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: 15 August 2024 | Viewed by 200

Special Issue Editors


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Guest Editor
Department of Biochemistry & Chemistry, La Trobe University, Kingsbury Drive, Melbourne 3086, Australia
Interests: apoptosis; structural biology; polarity; defensins
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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

Published Papers

This special issue is now open for submission.
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