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Viruses
Special Issues
The Role of Cell Death in Viral Infections
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The Role of Cell Death in Viral Infections

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

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 3490

Special Issue Editor

Prof. Kirsten Spann

E-Mail Website
Guest Editor
Centre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, South Brisbane, QLD 4007, Australia
Interests: respiratory viruses; innate immune signalling; innate immune evasion; host-virus interactions; virus transmission

Special Issue Information

Dear Colleagues,

Programmed cell death is a key component of the host’s innate immune response and serves to limit the spread of infection and tissue damage. Viruses have therefore evolved many mechanisms for modulating cell death pathways. Viral gene products may interfere with effector or regulatory mechanisms to confer a selective advantage to the virus by suppressing cell death and therefore promoting replication and spread. Other viruses do not suppress cell death but rather hijack cell death pathways to compromise the host. Apoptosis, pyroptosis and necroptosis are the most widely studied pathways of programmed cell death in response to virus infection. During apoptosis, the cell membrane remains intact and allows neighboring immune cells to remove both the cell and the invading virus. However, pyroptosis and necroptosis are lytic cell death processes, which facilitate the release of damage-associated molecular patterns (DAMPS) into the extracellular space, thus inducing an inflammatory response. However, these pathways are not necessarily discrete and may intersect during infection, increasing the complexity of virus–host interaction. Understanding this relationship will provide us with insights and novel approaches for antiviral therapies.

For this Special Issue, we invite the submission of original research papers and review articles pertaining to programmed cell death pathways in viral infection, virus–host interaction, the effect this has on disease, and ideas for novel therapeutics based on new knowledge in this area.

Prof. Kirsten Spann
Guest Editor

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

  • programmed cell death
  • inflammation
  • cellular damage
  • virus–host interactions
  • antiviral therapies

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Published Papers (2 papers)

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Research

29 pages, 11596 KiB  
Article
DHX15 and Rig-I Coordinate Apoptosis and Innate Immune Signaling by Antiviral RNase L
by Barkha Ramnani, Trupti Devale, Praveen Manivannan, Aiswarya Haridas and Krishnamurthy Malathi
Viruses 2024, 16(12), 1913; https://doi.org/10.3390/v16121913 - 13 Dec 2024
Viewed by 1462
Abstract
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2′-5′-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad [...] Read more.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2′-5′-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis. In RNase L-activated cells, DHX15 interacts with Rig-I and MAVS, and cells lacking MAVS expression were resistant to apoptosis. RL RNAs induced the transcription of genes for IFN and proinflammatory cytokines by interferon regulatory factor 3 (IRF-3) and nuclear factor kB (NF-kB), while cells lacking both DHX15 and Rig-I showed a reduced induction of cytokines. However, apoptotic cell death is independent of both IRF-3 and NF-kB, suggesting that cytokine and cell death induction by RL RNAs are uncoupled. The RNA binding of both DHX15 and Rig-I is required for apoptosis induction, and the expression of both single proteins in cells lacking both DHX15 and Rig-I is insufficient to promote cell death by RL RNAs. Cell death induced by RL RNAs suppressed Coxsackievirus B3 (CVB3) replication, and inhibiting caspase-3 activity or cells lacking IRF-3 showed that the induction of apoptosis directly resulted in the CVB3 antiviral effect, and the effects were independent of the role of IRF-3. Full article
(This article belongs to the Special Issue The Role of Cell Death in Viral Infections)
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22 pages, 9345 KiB  
Article
Human Coronavirus 229E Infection Inactivates Pyroptosis Executioner Gasdermin D but Ultimately Leads to Lytic Cell Death Partly Mediated by Gasdermin E
by Xavier Martiáñez-Vendrell, Jonna Bloeme-ter Horst, Roy Hutchinson, Coralie Guy, Andrew G. Bowie and Marjolein Kikkert
Viruses 2024, 16(6), 898; https://doi.org/10.3390/v16060898 - 1 Jun 2024
Cited by 1 | Viewed by 1268
Abstract
Human coronavirus 229E (HCoV-229E) is associated with upper respiratory tract infections and generally causes mild respiratory symptoms. HCoV-229E infection can cause cell death, but the molecular pathways that lead to virus-induced cell death as well as the interplay between viral proteins and cellular [...] Read more.
Human coronavirus 229E (HCoV-229E) is associated with upper respiratory tract infections and generally causes mild respiratory symptoms. HCoV-229E infection can cause cell death, but the molecular pathways that lead to virus-induced cell death as well as the interplay between viral proteins and cellular cell death effectors remain poorly characterized for HCoV-229E. Studying how HCoV-229E and other common cold coronaviruses interact with and affect cell death pathways may help to understand its pathogenesis and compare it to that of highly pathogenic coronaviruses. Here, we report that the main protease (Mpro) of HCoV-229E can cleave gasdermin D (GSDMD) at two different sites (Q29 and Q193) within its active N-terminal domain to generate fragments that are now unable to cause pyroptosis, a form of lytic cell death normally executed by this protein. Despite GSDMD cleavage by HCoV-229E Mpro, we show that HCoV-229E infection still leads to lytic cell death. We demonstrate that during virus infection caspase-3 cleaves and activates gasdermin E (GSDME), another key executioner of pyroptosis. Accordingly, GSDME knockout cells show a significant decrease in lytic cell death upon virus infection. Finally, we show that HCoV-229E infection leads to increased lytic cell death levels in cells expressing a GSDMD mutant uncleavable by Mpro (GSDMD Q29A+Q193A). We conclude that GSDMD is inactivated by Mpro during HCoV-229E infection, preventing GSDMD-mediated cell death, and point to the caspase-3/GSDME axis as an important player in the execution of virus-induced cell death. In the context of similar reported findings for highly pathogenic coronaviruses, our results suggest that these mechanisms do not contribute to differences in pathogenicity among coronaviruses. Nonetheless, understanding the interactions of common cold-associated coronaviruses and their proteins with the programmed cell death machineries may lead to new clues for coronavirus control strategies. Full article
(This article belongs to the Special Issue The Role of Cell Death in Viral Infections)
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