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Viruses
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Virus-Induced Syncytia
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Virus-Induced Syncytia

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (1 May 2022) | Viewed by 16020

Special Issue Editors

Dr. Markus Thali

E-Mail Website
Guest Editor
Microbiology and Molecular Genetics Department, University of Vermont, Stafford Hall, Room 320, Burlington, VT 05405, USA
Interests: HIV/retrovirus transmission and spread; virus-induced cell-cell fusion; syncytia; virus-host interactions; various quantitative imaging methods; viruses as overall positive biological entities
Special Issues, Collections and Topics in MDPI journals
Dr. Stefan Oliver

E-Mail Website1 Website2
Guest Editor
Department of Pediatrics, Stanford University School of Medicine, Grant Building Rm S366, 300 Pasteur Drive, Stanford, CA 94305, USA
Interests: varicella-zoster virus; fusion; glycoprotein; cell-cell fusion; pathogenesis; evolution; structural biology and cryo-EM

Special Issue Information

Dear Colleagues, 

Virus-induced cell-cell fusion, the formation of multinucleated cells, i.e. syncytia, often gets dismissed as a mere cytopathic effect (CPE) in cultured cells. However, it is becoming increasingly clear that syncytia can be much more than short-lived byproducts of virus-induced membrane fusion. Syncytia can enable unhindered transfer of viral genomes to neighboring cells, thus allowing for speedy viral spread. In vivo, syncytia also allow viruses to partially evade host defense mechanisms, including humoral immune responses as well as restriction factors that target assembly and the release of viral particles, or, their entry into target cells. Together, these features might allow syncytia to contribute significantly to virus propagation and dissemination. Critically, for some viruses, the formation of multinucleated cells in vivo contributes to pathogenesis. While distinct roles for syncytia induced by viruses (including SARS-CoV-2) remain to be demonstrated, recent studies have revealed that fusion alone of cells can lead to reprogramming/differentiation; thus, virus-induced syncytia are likely endowed with unique properties that distinguish them from infected mononucleated cells.

This special issue aims to cover recent developments in our understanding of how syncytia influence the etiology of virus propagation and their contributions to pathogenesis. We also welcome submissions reporting on other aspects of virus-induced syncytia, including, for example, their role in normal healthy development such as placenta formation with respect to endogenous retroviruses, or the therapeutic use of viral fusogens in oncology. It is our vision that this Special Issue will serve as a forum not only for regular research papers or “traditional” reviews but that some of the contributions will propose new ideas about the biological significance of virus-induced syncytia, or indeed about syncytia per se. We are delighted to announce that two eminent researchers have already committed to contributing articles for this Special Issue: Kathryn Holmes will write a review on how coronavirus-induced syncytia might contribute to virus spread, while Jennifer Lippincott-Schwartz along with Carolyn Ott will follow up on their recent study with which they documented that mere fusion of cells (induced by a viral fusogen, but without involvement of other viral components) can lead to cellular reprogramming. We are excited about these contributions and trust that they will lay a strong foundation for what we hope will be a forum to stimulate conversation within the syncytia community and beyond.

Markus Thali
Stefan Oliver
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.

Keywords

  • syncytia
  • cell-cell fusion
  • virus spread
  • pathogenesis

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Published Papers (4 papers)

