Antiviral Immunity and Vaccine Development

A special issue of Vaccines (ISSN 2076-393X). This special issue belongs to the section "Pathogens-Host Immune Boundaries".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1173

Special Issue Editors


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Guest Editor
School of Public Health (Shenzhen), Sun Yat-Sen University, Shenzhen 518107, China
Interests: vaccine; innate immunity; antiviral drugs; HIV-1; SARS-CoV-2; influenza
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Guest Editor
Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
Interests: antiviral immune responses; innate immunity; inflammation-mediated diseases; vaccine

Special Issue Information

Dear Colleagues,

Emerging infectious diseases and evolving viral threats have become severe challenges for public health, and understanding the regulatory mechanisms of the host’s antiviral immunity is of great importance for developing effective antiviral vaccines. This Special Issue of Vaccines aims to bring together cutting-edge research on host immune responses to viral pathogens, thus providing insights into developing innovative antiviral vaccine technologies.

This Special Issue will focus on a broad spectrum of topics, including the mechanisms of immune responses to viral infections, innovative adjuvants based on the modulation of immune signalling pathways, novel vaccine platforms (such as mRNA, vector-based, and protein subunit vaccines), and recent breakthroughs in vaccine design (such as reverse vaccinology, structure-based vaccine design, mucosal vaccines, etc.). We are particularly interested in highlighting research that expands the boundaries of current knowledge in vaccine development and contributes to our understanding of immunity against both emerging and established viral threats.

This Special Issue welcomes submissions of all types, including original research articles, reviews, commentaries, and clinical trial reports, that provide important insights and novel conceptions of antiviral immune responses and vaccine development. Additionally, studies focusing on viral immune evasion mechanisms and innovative vaccine therapeutics are also highly encouraged.

We look forward to your contributions.

Prof. Dr. Caijun Sun
Dr. Tao Yu
Guest Editors

Manuscript Submission Information

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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. Vaccines 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 2700 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

  • antiviral innate immunity
  • adaptive immune responses
  • viral pathogenesis
  • immune evasion
  • host–virus interactions
  • antiviral vaccine development
  • vaccine design
  • novel vaccine platforms
  • vaccine adjuvants
  • vaccines and therapeutics

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Published Papers (1 paper)

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Research

16 pages, 3286 KB  
Article
Poxvirus K3 Orthologs Regulate NF-κB-Dependent Inflammatory Responses by Targeting the PKR–eIF2α Axis in Multiple Species
by Huibin Yu, Mary Eloise L. Fernandez, Chen Peng, Dewi Megawati, Greg Brennan, Loubna Tazi and Stefan Rothenburg
Vaccines 2025, 13(8), 800; https://doi.org/10.3390/vaccines13080800 - 28 Jul 2025
Viewed by 838
Abstract
Background: Protein kinase R (PKR) inhibits general mRNA translation by phosphorylating the alpha subunit of eukaryotic translation initiation factor 2 (eIF2). PKR also modulates NF-κB signaling during viral infections, but comparative studies of PKR-mediated NF-κB responses across mammalian species and their regulation by [...] Read more.
Background: Protein kinase R (PKR) inhibits general mRNA translation by phosphorylating the alpha subunit of eukaryotic translation initiation factor 2 (eIF2). PKR also modulates NF-κB signaling during viral infections, but comparative studies of PKR-mediated NF-κB responses across mammalian species and their regulation by viral inhibitors remain largely unexplored. This study aimed to characterize the conserved antiviral and inflammatory roles of mammalian PKR orthologs and investigate their modulation by poxviral inhibitors. Methods: Using reporter gene assays and quantitative RT-PCR, we assessed the impact of 17 mammalian PKR orthologs on general translation inhibition, stress-responsive translation, and NF-κB-dependent induction of target genes. Congenic human and rabbit cell lines infected with a myxoma virus strain lacking PKR inhibitors were used to compare the effects of human and rabbit PKR on viral replication and inflammatory responses. Site-directed mutagenesis was employed to determine key residues responsible for differential sensitivity to the viral inhibitor M156. Results: All 17 mammalian PKR orthologs significantly inhibited general translation, strongly activated stress-responsive ATF4 translation, and robustly induced NF-κB target genes. Inhibition of these responses was specifically mediated by poxviral K3 orthologs that effectively suppressed PKR activation. Comparative analyses showed human and rabbit PKRs similarly inhibited virus replication and induced cytokine transcripts. Amino acid swaps between rabbit PKRs reversed their sensitivity to viral inhibitor M156 and NF-κB activation. Conclusions: Our data show that the tested PKR orthologs exhibit conserved dual antiviral and inflammatory regulatory roles, which can be antagonized by poxviral K3 orthologs that exploit eIF2α mimicry to modulate the PKR-NF-κB axis. Full article
(This article belongs to the Special Issue Antiviral Immunity and Vaccine Development)
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