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Viruses
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Viruses 2026—New Horizons in Virology
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Viruses 2026—New Horizons in Virology

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

Deadline for manuscript submissions: 1 October 2026 | Viewed by 4011

Editors

Dr. Eric O. Freed

E-Mail Website
Guest Editor
HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA
Interests: HIV dynamics and replication
Special Issues, Collections and Topics in MDPI journals
Dr. Albert Bosch

E-Mail Website
Guest Editor
Enteric Virus Laboratory, Section Microbiology, Virology and Biotechnology, Department of Genetics, Microbiology and Statistics, School of Biology, Avda. Diagonal 643, 08028 Barcelona, Spain
Interests: hepatitis A virus; astrovirus; enteroviruses, norovirus; rotavirus; gastroenteritis agents; enteric hepatitis agents, wastewater-based epidemiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to the conference, “Viruses 2026—New Horizons in Virology”, which will be held in Barcelona, Spain, 11–13 March 2026.

We are constantly reminded of the critical importance of virology research as new viral outbreaks impact people, animals, and plants worldwide. This conference aims to bring together international researchers studying various topics related to viral replication, pathogenesis, structure, immunology, epidemiology, public health, and other areas of virology.

Since the first edition of the conference, Viruses 2016, was held in Basel, followed by editions every two years in Barcelona (2018, 2020, and 2024) and online (2022), the Viruses conference series has clearly established itself as the premier forum for dedicated discussions on all aspects of virology research.

All editions of the Viruses conference series are characterized by the high quality of presentations. Hence, we are pleased to announce the publication of a Special Issue, in Viruses, featuring original manuscripts from abstract presenters and invited speakers.

We are very excited to promote this Special Issue and we look forward to your participation!

References

  1. Viruses 2016: https://sciforum.net/event/viruses-2016
  2. Viruses 2018: https://sciforum.net/event/Viruses-2018
  3. Viruses 2020: https://sciforum.net/event/viruses2020
  4. Viruses 2022: https://sciforum.net/event/viruses2022
  5. Viruses 2024: https://sciforum.net/event/viruses2024

Dr. Eric O. Freed
Dr. Albert Bosch
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • virus
  • replication
  • assembly
  • pathogenesis
  • outbreak
  • molecular biology
  • cell biology
  • public health
  • structural biology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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22 pages, 22383 KB  
Article
Non-Polio Enterovirus A71 and D68 Infection of Human Neuromuscular Organoids Reveals Distinct Mechanisms of Neuromuscular Impairment
by Amber J. Schotting, Inés García-Rodríguez, Eline Freeze, Anoop T. Ambikan, Michael Wagner, Mira Mioch, Aymeric P. Y. L. Moffelein, William Jackson, Dasja Pajkrt, Katja C. Wolthers, Renata Vieira de Sá and Adithya Sridhar
Viruses 2026, 18(8), 853; https://doi.org/10.3390/v18080853 - 4 Aug 2026
Viewed by 384
Abstract
Enterovirus A71 (EV-A71) and enterovirus D68 (EV-D68) are recognised as causative agents of severe neurological complications, including acute flaccid myelitis (AFM). However, the molecular mechanisms underlying the neurovirulence and effects on neuromuscular integrity remain poorly understood. Here, we employed human induced pluripotent stem [...] Read more.
Enterovirus A71 (EV-A71) and enterovirus D68 (EV-D68) are recognised as causative agents of severe neurological complications, including acute flaccid myelitis (AFM). However, the molecular mechanisms underlying the neurovirulence and effects on neuromuscular integrity remain poorly understood. Here, we employed human induced pluripotent stem cell-derived neuromuscular organoids (NMOs) to investigate the cellular tropism and pathogenic effects of EV-A71 and EV-D68 in a human-relevant context. Both viruses infected neuronal populations within NMOs, with EV-A71 exhibiting higher levels of viral replication than EV-D68. Transcriptomic analysis revealed downregulation of neuronal and muscular gene networks following infection. EV-A71 preferentially suppressed neuronal pathways, while both viruses exerted comparable effects on muscle-associated gene expression. These transcriptional changes highlighted alterations in pathways governing neuronal and muscle function and communication, prompting examination of synaptic vesicle machinery components. At the protein level, both viruses were associated with sporadic cleavage of the neuronal SNARE protein synaptosomal-associated protein 25 (SNAP25). In addition, infection with either virus increased cleaved caspase-3 levels, consistent with activation of apoptotic signalling. Together, these findings indicate virus-specific downstream effects and establish NMOs as a robust platform for dissecting enterovirus–host interactions relevant to AFM. Full article
(This article belongs to the Special Issue Viruses 2026—New Horizons in Virology)
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16 pages, 1938 KB  
Article
The Innate Antiviral Factors APOBEC3G and APOBEC3H Interact with the Nucleocapsids of Human Coronaviruses in an RNA-Dependent Manner
by Jordi Exposito Trivino, Alexandra Decloux, Margaux Renier, Théo Massart, Justine Petit, Maxence Collard, Kévin Willemart, Aurélien Sellier, Rodrigue Tesse, Samuel Kindylides, Jean-Claude Twizere, Charles Nicaise, Lionel Tafforeau and Nicolas A. Gillet
Viruses 2026, 18(8), 830; https://doi.org/10.3390/v18080830 - 28 Jul 2026
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Abstract
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) evolution has been marked by the rapid accumulation of mutations, among which cytosine-to-uracil (C-to-U) transitions represent a major proportion of observed genomic changes. These mutations have been proposed to result from the activity of host APOBEC3 [...] Read more.
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) evolution has been marked by the rapid accumulation of mutations, among which cytosine-to-uracil (C-to-U) transitions represent a major proportion of observed genomic changes. These mutations have been proposed to result from the activity of host APOBEC3 cytidine deaminases, innate immune enzymes capable of editing viral RNA. However, the molecular mechanisms underlying APOBEC3 involvement in SARS-CoV-2 biology remain poorly understood. Here, we systematically investigated physical interactions between APOBEC family members and the SARS-CoV-2 proteins using a Gaussia princeps protein complementation assay. Screening of APOBEC family proteins against the viral proteome identified specific interactions between APOBEC3G (A3G) and APOBEC3H (A3H) with the viral nucleocapsid (N) protein. These interactions were validated by co-immunoprecipitation and were found to be conserved across nucleocapsid proteins from all seven human coronaviruses, suggesting conserved structural determinants. Mechanistic analyses revealed that the RNA-binding and oligomerization capacities of A3G and A3H are key for their interaction with the SARS-CoV-2 nucleocapsid. Mapping experiments further showed that the C-terminal domain of N constitutes the minimal interacting region, with stronger binding observed in larger constructs encompassing adjacent regions, indicating cooperative stabilization. Further work will be needed to determine whether A3G and/or A3H can restrict viral replication and whether their interaction with the nucleocapsid allows them to access and mutate the viral genome. Full article
(This article belongs to the Special Issue Viruses 2026—New Horizons in Virology)
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Review

