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Viruses
Special Issues
Interaction between Virus and Host Innate Immune Systems
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Interaction between Virus and Host Innate Immune Systems

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 (20 April 2022) | Viewed by 15701

Special Issue Editors

Prof. Dr. Moon Jung Song

E-Mail Website
Guest Editor
College of Life Sciences and Biotechnology, Korea University, Seoul, Korea
Interests: virus–host interactions; innate immunity; viral immune evasion; regulation of viral life cycle; viral modulation of cellular NAD+ system; viral genetics; herpesviruses; influenza virus; noroviruses; coronaviruses; SARS-CoV-2
Dr. Ok Sarah Shin

E-Mail Website
Guest Editor
College of Medicine, Korea University, Seoul, Korea
Interests: host–pathogen interactions; innate immunity; virus-induced cell death; immune evasion; Zika virus
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The complex interplay between pathogens and host immune response is considered a highly dynamic process. When confronted with viral infection, the innate immune system provides the first line of host defense against pathogens by triggering host inflammatory and antiviral cytokine responses. Sensing viral nucleic acids and activating downstream signaling pathways are highly orchestrated to induce interferons (IFNs) and IFN-stimulated genes (ISGs), ultimately setting an antiviral stage. In addition, autophagy/mitophagy is an essential process that can initiate an innate immune response via crosstalk with innate immune receptors to modulate the expression of antiviral IFNs, thereby maintaining cellular homeostasis and clearing pathogens. Consequently, viruses have evolved mechanisms to evade host defenses at various stages of the innate immune response.

In this Special Issue, we aim to assemble a collection of research papers and reviews that highlight critical advancements in our understanding of the interactions between viruses and host innate immune system. Of particular interest are the innate immune responses to RNA or DNA virus infection, evasions strategies employed by viruses, characterizing the function of autophagy/mitophagy for modulating antiviral innate immunity, and innate immune pathways modulated by viral proteins. This knowledge will allow us to uncover novel viral evasion strategies and to identify novel viral and host factors in modulation of viral replication and disease outcome. We look forward to your submissions.

Prof. Dr. Moon Jung Song
Dr. Ok Sarah Shin
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

  • DNA viruses
  • RNA viruses
  • innate immunity
  • interferons
  • interferon stimulated genes
  • inflammasome
  • cytokines
  • autophagy
  • mitophagy
  • virus-induced cell death
  • immune evasion

Published Papers (5 papers)

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Research

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16 pages, 4170 KiB  
Article
Nonstructural Protein NS1 of Influenza Virus Disrupts Mitochondrial Dynamics and Enhances Mitophagy via ULK1 and BNIP3
by Jae-Hwan Lee, Soo-Jin Oh, Jeanho Yun and Ok Sarah Shin
Viruses 2021, 13(9), 1845; https://doi.org/10.3390/v13091845 - 15 Sep 2021
Cited by 13 | Viewed by 2859
Abstract
Nonstructural protein 1 (NS1) of influenza virus (IFV) is essential for evading interferon (IFN)-mediated antiviral responses, thereby contributing to the pathogenesis of influenza. Mitophagy is a type of autophagy that selectively removes damaged mitochondria. The role of NS1 in IFV-mediated mitophagy is currently [...] Read more.
Nonstructural protein 1 (NS1) of influenza virus (IFV) is essential for evading interferon (IFN)-mediated antiviral responses, thereby contributing to the pathogenesis of influenza. Mitophagy is a type of autophagy that selectively removes damaged mitochondria. The role of NS1 in IFV-mediated mitophagy is currently unknown. Herein, we showed that overexpression of NS1 protein led to enhancement of mitophagy. Mitophagy induction via carbonyl cyanide 3-chlorophenylhydrazone treatment in IFV-infected A549 cells led to increased viral replication efficiency, whereas the knockdown of PTEN-induced kinase 1 (PINK1) led to the opposite effect on viral replication. Overexpression of NS1 protein led to changes in mitochondrial dynamics, including depolarization of mitochondrial membrane potential. In contrast, infection with NS1-deficient virus resulted in impaired mitochondrial fragmentation, subsequent mitolysosomal formation, and mitophagy induction, suggesting an important role of NS1 in mitophagy. Meanwhile, NS1 protein increased the phosphorylation of Unc-51-like autophagy activating kinase 1 (ULK1) and the mitochondrial expression of BCL2- interacting protein 3 (BNIP3), both of which were found to be important for IFV-mediated mitophagy. Overall, these data highlight the importance of IFV NS1, ULK1, and BNIP3 during mitophagy activation. Full article
(This article belongs to the Special Issue Interaction between Virus and Host Innate Immune Systems)
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Review

