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Biomolecules
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Recent Advances in Retroviruses and Endogenous Retroviruses (ERVs) in Mammalian...
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Recent Advances in Retroviruses and Endogenous Retroviruses (ERVs) in Mammalian Placenta and Beyond 2025

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Nucleic Acids".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 782

Special Issue Editors

Prof. Dr. Kazuhiko Imakawa

E-Mail Website
Guest Editor
Research Institute of Agriculture, Tokai University, Tokyo, Japan
Interests: genetics; molecular biology; mammalian evolution; implantation/placentation; reproduction
Special Issues, Collections and Topics in MDPI journals
Dr. Jun Sugimoto

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Hiroshima University, Hiroshima, Japan
Interests: suppressyn; trophoblast; cell fusion; HERV
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Retroviruses are well known for their ability to alter host cellular functions via integration into the host genome, which can lead to diseases such as cancer and immune disorders. While the pathogenic consequences of retroviral infection have been extensively studied, retroviral sequences that have become endogenized throughout evolution are increasingly recognized for their pivotal roles in host development and physiology. For instance, endogenous retroviral elements have been co-opted to support essential functions such as placental development in mammals. This dual nature of retroviruses—both as agents of disease and as contributors to evolutionary advantage—provides a compelling framework for understanding the dynamic interplay between viruses and their hosts. A more comprehensive understanding of how retroviruses shape both pathology and evolution could yield novel insights into gene regulation, immune function, and developmental biology. This Special Issue aims to highlight recent advances in retrovirus research, and we invite the submission of original research articles and reviews that explore both endogenous and exogenous retroviruses.

Prof. Dr. Kazuhiko Imakawa
Dr. Jun Sugimoto
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. Biomolecules 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

  • retroviruses
  • ERVs (endogenous retroviruses)
  • placental diversity
  • organ development (stem cells)
  • immunoregulation

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Published Papers (1 paper)

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Research

13 pages, 1988 KB  
Article
Genetic Diversity in the Suppressyn Gene Sequence: From Polymorphisms to Loss-of-Function Mutations
by Jun Sugimoto, Danny J. Schust, Takeshi Nagamatsu, Yoshihiro Jinno and Yoshiki Kudo
Biomolecules 2025, 15(7), 1051; https://doi.org/10.3390/biom15071051 - 21 Jul 2025
Viewed by 538
Abstract
The suppressive regulator of cell fusion, suppressyn, is specifically expressed in the human placenta and is thought to play a crucial role in trophoblast fusion or syncytialization. Previous studies have suggested that alterations in its expression are associated with aberrant placental development, [...] Read more.
The suppressive regulator of cell fusion, suppressyn, is specifically expressed in the human placenta and is thought to play a crucial role in trophoblast fusion or syncytialization. Previous studies have suggested that alterations in its expression are associated with aberrant placental development, such as the immature placental morphology observed in Down syndrome, and may contribute to the pathogenesis of fetal growth restriction. While syncytialization in trophoblasts is an essential process for normal placental development, the precise molecular causes of its dysregulation remain poorly understood. In the present study, we aimed to elucidate the potential contribution of genomic variation to the loss of suppressyn function, extending previous analyses of expression abnormalities in perinatal disorders. Through sequence analysis, (1) we identified six polymorphisms within the coding region of the suppressyn gene, and (2) discovered that certain deletions and specific amino acid substitutions result in a complete loss of suppressyn-mediated inhibition of cell fusion. Although these mutations have not yet been reported in disease-associated genomic databases, our findings suggest that comprehensive genomic studies of perinatal and other disorders may reveal pathogenic variants of suppressyn, thereby uncovering novel genetic contributions to placental dysfunction. It is also anticipated that these findings might direct the development of therapeutic strategies targeting loss-of-function mutations. Full article
(This article belongs to the Special Issue Recent Advances in Retroviruses and Endogenous Retroviruses (ERVs) in Mammalian Placenta and Beyond 2025)
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