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31 pages, 4716 KB  
Review
Retrovirus-Induced Immunosuppression: Role of the Transmembrane Envelope Protein
by Joachim Denner
Viruses 2026, 18(7), 740; https://doi.org/10.3390/v18070740 - 3 Jul 2026
Viewed by 916
Abstract
Retroviruses induce immunosuppression in their infected hosts. This phenomenon is well described for the immunodeficiency viruses, with human immunodeficiency virus type 1 (HIV-1) representing the best-studied example, but it also occurs in other retroviral infections. Immunosuppressive properties were first characterized in murine leukemia [...] Read more.
Retroviruses induce immunosuppression in their infected hosts. This phenomenon is well described for the immunodeficiency viruses, with human immunodeficiency virus type 1 (HIV-1) representing the best-studied example, but it also occurs in other retroviral infections. Immunosuppressive properties were first characterized in murine leukemia viruses (MuLV). Additional well-studied examples include feline leukemia virus (FeLV) and koala retrovirus (KoRV). Investigations into the mechanisms underlying retrovirus-induced immunosuppression revealed that not only inactivated viral particles but also their purified transmembrane (TM) envelope proteins exhibit immunosuppressive activity. However, in certain retroviral infections, additional viral proteins contribute to the immunosuppression in vivo. Within the TM envelope proteins, a highly conserved region—designated the immunosuppressive (isu) domain—was identified. Synthetic peptides corresponding to this domain suppress a wide range of in vitro immune responses, possibly by regulating Ras-Raf-MEK-MAPK and PI3K-AKT-mTOR pathways. They modulate cytokine release and alter gene expression in immune cells, mirroring the activity of the corresponding TM envelope protein. Mutations in the sequence abrogate the effect. Numerous TM envelope proteins have demonstrated immunosuppressive activity in vivo in a tumor rejection model, and mutations within the isu domain also abrogate this function. These studies have important implications for reproduction, particularly through the immunosuppressive syncytins in the placenta, for tumor development, where similar mechanisms may protect cancer cells from the host immune system, and for vaccine development and xenotransplantation. Notably, immunization with TM envelope proteins carrying mutations in the isu domain elicits stronger immune responses compared with the wild-type proteins. Finally, the potential of retroviral TM envelope proteins to protect xenotransplants from immune rejection will be discussed. Full article
(This article belongs to the Special Issue Viruses 2026—New Horizons in Virology)
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