Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.3
3.8
Journals
Viruses
Special Issues
Innate Immunity to Virus Infection 2nd Edition
share announcement

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: 15 April 2025 | Viewed by 7933

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

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 (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

15 pages, 3990 KiB  
Article
Long Non-Coding RNA THRIL Promotes Influenza Virus Replication by Inhibiting the Antiviral Innate Immune Response
by Mengying Chen, Jingyun Hu, Xinni Zhou, Ming Gao, Ning Li, Guihong Yang, Xiaojuan Chi and Song Wang
Viruses 2025, 17(2), 153; https://doi.org/10.3390/v17020153 - 23 Jan 2025
Viewed by 386
Abstract
Long non-coding RNAs (lncRNAs) have been recognized for their crucial roles in the replication processes of various viruses. However, the specific functions and regulatory mechanisms of many lncRNAs in influenza A virus (IAV) pathogenesis remain poorly understood. In this study, we identified lncRNA [...] Read more.
Long non-coding RNAs (lncRNAs) have been recognized for their crucial roles in the replication processes of various viruses. However, the specific functions and regulatory mechanisms of many lncRNAs in influenza A virus (IAV) pathogenesis remain poorly understood. In this study, we identified lncRNA THRIL and observed a significant reduction in its expression following IAV infection in A549 cells. The treatment of cells with the viral mimic poly (I:C), or with type I and type III interferons, resulted in a substantial decrease in THRIL expression. Furthermore, THRIL overexpression significantly enhanced IAV replication, while its silencing markedly reduced IAV replication. Additionally, IAV infection led to notable reductions in the expression levels of type I and type III interferons in cell lines overexpressing THRIL compared to control groups; conversely, cell lines with THRIL knockdown exhibited significantly higher interferon levels than control groups. Moreover, THRIL was found to inhibit the expression of several critical interferon-stimulated genes (ISGs), which are essential for an effective antiviral response. Notably, our findings demonstrated that THRIL impaired the activation of IRF3, a key transcription factor in the interferon signaling pathway, thereby suppressing host innate immunity. These results highlight THRIL’s potential as a therapeutic target for antiviral strategies. Full article
(This article belongs to the Special Issue Innate Immunity to Virus Infection 2nd Edition)
►▼ Show Figures

Figure 1

16 pages, 2538 KiB  
Article
Association Between Single-Nucleotide Polymorphisms in Toll-like Receptor 3 (tlr3), tlr7, tlr8 and tirap Genes with Severe Symptoms in Children Presenting COVID-19
by Adriana Souza Andrade, Aline Almeida Bentes, Lilian Martins Diniz, Silvia Hees Carvalho, Erna Geessien Kroon and Marco Antonio Campos
Viruses 2025, 17(1), 35; https://doi.org/10.3390/v17010035 - 30 Dec 2024
Viewed by 899
Abstract
The global number of COVID-19 deaths has reached 7 million, with 4% of these deaths occurring in children and adolescents. In Brazil, around 1500 children up to 11 years old died from the disease. The most common symptoms in children are respiratory, potentially [...] Read more.
The global number of COVID-19 deaths has reached 7 million, with 4% of these deaths occurring in children and adolescents. In Brazil, around 1500 children up to 11 years old died from the disease. The most common symptoms in children are respiratory, potentially progressing to severe illnesses, such as severe acute respiratory syndrome (SARS) and MIS-C. Studies indicate that comorbidities and genetic factors, such as polymorphisms in immune response genes, can influence the severity of COVID-19. This study investigates the occurrence of single-nucleotide polymorphisms (SNPs) in innate immune response genes in children with COVID-19. Seventy-three samples were analyzed from children under 13 years old hospitalized at João Paulo II Children’s Hospital due to COVID-19. The evaluated SNPs were tlr8 (1) (rs3764879), tlr8 (2) (rs2407992), tlr7 (rs179008), tlr3 (rs3775291), tirap (rs8177374), and mcp-1 (rs1024611), considering four categories of severity: mild, moderate, severe, and critical COVID-19. To identify the SNPs, PCR and sequencing were performed. The frequencies of the SNPs obtained were not discrepant when compared to the frequencies described in the Global ALFA, Global 1000 Genomes, Global gnomAD, American 1000 Genomes, and American gnomAD databases, except for the SNP in TLR7. Comparing severe and critical cases to mild and moderate cases, we found a higher relative risk associated with mutations in tlr8 (1), tlr7, tlr3, and tirap (p < 0.05). No association was found for SNPs in tlr8 (2) and mcp-1. Our analyses suggest an association between SNPs in innate immune response genes and severity of symptoms in children with COVID-19 (or SARS-CoV-2 infected children). Full article
(This article belongs to the Special Issue Innate Immunity to Virus Infection 2nd Edition)
►▼ Show Figures