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Research

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29 pages, 19936 KiB  
Article
Proline–Proline Dyad in the Fusion Peptide of the Murine β–Coronavirus Spike Protein’s S2 Domain Modulates Its Neuroglial Tropism
by Abass Alao Safiriyu, Vaishali Mulchandani, Mohammed Nahaf Anakkacheri, Debnath Pal and Jayasri Das Sarma
Viruses 2023, 15(1), 215; https://doi.org/10.3390/v15010215 - 12 Jan 2023
Cited by 2 | Viewed by 2321
Abstract
The β-Coronavirus mouse hepatitis virus (MHV-A59)-RSA59 has a patent stretch of fusion peptide (FP) containing two consecutive central prolines (PP) in the S2 domain of the Spike protein. Our previous studies compared the PP-containing fusogenic-demyelinating strain RSA59(PP) to its one proline-deleted mutant strain [...] Read more.
The β-Coronavirus mouse hepatitis virus (MHV-A59)-RSA59 has a patent stretch of fusion peptide (FP) containing two consecutive central prolines (PP) in the S2 domain of the Spike protein. Our previous studies compared the PP-containing fusogenic-demyelinating strain RSA59(PP) to its one proline-deleted mutant strain RSA59(P) and one proline-containing non-fusogenic non-demyelinating parental strain RSMHV2(P) to its one proline inserted mutant strain RSMHV2(PP). These studies highlighted the crucial role of PP in fusogenicity, hepato-neuropathogenesis, and demyelination. Computational studies combined with biophysical data indicate that PP at the center of the FP provides local rigidity while imparting global fluctuation to the Spike protein that enhances the fusogenic properties of RSA59(PP) and RSMHV2(PP). To elaborate on the understanding of the role of PP in the FP of MHV, the differential neuroglial tropism of the PP and P mutant strains was investigated. Comparative studies demonstrated that PP significantly enhances the viral tropism for neurons, microglia, and oligodendrocytes. PP, however, is not essential for viral tropism for either astroglial or oligodendroglial precursors or the infection of meningeal fibroblasts in the blood–brain and blood–CSF barriers. PP in the fusion domain is critical for promoting gliopathy, making it a potential region for designing antivirals for neuro-COVID therapy. Full article
(This article belongs to the Special Issue Virus-Induced Syncytia)
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17 pages, 12639 KiB  
Article
Reduction of Cell Fusion by Deletion in the Hypervariable Region of the Spike Protein of Mouse Hepatitis Virus
by Nipuna Tennakoon, Jihoon Ryu, Makoto Ujike, Fumihiro Taguchi and Hyun-Jin Shin
Viruses 2022, 14(2), 398; https://doi.org/10.3390/v14020398 - 15 Feb 2022
Cited by 1 | Viewed by 2257
Abstract
Deletions in the spike gene of mouse hepatitis virus (MHV) produce several variants with diverse biological characteristics, highlighting the significance of the spike gene in viral pathogenesis. In this study, we characterized the JHM-X strain, which has a deletion in the hypervariable region [...] Read more.
Deletions in the spike gene of mouse hepatitis virus (MHV) produce several variants with diverse biological characteristics, highlighting the significance of the spike gene in viral pathogenesis. In this study, we characterized the JHM-X strain, which has a deletion in the hypervariable region (HVR) of the spike gene, compared with the cl-2 strain, which has a full spike gene. Cytopathic effects (CPEs) induced by the two strains revealed that the size of the CPE produced by cl-2 is much greater than that produced by JHM-X in delayed brain tumor (DBT) cells. Thus, this finding explains the greater fusion activity of cl-2 than JHM-X in cultured cells, and we speculate that the deletion region of the spike protein is involved in the fusion activity differences. In contrast with the fusion activity, a comparison of the virus growth kinetics revealed that the titer of JHM-X was approximately 100 times higher than that of cl-2. We found that the deletion region of the spike protein was involved in fusion activity differences, whereas cl-2 produced significantly higher luciferase activity than JHM-X upon similar expression levels of the spike protein. However, the reason behind the growth difference is still unknown. Overall, we discovered that deletion in the HVR of the spike gene could be involved in the fusion activity differences between the two strains. Full article
(This article belongs to the Special Issue Virus-Induced Syncytia)
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15 pages, 2803 KiB  
Article
Human Cytomegalovirus Replication and Infection-Induced Syncytia Formation in Labial, Foreskin, and Fetal Lung Fibroblasts
by Alexis Aguiar, Melissa Galinato, Maite’ Bradley Silva, Bryant Toth, Michael A. McVoy and Laura Hertel
Viruses 2021, 13(12), 2355; https://doi.org/10.3390/v13122355 - 24 Nov 2021
Cited by 5 | Viewed by 2641
Abstract
Only a handful of cell types, including fibroblasts, epithelial, and endothelial cells, can support human cytomegalovirus (CMV) replication in vitro, in striking contrast to the situation in vivo. While the susceptibility of epithelial and endothelial cells to CMV infection is strongly modulated by [...] Read more.
Only a handful of cell types, including fibroblasts, epithelial, and endothelial cells, can support human cytomegalovirus (CMV) replication in vitro, in striking contrast to the situation in vivo. While the susceptibility of epithelial and endothelial cells to CMV infection is strongly modulated by their anatomical site of origin, multiple CMV strains have been successfully isolated and propagated on fibroblasts derived from different organs. As oral mucosal cells are likely involved in CMV acquisition, we sought to evaluate the ability of infant labial fibroblasts to support CMV replication, compared to that of commonly used foreskin and fetal lung fibroblasts. No differences were found in the proportion of cells initiating infection, or in the amounts of viral progeny produced after exposure to the fibroblast-adapted CMV strain AD169 or to the endothelial cell-adapted strain TB40/E. Syncytia formation was, however, significantly enhanced in infected labial and lung fibroblasts compared to foreskin-derived cells, and did not occur after infection with AD169. Together, these data indicate that fibroblast populations derived from different tissues are uniformly permissive to CMV infection but retain phenotypic differences of potential importance for infection-induced cell–cell fusion, and ensuing viral spread and pathogenesis in different organs. Full article
(This article belongs to the Special Issue Virus-Induced Syncytia)
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Review