Jump to: Research

14 pages, 14014 KiB  
Review
Aminoacyl-tRNA Synthetase: A Non-Negligible Molecule in RNA Viral Infection
by Min Feng and Han Zhang
Viruses 2022, 14(3), 613; https://doi.org/10.3390/v14030613 - 15 Mar 2022
Cited by 4 | Viewed by 2504
Abstract
Infectious diseases such as the ongoing coronavirus disease 2019 (COVID-19) continue to have a huge impact on global health, and the host-virus interaction remains incompletely understood. To address the global threat, in-depth investigations in pathogenesis are essential for interventions in infectious diseases and [...] Read more.
Infectious diseases such as the ongoing coronavirus disease 2019 (COVID-19) continue to have a huge impact on global health, and the host-virus interaction remains incompletely understood. To address the global threat, in-depth investigations in pathogenesis are essential for interventions in infectious diseases and vaccine development. Interestingly, aminoacyl-transfer RNA (tRNA) synthetases (aaRSs), an ancient enzyme family that was once considered to play housekeeping roles in protein synthesis, are involved in multiple viral infectious diseases. Many aaRSs in eukaryotes present as the components of a cytoplasmic depot system named the multi-synthetase complex (MSC). Upon viral infections, several components of the MSC are released and exert nonenzymatic activities. Host aaRSs can also be utilized to facilitate viral entry and replication. In addition to their intracellular roles, some aaRSs and aaRS-interacting multi-functional proteins (AIMPs) are secreted as active cytokines or function as “molecule communicators” on the cell surface. The interactions between aaRSs and viruses ultimately affect host innate immune responses or facilitate virus invasion. In this review, we summarized the latest advances of the interactions between aaRSs and RNA viruses, with a particular emphasis on the therapeutic potentials of aaRSs in viral infectious diseases. Full article
(This article belongs to the Special Issue Interaction between Virus and Host Innate Immune Systems)
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18 pages, 7004 KiB  
Review
Escape and Over-Activation of Innate Immune Responses by SARS-CoV-2: Two Faces of a Coin
by Sameer-ul-Salam Mattoo, Seong-Jun Kim, Dae-Gyun Ahn and Jinjong Myoung
Viruses 2022, 14(3), 530; https://doi.org/10.3390/v14030530 - 04 Mar 2022
Cited by 10 | Viewed by 2440
Abstract
In the past 20 years, coronaviruses (CoVs), including SARS-CoV-1, MERS-CoV, and SARS-CoV-2, have rapidly evolved and emerged in the human population. The innate immune system is the first line of defense against invading pathogens. Multiple host cellular receptors can trigger the innate immune [...] Read more.
In the past 20 years, coronaviruses (CoVs), including SARS-CoV-1, MERS-CoV, and SARS-CoV-2, have rapidly evolved and emerged in the human population. The innate immune system is the first line of defense against invading pathogens. Multiple host cellular receptors can trigger the innate immune system to eliminate invading pathogens. However, these CoVs have acquired strategies to evade innate immune responses by avoiding recognition by host sensors, leading to impaired interferon (IFN) production and antagonizing of the IFN signaling pathways. In contrast, the dysregulated induction of inflammasomes, leading to uncontrolled production of IL-1 family cytokines (IL-1β and IL-18) and pyroptosis, has been associated with COVID-19 pathogenesis. This review summarizes innate immune evasion strategies employed by SARS-CoV-1 and MERS-CoV in brief and SARS-CoV-2 in more detail. In addition, we outline potential mechanisms of inflammasome activation and evasion and their impact on disease prognosis. Full article
(This article belongs to the Special Issue Interaction between Virus and Host Innate Immune Systems)
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20 pages, 1252 KiB  
Review
Schlafens Can Put Viruses to Sleep
by Eui Tae Kim and Matthew D. Weitzman
Viruses 2022, 14(2), 442; https://doi.org/10.3390/v14020442 - 21 Feb 2022
Cited by 8 | Viewed by 4386
Abstract
The Schlafen gene family encodes for proteins involved in various biological tasks, including cell proliferation, differentiation, and T cell development. Schlafens were initially discovered in mice, and have been studied in the context of cancer biology, as well as their role in protecting [...] Read more.
The Schlafen gene family encodes for proteins involved in various biological tasks, including cell proliferation, differentiation, and T cell development. Schlafens were initially discovered in mice, and have been studied in the context of cancer biology, as well as their role in protecting cells during viral infection. This protein family provides antiviral barriers via direct and indirect effects on virus infection. Schlafens can inhibit the replication of viruses with both RNA and DNA genomes. In this review, we summarize the cellular functions and the emerging relationship between Schlafens and innate immunity. We also discuss the functions and distinctions of this emerging family of proteins as host restriction factors against viral infection. Further research into Schlafen protein function will provide insight into their mechanisms that contribute to intrinsic and innate host immunity. Full article
(This article belongs to the Special Issue Interaction between Virus and Host Innate Immune Systems)
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18 pages, 9780 KiB  
Review
Interaction between the Hepatitis B Virus and Cellular FLIP Variants in Viral Replication and the Innate Immune System
by Ah Ram Lee, Yong Kwang Park, Mehrangiz Dezhbord and Kyun-Hwan Kim
Viruses 2022, 14(2), 373; https://doi.org/10.3390/v14020373 - 11 Feb 2022
Cited by 3 | Viewed by 2416
Abstract
During viral evolution and adaptation, many viruses have utilized host cellular factors and machinery as their partners. HBx, as a multifunctional viral protein encoded by the hepatitis B virus (HBV), promotes HBV replication and greatly contributes to the development of HBV-associated hepatocellular carcinoma [...] Read more.
During viral evolution and adaptation, many viruses have utilized host cellular factors and machinery as their partners. HBx, as a multifunctional viral protein encoded by the hepatitis B virus (HBV), promotes HBV replication and greatly contributes to the development of HBV-associated hepatocellular carcinoma (HCC). HBx interacts with several host factors in order to regulate HBV replication and evolve carcinogenesis. The cellular FADD-like IL-1β-converting enzyme (FLICE)-like inhibitory protein (c-FLIP) is a major factor that functions in a variety of cellular pathways and specifically in apoptosis. It has been shown that the interaction between HBx and c-FLIP determines HBV fate. In this review, we provide a comprehensive and detailed overview of the interplay between c-FLIP and HBV in various environmental circumstances. We describe strategies adapted by HBV to establish its chronic infection. We also summarize the conventional roles of c-FLIP and highlight the functional outcome of the interaction between c-FLIP and HBV or other viruses in viral replication and the innate immune system. Full article
(This article belongs to the Special Issue Interaction between Virus and Host Innate Immune Systems)
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