Special Issue "KSHV-Host Stand-Off (or Interaction)"

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: 1 March 2021.

Special Issue Editor

Prof. Hye-ra Lee
Website
Guest Editor
Department of Biotechonology and Bioinformatics, Korea University, Sejong Campus, South Korea
Interests: cancer-associated pathogens; respiratory infection; innate immunity; post-translational modification; angiogenesis

Special Issue Information

Dear Colleagues,

Virus-associated cancers comprise approximately 15%–20% of all human tumors worldwide. It is the second most important risk factor for the development of cancer in humans, exceeded only by tobacco consumption. Herpesvirus represents the most ubiquitous pathogen in humans, and their infections are implicated in diverse malignancies. Human Kaposi’s-sarcoma-associated herpesvirus (KSHV) and Epstein–Barr virus (EBV) belong to gamma-2 herpesvirinae and are associated with tumors of lymphoid, epithelial, and endothelial origin in immune-compromised patients such as HIV/AIDS patients and organ transplant patients. Approximately 600,000 new cases of KSHV- and EBV-associated cancers are annually reported worldwide. Despite being a pressing human health problem, very little has been done thus far to develop therapeutic agents that specifically target these virus-associated diseases. Furthermore, the mechanisms that govern gamma-2 herpesvirus immunity and pathogenesis are poorly understood.

For this Special Issue of Pathogens, we aim to understand the molecular mechanisms deployed by gamma-2 herpesvirus to evade and survive the host’s immune responses as well as viral host interactions at the cellular level to reshape the cellular environment for their life cycle. Thereby, we welcome to invite you to submit either an original research article or an insightful review.

Prof. Hye-ra Lee
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 papers will be 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 1400 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

  • Kaposi’s-sarcoma-associated herpesvirus (KSHV)
  • Epstein–Barr virus (EBV)
  • gamma-2-herpesviruses-associated malignancies
  • evasion of immune responses
  • virus–host interaction
  • viral gene expression and replication

Published Papers (1 paper)

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Review

Open AccessReview
Kaposi’s Sarcoma-Associated Herpesvirus and Host Interaction by the Complement System
Pathogens 2020, 9(4), 260; https://doi.org/10.3390/pathogens9040260 - 03 Apr 2020
Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV) modulates the immune response to allow the virus to establish persistent infection in the host and facilitate the development of KSHV-associated cancer. The complement system has a central role in the defense against pathogens. Hence, KSHV has adopted an [...] Read more.
Kaposi’s sarcoma-associated herpesvirus (KSHV) modulates the immune response to allow the virus to establish persistent infection in the host and facilitate the development of KSHV-associated cancer. The complement system has a central role in the defense against pathogens. Hence, KSHV has adopted an evasion strategy for complement attack using the viral protein encoded by KSHV open reading frame 4. However, despite this defense mechanism, the complement system appears to become activated in KSHV-infected cells as well as in the region surrounding Kaposi’s sarcoma tumors. Given that the complement system can affect cell fate as well as the inflammatory microenvironment, complement activation is likely associated with KSHV pathogenesis. A better understanding of the interplay between KSHV and the complement system may, therefore, translate into the development of novel therapeutic interventions for KSHV-associated tumors. In this review, the mechanisms and functions of complement activation in KSHV-infected cells are discussed. Full article
(This article belongs to the Special Issue KSHV-Host Stand-Off (or Interaction))
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