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Journals
Viruses
Special Issues
Innate Immunity to Virus Infection 2nd Edition
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Innate Immunity to Virus Infection 2nd Edition

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

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 2285

Special Issue Editors

Prof. Dr. Caijun Sun

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Feng Ma

E-Mail Website
Guest Editor
Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Suzhou 215123, China
Interests: antiviral immunity; immunometabolism; infectious diseases; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Emerging and re-emerging outbreaks of highly pathogenic viruses have been becoming a severe crisis for global public health. As the first line of host defense against viral infections, the interferon (IFN)-mediated innate immunity and a variety of IFN-stimulated genes (ISGs) are well-known to play a critical role in interfering with virus entry and replication. Thus, it is of great importance to deeply understand the comprehensive interplay between innate immunity and virus infection, which will provide insights into developing novel antiviral therapeutics and vaccines. In this special issue, we welcome novel findings related to innate immunity to viral infection, including but not limited to interferon (IFN)-stimulated genes (ISGs), IFN signaling pathways, antiviral immunity, inflammation, immunometabolism, non-coding RNA, vaccine-related innate immunity, broadly antiviral drugs, and so on.

Prof. Dr. Caijun Sun
Prof. Dr. Feng Ma
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

  • innate immunity
  • interferon (IFN)
  • IFN-stimulated genes (ISGs)
  • IFN signaling pathways
  • antiviral immunity
  • inflammation
  • immunometabolism
  • non-coding RNA
  • vaccine
  • broadly antiviral drug

Published Papers (2 papers)

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16 pages, 10470 KiB  
Article
CD8+ T Cells Mediate Lethal Lung Pathology in the Absence of PD-L1 and Type I Interferon Signalling following LCMV Infection
by Alanna G. Spiteri, Tamara Suprunenko, Erin Cutts, Andrew Suen, Thomas M. Ashhurst, Barney Viengkhou, Nicholas J. C. King and Markus J. Hofer
Viruses 2024, 16(3), 390; https://doi.org/10.3390/v16030390 - 01 Mar 2024
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Abstract
CD8+ T cells are critical to the adaptive immune response against viral pathogens. However, overwhelming antigen exposure can result in their exhaustion, characterised by reduced effector function, failure to clear virus, and the upregulation of inhibitory receptors, including programmed cell death 1 [...] Read more.
CD8+ T cells are critical to the adaptive immune response against viral pathogens. However, overwhelming antigen exposure can result in their exhaustion, characterised by reduced effector function, failure to clear virus, and the upregulation of inhibitory receptors, including programmed cell death 1 (PD-1). However, exhausted T cell responses can be “re-invigorated” by inhibiting PD-1 or the primary ligand of PD-1: PD-L1. Further, the absence of the type I interferon receptor IFNAR1 also results in T cell exhaustion and virus persistence in lymphocytic choriomeningitis virus Armstrong (LCMV-Arm)-infected mice. In this study, utilizing single- and double-knockout mice, we aimed to determine whether ablation of PD-1 could restore T cell functionality in the absence of IFNAR1 signalling in LCMV-Arm-infected mice. Surprisingly, this did not re-invigorate the T cell response and instead, it converted chronic LCMV-Arm infection into a lethal disease characterized by severe lung inflammation with an infiltration of neutrophils and T cells. Depletion of CD8+ T cells, but not neutrophils, rescued mice from lethal disease, demonstrating that IFNAR1 is required to prevent T cell exhaustion and virus persistence in LCMV-Arm infection, and in the absence of IFNAR1, PD-L1 is required for survival. This reveals an important interplay between IFNAR1 and PD-L1 with implications for therapeutics targeting these pathways. Full article
(This article belongs to the Special Issue Innate Immunity to Virus Infection 2nd Edition)
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11 pages, 982 KiB  
Systematic Review
Association between Statins Administration and Influenza Susceptibility: A Systematic Review and Meta-Analysis of Longitudinal Studies
by Fan Wu, Congcong Wang, Shunran Li, Ying Ye, Mingting Cui, Yajie Liu, Shiqiang Jiang, Jun Qian, Jianhui Yuan, Yuelong Shu and Caijun Sun
Viruses 2024, 16(2), 278; https://doi.org/10.3390/v16020278 - 10 Feb 2024
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Abstract
Previous studies reported that the association between statins use and influenza infection was contradictory. A systematic review and meta-analysis of longitudinal studies were performed to determine the association between statins use and influenza susceptibility. The literature search was conducted in PubMed, Embase, and [...] Read more.
Previous studies reported that the association between statins use and influenza infection was contradictory. A systematic review and meta-analysis of longitudinal studies were performed to determine the association between statins use and influenza susceptibility. The literature search was conducted in PubMed, Embase, and Web of Science, from each database’s inception to 21 May 2023. The fixed effect model and random effects model were used for data synthesis. In our study, a total of 1,472,239 statins users and 1,486,881 statins non-users from five articles were included. The pooled risk ratio (RR) of all included participants was 1.05 (95% CI: 1.03–1.07), and there were still significant differences after adjusting for vaccination status. Of note, RR values in statins users were 1.06 (95% CI: 1.03–1.08) in people aged ≥60 years old and 1.05 (95% CI: 1.03–1.07) in participant groups with a higher proportion of females. Administration of statins might be associated with an increased risk of influenza infection, especially among females and elderly people. For those people using statins, we should pay more attention to surveillance of their health conditions and take measures to prevent influenza infection. Full article
(This article belongs to the Special Issue Innate Immunity to Virus Infection 2nd Edition)
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