Figure 1

14 pages, 6160 KiB  
Article
RNA-Seq Reveals Transcriptome Changes Following Zika Virus Infection in Fetal Brains in c-Flip Knockdown Mice
by Ting Xie, Qiqi Chen, Nina Li, Shengze Zhang, Lin Zhu, Shaohui Bai, Haolu Zha, Weijian Tian, Chuming Luo, Nan Wu, Xuan Zou, Shisong Fang, Yuelong Shu, Jianhui Yuan, Ying Jiang and Huanle Luo
Viruses 2024, 16(11), 1712; https://doi.org/10.3390/v16111712 - 31 Oct 2024
Viewed by 1193
Abstract
The FADD-like interleukin-1β converting enzyme (FLICE)-inhibitory protein (c-FLIP) plays a crucial role in various biological processes, including apoptosis and inflammation. However, the complete transcriptional profile altered by the c-FLIP is not fully understood. Furthermore, the impact of the c-FLIP deficiency on the transcriptome [...] Read more.
The FADD-like interleukin-1β converting enzyme (FLICE)-inhibitory protein (c-FLIP) plays a crucial role in various biological processes, including apoptosis and inflammation. However, the complete transcriptional profile altered by the c-FLIP is not fully understood. Furthermore, the impact of the c-FLIP deficiency on the transcriptome during a Zika virus (ZIKV) infection, which induces apoptosis and inflammation in the central nervous system (CNS), has not yet been elucidated. In this study, we compared transcriptome profiles between wild-type (WT) and the c-Flip heterozygous knockout mice (c-Flip+/−) fetal heads at embryonic day 13.5 from control and PBS-infected WT dams mated with c-Flip+/− sires. In the non-infected group, we observed differentially expressed genes (DEGs) mainly involved in embryonic development and neuron development. However, the ZIKV infection significantly altered the transcriptional profile between WT and the c-Flip+/− fetal heads. DEGs in pattern recognition receptor (PRR)-related signaling pathways, such as the RIG-I-like receptor signaling pathway and Toll-like receptor signaling pathway, were enriched. Moreover, the DEGs were also enriched in T cells, indicating that the c-FLIP participates in both innate and adaptive immune responses upon viral infection. Furthermore, our observations indicate that DEGs are associated with sensory organ development and eye development, suggesting a potential role for the c-FLIP in ZIKV-induced organ development defects. Overall, we have provided a comprehensive transcriptional profile for the c-FLIP and its modulation during a ZIKV infection. Full article
(This article belongs to the Special Issue Innate Immunity to Virus Infection 2nd Edition)
►▼ Show Figures

Figure 1

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 - 1 Mar 2024
Viewed by 2245
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)
►▼ Show Figures

Figure 1

Review

Jump to: Research, Other

18 pages, 1511 KiB  
Review
The Role of Sustained Type I Interferon Secretion in Chronic HIV Pathogenicity: Implications for Viral Persistence, Immune Activation, and Immunometabolism
by Eman Teer, Nyasha C. Mukonowenzou and M. Faadiel Essop
Viruses 2025, 17(2), 139; https://doi.org/10.3390/v17020139 - 22 Jan 2025
Viewed by 651
Abstract
Human immunodeficiency virus (HIV) infection induces chronic immune activation by stimulating both the innate and adaptive immune systems, resulting in persistent inflammation and immune cell exhaustion. Of note, the modulation of cytokine production and its release can significantly influence the immune response. Type [...] Read more.
Human immunodeficiency virus (HIV) infection induces chronic immune activation by stimulating both the innate and adaptive immune systems, resulting in persistent inflammation and immune cell exhaustion. Of note, the modulation of cytokine production and its release can significantly influence the immune response. Type I interferons (IFN-Is) are cytokines that play a crucial role in innate immunity due to their potent antiviral effects, regulation of IFN-stimulated genes essential for viral clearance, and the initiation of both innate and adaptive immune responses. Thus, an understanding of the dual role of IFN-I (protective versus harmful) during HIV-1 infections and elucidating its contributions to HIV pathogenesis is crucial for advancing HIV therapeutic interventions. This review therefore delves into the intricate involvement of IFN-I in both the acute and chronic phases of HIV infection and emphasizes its impact on viral persistence, immune activation, and immunometabolism in treated HIV-infected individuals. Full article
(This article belongs to the Special Issue Innate Immunity to Virus Infection 2nd Edition)
►▼ Show Figures

Graphical abstract

Other

Jump to: Research, Review

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
Viewed by 1679
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)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop