Host Defense, Viruses and Cell Death Pathways

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 437

Special Issue Editor


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Guest Editor
CYROI Technological Platform, Mixed Unit for Infectious Processes in Tropical Island Environments, University of Réunion, Réunion, France
Interests: viruses–human host cell interactions and pathogenicity; host cell defenses to infection (cell death, autophagy, stresses, and innate immunity)
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Special Issue Information

Dear Colleagues,

Over the last few decades, marked by the coronavirus, HIV, and Dengue pandemics, among others, despite rapid advances in our knowledge of host–virus interactions and host defense mechanisms, viruses have continued to threaten global health. The scientific community is working hard to identify ways of limiting the spread of emerging viruses and develop antiviral treatments and vaccines. Therefore, it is increasingly important to better understand cell-level host responses and their manipulation by viruses in order to consider the best control strategies. Among these responses, cell suicide is a common pathway chosen by infected cells: indeed, apoptosis and other forms of cell death, such as programmed necrosis and pyroptosis, serve to limit pathogen replication in infected cells, simultaneously promoting the inflammatory and innate responses which shape effective long-term host immunity. Viruses have developed multiple strategies to modify cell death pathways to their advantage, not always by limiting them. The complete resolution of infection, disease pathogenesis and progression, and the possible persistence of viruses are largely due to the latter’s ability to deal with cell death pathways. At the same time, the discovery that viruses have a tropism influenced by the cellular metabolism and, therefore, a liking for tumor cells makes them oncolytic tools capable of inducing targeted cell death.

This Special Issue will present original research papers and review articles that provide an overview of the latest findings on host defense mechanisms to viral infections involving cell death. Understanding the viral control of cell fate remains a highly topical subject, providing inspiration for the development of new therapeutic strategies. Particular attention will be given to studies identifying the fine-tuning mechanisms by which viruses or viral factors can induce targeted cell death and those enhancing our understanding of certain viruses’ potential to become therapeutic weapons.

Dr. Pascale Krejbich-Trotot
Guest Editor

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Keywords

  • virus–host
  • programmed cell death
  • apoptosis
  • necroptosis
  • pyroptosis
  • viral factors and cell death effector interplay
  • oncolytic

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Published Papers (1 paper)

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Research

14 pages, 2160 KiB  
Article
Dengue Viral Infection Induces Alteration of CD95 Expression in B Cell Subsets with Potential Involvement of Dengue Viral Non-Structural Protein 1
by Siyu Wang, Premrutai Thitilertdecha, Ladawan Khowawisetsut, Theeraporn Maneesawat, Ampaiwan Chuansumrit, Kulkanya Chokephaibulkit, Kovit Pattanapanyasat and Nattawat Onlamoon
Viruses 2025, 17(4), 541; https://doi.org/10.3390/v17040541 - 8 Apr 2025
Viewed by 274
Abstract
Little is known about the regulation of B cell subpopulations in association with programmed cell death during dengue virus (DENV) infection. Therefore, blood samples from dengue-infected patients and healthy donors were obtained for B cell subset characterization and the analysis of pro-apoptotic CD95 [...] Read more.
Little is known about the regulation of B cell subpopulations in association with programmed cell death during dengue virus (DENV) infection. Therefore, blood samples from dengue-infected patients and healthy donors were obtained for B cell subset characterization and the analysis of pro-apoptotic CD95 expression in these cell subsets. The results showed that the activated memory (AM) subset in the patients remained unchanged compared to the healthy donors. In contrast, tissue memory (TM) and antibody-secreting cells (ASCs) were notably increased, whereas naïve cells and resting memory (RM) cells were considerably decreased. Although the ASCs maintained comparably high levels of CD95 expression in both groups, significantly increased percentages of CD95-expressing cells in the other B cell subsets were found in the patients. When B cells from the healthy donors were treated with DENV non-structural protein 1 (NS1), the results showed that the NS1 protein at 2 µg/mL could induce CD95 expression and the exposure of phosphatidylserine on the cell membrane in most B cell subsets, except for the RM. This study demonstrates that DENV infection could induce CD95 expression in both activated and resting B cell subsets in all patients. The results also suggest a potential mechanism of apoptotic regulation in B cell subsets through the increased CD95 expression caused by the interaction between the B cells and the NS1 protein. Full article
(This article belongs to the Special Issue Host Defense, Viruses and Cell Death Pathways)
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