Apoptosis and Necroptosis as Host Defense Strategies to Prevent Viral Infection

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

Deadline for manuscript submissions: 20 November 2024 | Viewed by 1755

Special Issue Editors


E-Mail Website
Guest Editor
Department of Biochemistry & Chemistry, La Trobe University, Kingsbury Drive, Melbourne 3086, Australia
Interests: apoptosis; structural biology; polarity; defensins
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601, Australia
Interests: apoptosis; virus-host interaction; structural biology; pox virus; bacteriophages

Special Issue Information

Dear Colleagues,

Apoptosis and necroptosis are powerful host defense mechanisms deployed by hosts against viral pathogens. Apoptosis plays a fundamental role in development, immune regulation, tissue homeostasis and viral pathogenesis. Dysregulation of apoptosis is associated with a wide variety of diseases, including immunological and developmental disorders, neurodegenerative disorders and cancer. In contrast, necroptosis is a lytic and highly inflammatory form of cell death with important antiviral functions.

Numerous viruses have evolved sophisticated immunomodulatory strategies to counter host-cell-innate and adaptive immune responses to viral infection. One such strategy is to prevent host-cell intracellular responses to infections such as host cell apoptosis to counter viral proliferation, with successful blockade of apoptosis allowing establishment of infection. This is often achieved via the expression of direct inhibitors against caspases and mimicry of cellular Bcl-2 proteins to inactivate host pro-apoptotic proteins and block host-cell-intrinsic apoptosis. However, blockade of the proteolytic activity of caspase-8, the initiator caspase of extrinsic apoptosis, greatly sensitizes cells to the induction of necroptosis. Proteins that contain receptor-interacting protein (RIP) homotypic interaction motifs (RHIMs) play central roles in necroptotic signaling. This Special Issue welcomes articles exploring viral–host interactions with an emphasis on biochemical signaling pathways such as apoptosis and necroptosis, subcellular compartmentalization, viral structural organization and cellular structure as it relates to viral infection in battling for control of host cell death checkpoints.

Prof. Dr. Marc Kvansakul
Dr. Chathura Suraweera
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

  • apoptosis
  • necroptosis
  • host defense
  • caspases

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 7923 KiB  
Article
Fas/FasL-Mediated Apoptosis and Inflammation Contribute to Recovery from HSV-2-Mediated Spinal Cord Infection
by Malgorzata Krzyzowska, Magdalena Patrycy, Marcin Chodkowski, Martyna Janicka, Andrzej Kowalczyk, Katarzyna Skulska, Karolina Thörn and Kristina Eriksson
Viruses 2024, 16(9), 1363; https://doi.org/10.3390/v16091363 - 26 Aug 2024
Viewed by 372
Abstract
Herpes simplex virus type 2 (HSV-2) is a sexually transmitted pathogen that causes a persistent infection in sensory ganglia. The infection manifests itself as genital herpes but in rare cases it can cause meningitis. In this study, we used a murine model of [...] Read more.
Herpes simplex virus type 2 (HSV-2) is a sexually transmitted pathogen that causes a persistent infection in sensory ganglia. The infection manifests itself as genital herpes but in rare cases it can cause meningitis. In this study, we used a murine model of HSV-2 meningitis to show that Fas and FasL are induced within the CNS upon HSV-2 infection, both on resident microglia and astrocytes and on infiltrating monocytes and lymphocytes. Mice lacking Fas or FasL had a more severe disease development with significantly higher morbidity, mortality, and an overall higher CNS viral load. In parallel, these Fas/FasL-deficient mice showed a severely impaired infection-induced CNS inflammatory response with lower levels of infiltrating CD4+ T-cells, lower levels of Th1 cytokines and chemokines, and a shift in the balance between M1 and M2 microglia/monocytes. In vitro, we confirmed that Fas and FasL is required for the induction of leucocyte apoptosis, but also show that the Fas/FasL pathway is required for adequate cytokine and chemokine production by glial cells. In summary, our data show that the Fas/FasL cell death receptor pathway is an important defense mechanism in the spinal cord as it down-regulates HSV-2-induced inflammation while at the same time promoting adequate anti-viral immune responses against infection. Full article
Show Figures

Figure 1

Review

Jump to: Research

22 pages, 5418 KiB  
Review
Mastering Death: The Roles of Viral Bcl-2 in dsDNA Viruses
by Chathura D. Suraweera, Benjamin Espinoza, Mark G. Hinds and Marc Kvansakul
Viruses 2024, 16(6), 879; https://doi.org/10.3390/v16060879 - 30 May 2024
Viewed by 987
Abstract
Proteins of the Bcl-2 family regulate cellular fate via multiple mechanisms including apoptosis, autophagy, senescence, metabolism, inflammation, redox homeostasis, and calcium flux. There are several regulated cell death (RCD) pathways, including apoptosis and autophagy, that use distinct molecular mechanisms to elicit the death [...] Read more.
Proteins of the Bcl-2 family regulate cellular fate via multiple mechanisms including apoptosis, autophagy, senescence, metabolism, inflammation, redox homeostasis, and calcium flux. There are several regulated cell death (RCD) pathways, including apoptosis and autophagy, that use distinct molecular mechanisms to elicit the death response. However, the same proteins/genes may be deployed in multiple biochemical pathways. In apoptosis, Bcl-2 proteins control the integrity of the mitochondrial outer membrane (MOM) by regulating the formation of pores in the MOM and apoptotic cell death. A number of prosurvival genes populate the genomes of viruses including those of the pro-survival Bcl-2 family. Viral Bcl-2 proteins are sequence and structural homologs of their cellular counterparts and interact with cellular proteins in apoptotic and autophagic pathways, potentially allowing them to modulate these pathways and determine cellular fate. Full article
Show Figures

Figure 1

Back to TopTop