Special Issue "The Host Interferon Response against RNA and DNA Viruses"

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 1799

Special Issue Editors

Dr. Melody Li
E-Mail Website
Guest Editor
Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA
Interests: RNA viruses; alphaviruses; flaviviruses; virus-host interactions; innate immune responses; interferon; interferon-stimulated genes; broad-spectrum antiviral host factors
Dr. Christel Uittenbogaart
E-Mail Website
Guest Editor
Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA
Interests: human T cell development; T cell receptor (TCR) alpha/beta cells; TCR gamma/delta cells; plasmacytoid (lymphoid -derived) dendritic cells; myeloid derived dendritic cells; Natural Killer (NK) cells; NK-T cells and regulatory T cells; HIV
Dr. Ting-Ting Wu
E-Mail Website
Guest Editor
Molecular & Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90095, USA
Interests: innate immunity; vaccine; gene regulation; herpesvirus; Kaposi Sarcoma-associated herpesvirus

Special Issue Information

Dear Colleagues,

The type I (α/β) interferon (IFN) response is the first and most critical line of host defense against viruses. Upon viral invasion, the host cell recognizes pathogen-associated molecular patterns (PAMPs), such as viral double-stranded RNA or DNA, and activates transcription factors IFN regulatory factors 3 or 7 (IRF3/7), leading to the production of type I IFN. Secreted IFN binds to the cell surface receptor on the infected or neighboring cells and activates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway, inducing expression of an array of IFN-stimulated genes (ISGs) that establish the antiviral state.

Many ISGs with antiviral activity have been identified and shown to inhibit different stages of the viral life cycle, such as endosomal fusion, translation, and release. However, they are just the tip of the iceberg. For some ISGs, it is not clear what the exact mechanisms underlying their inhibitory effects are. As we combat emerging viruses like SARS-CoV-2, a better understanding of the mechanism of broadly active ISGs is urgently needed. In addition, the antiviral role of a plethora of ISGs is yet to be uncovered. Moreover, viruses that are not sensitive to the antiviral action of well-characterized ISGs might have evolved strategies to evade or antagonize the IFN response. Characterizing the function of ISGs will illuminate viral processes targeted by innate immunity, cellular pathways usurped for antiviral activity, and uncover novel viral evasion strategies. This knowledge will allow us to develop new therapies that either mimic ISG action or reinforce the weak points of the IFN system.

This Special Issue is intended to provide an up-to-date view of the contribution of IFN and ISGs to immune control of viral infections. The emphasis is on the antiviral role and mechanism of ISGs that have been or are yet to be identified and evasions strategies employed by RNA and DNA viruses to evade these ISGs.

Dr. Melody Li
Dr. Christel Uittenbogaart
Dr. Ting-Ting Wu
Guest Editors

Manuscript Submission Information

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Keywords

  • antiviral proteins
  • antiviral ISGs
  • virus-host interactions
  • viral evasion of IFN

Published Papers (3 papers)

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Research

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Article
HIV-1 Accessory Proteins Impart a Modest Interferon Response and Upregulate Cell Cycle-Related Genes in Macrophages
Pathogens 2022, 11(2), 163; https://doi.org/10.3390/pathogens11020163 - 26 Jan 2022
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Abstract
HIV-1 infection of myeloid cells is associated with the induction of an IFN response. How HIV-1 manipulates and subverts the IFN response is of key interest for the design of therapeutics to improve immune function and mitigate immune dysregulation in people living with [...] Read more.
HIV-1 infection of myeloid cells is associated with the induction of an IFN response. How HIV-1 manipulates and subverts the IFN response is of key interest for the design of therapeutics to improve immune function and mitigate immune dysregulation in people living with HIV. HIV-1 accessory genes function to improve viral fitness by altering host pathways in ways that enable transmission to occur without interference from the immune response. We previously described changes in transcriptomes from HIV-1 infected and from IFN-stimulated macrophages and noted that transcription of IFN-regulated genes and genes related to cell cycle processes were upregulated during HIV-1 infection. In the present study, we sought to define the roles of individual viral accessory genes in upregulation of IFN-regulated and cell cycle-related genes using RNA sequencing. We observed that Vif induces a set of genes involved in mitotic processes and that these genes are potently downregulated upon stimulation with type-I and -II IFNs. Vpr also upregulated cell cycle-related genes and was largely responsible for inducing an attenuated IFN response. We note that the induced IFN response most closely resembled a type-III IFN response. Vpu and Nef-regulated smaller sets of genes whose transcriptomic signatures upon infection related to cytokine and chemokine processes. This work provides more insight regarding processes that are manipulated by HIV-1 accessory proteins at the transcriptional level. Full article
(This article belongs to the Special Issue The Host Interferon Response against RNA and DNA Viruses)
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Review

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Review
The Evolutionary Dance between Innate Host Antiviral Pathways and SARS-CoV-2
Pathogens 2022, 11(5), 538; https://doi.org/10.3390/pathogens11050538 - 03 May 2022
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Abstract
Compared to what we knew at the start of the SARS-CoV-2 global pandemic, our understanding of the interplay between the interferon signaling pathway and SARS-CoV-2 infection has dramatically increased. Innate antiviral strategies range from the direct inhibition of viral components to reprograming the [...] Read more.
Compared to what we knew at the start of the SARS-CoV-2 global pandemic, our understanding of the interplay between the interferon signaling pathway and SARS-CoV-2 infection has dramatically increased. Innate antiviral strategies range from the direct inhibition of viral components to reprograming the host’s own metabolic pathways to block viral infection. SARS-CoV-2 has also evolved to exploit diverse tactics to overcome immune barriers and successfully infect host cells. Herein, we review the current knowledge of the innate immune signaling pathways triggered by SARS-CoV-2 with a focus on the type I interferon response, as well as the mechanisms by which SARS-CoV-2 impairs those defenses. Full article
(This article belongs to the Special Issue The Host Interferon Response against RNA and DNA Viruses)
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Review
Surgical Strikes on Host Defenses: Role of the Viral Protease Activity in Innate Immune Antagonism
Pathogens 2022, 11(5), 522; https://doi.org/10.3390/pathogens11050522 - 28 Apr 2022
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Abstract
As a frontline defense mechanism against viral infections, the innate immune system is the primary target of viral antagonism. A number of virulence factors encoded by viruses play roles in circumventing host defenses and augmenting viral replication. Among these factors are viral proteases, [...] Read more.
As a frontline defense mechanism against viral infections, the innate immune system is the primary target of viral antagonism. A number of virulence factors encoded by viruses play roles in circumventing host defenses and augmenting viral replication. Among these factors are viral proteases, which are primarily responsible for maturation of viral proteins, but in addition cause proteolytic cleavage of cellular proteins involved in innate immune signaling. The study of these viral protease-mediated host cleavages has illuminated the intricacies of innate immune networks and yielded valuable insights into viral pathogenesis. In this review, we will provide a brief summary of how proteases of positive-strand RNA viruses, mainly from the Picornaviridae, Flaviviridae and Coronaviridae families, proteolytically process innate immune components and blunt their functions. Full article
(This article belongs to the Special Issue The Host Interferon Response against RNA and DNA Viruses)
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