodgkin lymphoma (HL), post-transplant lymphoproliferative disorder (PTLD), and nasopharyngeal carcinoma. EBV latency proteins, notably LMP1 and EBNA3C, use ubiquitin-mediated mechanisms to inhibit apoptosis, promote cell proliferation, and interfere with DNA repair, contributing to tumorigenesis. EBV’s lytic proteins, including BZLF1 and BPLF1, further disrupt cellular processes to favor oncogenesis. Similarly, KSHV, a causative agent of Kaposi’s Sarcoma and lymphoproliferative disorders, has a latency-associated nuclear antigen (LANA) and other latency proteins that manipulate ubiquitin pathways to degrade tumor suppressors, stabilize oncogenic proteins, and evade immune responses. KSHV’s lytic cycle proteins, such as RTA and Orf64, also use ubiquitin-mediated strategies to impair immune functions and promote oncogenesis. This review explores the ubiquitin-mediated interactions of EBV and KSHV proteins, elucidating their roles in viral oncogenesis. Understanding these mechanisms offers insights into the similarities between the viruses, as well as provoking thought about potential therapeutic targets for herpesvirus-associated cancers. Full article
(This article belongs to the Special Issue Understanding the Oncogenesis of Human Herpesviruses through Their Critical Comparisons)
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