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19 pages, 15747 KiB  
Review
Cell Fusion and Syncytium Formation in Betaherpesvirus Infection
by Jiajia Tang, Giada Frascaroli, Xuan Zhou, Jan Knickmann and Wolfram Brune
Viruses 2021, 13(10), 1973; https://doi.org/10.3390/v13101973 - 30 Sep 2021
Cited by 11 | Viewed by 4490
Abstract
Cell–cell fusion is a fundamental and complex process that occurs during reproduction, organ and tissue growth, cancer metastasis, immune response, and infection. All enveloped viruses express one or more proteins that drive the fusion of the viral envelope with cellular membranes. The same [...] Read more.
Cell–cell fusion is a fundamental and complex process that occurs during reproduction, organ and tissue growth, cancer metastasis, immune response, and infection. All enveloped viruses express one or more proteins that drive the fusion of the viral envelope with cellular membranes. The same proteins can mediate the fusion of the plasma membranes of adjacent cells, leading to the formation of multinucleated syncytia. While cell–cell fusion triggered by alpha- and gammaherpesviruses is well-studied, much less is known about the fusogenic potential of betaherpesviruses such as human cytomegalovirus (HCMV) and human herpesviruses 6 and 7 (HHV-6 and HHV-7). These are slow-growing viruses that are highly prevalent in the human population and associated with several diseases, particularly in individuals with an immature or impaired immune system such as fetuses and transplant recipients. While HHV-6 and HHV-7 are strictly lymphotropic, HCMV infects a very broad range of cell types including epithelial, endothelial, mesenchymal, and myeloid cells. Syncytia have been observed occasionally for all three betaherpesviruses, both during in vitro and in vivo infection. Since cell–cell fusion may allow efficient spread to neighboring cells without exposure to neutralizing antibodies and other host immune factors, viral-induced syncytia may be important for viral dissemination, long-term persistence, and pathogenicity. In this review, we provide an overview of the viral and cellular factors and mechanisms identified so far in the process of cell–cell fusion induced by betaherpesviruses and discuss the possible consequences for cellular dysfunction and pathogenesis. Full article
(This article belongs to the Special Issue Virus-Induced Syncytia)
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