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Viruses
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Interferon-Stimulated Genes in Antiviral Immunity
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Interferon-Stimulated Genes in Antiviral Immunity

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

Deadline for manuscript submissions: 31 May 2026 | Viewed by 2200

Special Issue Editor

Prof. Dr. Chen Liang

E-Mail Website
Guest Editor
Lady Davis Institute, Jewish General Hospital, McGill University, Montreal, QC H3T 1E2, Canada
Interests: pandemic and emerging viruses; host antiviral responses and HIV cure
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are excited to launch this Special Issue on interferon-stimulated genes (ISGs) that protect hosts against viral infections through a rich variety of molecular mechanisms. In recent decades, significant progress has been made in elucidating the antiviral functions of individual ISGs and in deciphering the molecular details of their actions, ranging from early studies of OAS/RNase L and Mx proteins to systematic screening for ISGs that inhibit different classes of viruses. Despite these efforts, the functions of many ISGs remain unexplored, and there is limited research on how they act in concert to protect cells against viral infections and mitigate viral diseases in vivo. It is expected that much more work will be conducted on these fast-evolving fronts. 

This Special Issue invites the submission of manuscripts describing the antiviral functions of ISGs as well as viral counter-attack mechanisms. We particularly welcome studies on ISGs that encode non-coding RNA and on their roles during viral infections, as well as those on ISGs from species such as bats, birds, pigs, and other natural reservoirs of viruses that are sporadically transmitted to humans and cause pandemics. We encourage the submission of studies on how ISGs modulate cellular environments such as the metabolic state to deter viral replication. We also welcome studies aimed at revealing the operation of the ISG network with the application of systems biology and deep learning tools.

Prof. Dr. Chen Liang
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 250 words) can be sent to the Editorial Office for assessment.

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

  • interferon-stimulated genes
  • ISGs
  • non-coding RNA
  • viral replication
  • deep learning tools

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Published Papers (3 papers)

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Research

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19 pages, 2375 KB  
Article
The Intrinsic Innate Immunity of Hepatocytes Suppresses HBV Replication and Is Antagonized by HBx
by Chui Zeng, Fayed Attia Koutb Megahed, Yiqiong Guo, Dongmei Sun, Yaru Wang, Qin Liu, Yanwei Bi, Jinghang Li, Qi Zhou, Qingdong Xie, Pingnan Sun and Xiaoling Zhou
Viruses 2025, 17(12), 1599; https://doi.org/10.3390/v17121599 - 10 Dec 2025
Viewed by 866
Abstract
(1) Background: Hepatitis B virus (HBV) belongs to the Hepadnaviridae family of viruses that interact with hepatocytes. HBV infection is a major global health problem. Most adults clear the infection quickly after being infected with HBV, while a few people develop chronic HBV [...] Read more.
(1) Background: Hepatitis B virus (HBV) belongs to the Hepadnaviridae family of viruses that interact with hepatocytes. HBV infection is a major global health problem. Most adults clear the infection quickly after being infected with HBV, while a few people develop chronic HBV infection. It is well-known that the early innate immune response of host cells plays an important role in the fight against virus infection. However, the interactions between HBV and the intrinsic innate immune system of hepatocytes are still not fully understood. The aim of this study was to confirm the interaction between HBV and hepatocytes, and to identify the interferon-stimulated genes (ISGs) regulated by HBx and their expression in association with HBV-associated HCC (HBV-HCC), so that we can refine our understanding of the interaction between HBV and ISGs and its potential influence on HBV-HCC. (2) Methods: We analyzed data concerning the stimulation of IFN-dependent genes in primary human hepatocytes (PHHs) transfected with pathogen DNA mimetics or infected with HBV in the GSE69590 database. Bioinformatic methods, such as GSEA, GO, and KEGG, were used to analyze the differentially expressed innate immunity genes and their related pathways to identify candidate intrinsic innate immune factors. qPCR on HepG2 and Huh7 cells, which highly express HBx, was used to detect relevant intrinsic innate immune factors. qPCR, RNAi, and Elisa methods were used to identify intrinsic innate immune factors in HBV-integrated HepG2.2.15 cells, and bioinformatics analysis was conducted on the HBV-infected tissues and cells in the GEO database. (3) Results: Inhibition of the JAK-STAT pathway enhanced HBV replication in HepG2 cells transfected with HBV plasmid and HepG2-NTCP cells infected with HBV. GSEA analysis of the GSE69590 data revealed significant changes in intrinsic innate immune pathways during HBV infection with PHH for 40 h. A total of 84 differentially expressed, candidate innate immunity genes were identified in GSE69590. Validation showed that TRIM22 and TRIM56 were down-regulated when HBx was expressed. Consistently, TRIM22 and TRIM56 were up-regulated following inhibition of HBx by transfection of HBx siRNA into HepG2.2.15 cells, and HBV pgRNA was up-regulated following down-regulated expression of TRIM22 and TRIM56 in HEK293 cells. Receiver operating characteristics (ROC) and overall survival (OS) analysis of 204 HBV-HCC patients showed that expression of TRIM22 was closely associated with HBV-HCC, and high expression of TRIM22 was associated with longer survival. (4) Conclusions: Innate immunity genes TRIM22 and TRIM56 are regulated by HBx, and higher expression of TRIM22 is closely related to longer survival of HBV-HCC patients. Full article
(This article belongs to the Special Issue Interferon-Stimulated Genes in Antiviral Immunity)
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Review

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21 pages, 391 KB  
Review
Identification of Fish Interferon-Stimulated Genes and Their Antiviral Mechanisms
by Emily Yang
Viruses 2026, 18(3), 296; https://doi.org/10.3390/v18030296 - 28 Feb 2026
Viewed by 460
Abstract
The frontlines of innate antiviral immunity center on type I interferons (IFNs), which are expressed by nearly all cell types as a cellular alarm signal. IFNs drive the expression of IFN-stimulated genes (ISGs), which can both generate an intracellular antiviral state and regulate [...] Read more.
The frontlines of innate antiviral immunity center on type I interferons (IFNs), which are expressed by nearly all cell types as a cellular alarm signal. IFNs drive the expression of IFN-stimulated genes (ISGs), which can both generate an intracellular antiviral state and regulate the IFN response itself. This key antiviral line of defense is conserved in all jawed vertebrates, including teleost fish. Since their identification nearly 70 years ago, many mammalian ISGs have been identified and characterized However, fish ISGs represent an exciting, largely unexplored avenue of antiviral effector research and present an opportunity to assess how IFN systems have been shaped by whole genome duplication events. This review summarizes advances in the identification of bona fide teleost ISGs and examines studies elucidating the antiviral mechanisms of conserved ISGs, including IFIT1, Mx, Nmi and IFP35, Viperin, TRIMs, and ISG15. Teleost-specific gene expansions and isoform divergence, particularly in the development of the fish novel TRIM family, will be considered under each relevant ISG. Understanding teleost ISG biology promises not only to improve antiviral strategies in aquaculture but also to reveal novel antiviral principles with translational relevance for human health. Full article
(This article belongs to the Special Issue Interferon-Stimulated Genes in Antiviral Immunity)
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Graphical abstract

19 pages, 1058 KB  
Review
Beyond Viral Restriction: The Metabolic Dimensions of Interferon-Stimulated Genes in Antiviral Immunity
by Xiaoyu Ding, Libao Liu and Haiming Wei
Viruses 2026, 18(2), 160; https://doi.org/10.3390/v18020160 - 25 Jan 2026
Viewed by 486
Abstract
Interferon-stimulated genes (ISGs) are classically recognized for their direct antiviral functions, such as viral genome degradation or replication blockade. However, emerging evidence reveals that ISGs orchestrate a broader landscape of host defense by rewiring cellular metabolism. These mechanisms are still not fully understood [...] Read more.
Interferon-stimulated genes (ISGs) are classically recognized for their direct antiviral functions, such as viral genome degradation or replication blockade. However, emerging evidence reveals that ISGs orchestrate a broader landscape of host defense by rewiring cellular metabolism. These mechanisms are still not fully understood in the context of antiviral immunity. This review synthesizes recent advances in understanding how ISGs modulate metabolic pathways (e.g., glycolysis, lipid metabolism, amino acids, and nucleotide metabolism) to create an antiviral cellular environment. However, viruses have developed strategies to evade or counteract ISG-encoded proteins, and some even hijack certain ISGs to their advantage. Therefore, we further explore how viruses subvert these ISG-driven metabolic to evade host defenses. Overall, we summarize the current state of knowledge on the interactions between viruses and ISGs and propose that ISGs act as “protective” or “pathogenic” regulators at the dimensions of metabolism, offering new perspectives for targeting host-centered pathways to combat viral infections. Full article
(This article belongs to the Special Issue Interferon-Stimulated Genes in Antiviral Immunity)
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