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Viral Strategies to Regulate Host Immunity or Signal Pathways

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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 July 2024 | Viewed by 5263

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Special Issue Editor

Dr. Bumsuk Hahm

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Guest Editor

Departments of Surgery and Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212, USA
Interests: viral immunity; RNA virus-host interaction; influenza; LCMV; sphingolipid network
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Viruses appear to have developed diverse strategies to regulate host immunity and cellular signal pathways in order to facilitate viral propagation. Highly pathogenic viruses effectively elude or suppress the host protective immune system and even utilize host machinery for robust viral replication or spread. Therefore, determining the mechanisms for pathogenic virus–host interactions and viral methodologies to escape the host immunity could help us understand how viruses cause diseases and ultimately help to design new therapeutics to cure the viral diseases.

This Special Issue will cover research on recent scientific discoveries about virus–host interaction, viral disruption of cellular signal pathways, viral utilization of host machinery, and viral tactics to escape or inhibit the host innate or adaptive immune responses. You are cordially invited to contribute unique research or review articles on the related research topics.

Dr. Bumsuk Hahm
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 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

virus–host interaction
viral immunity
viral pathogenesis
immune evasion
innate immunity
adaptive immunity
signal pathway

Published Papers (4 papers)

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Research

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18 pages, 2397 KiB

Open AccessArticle

Hypoxia and Activation of Neutrophil Degranulation-Related Genes in the Peripheral Blood of COVID-19 Patients

by Hongxing Lei

Viruses 2024, 16(2), 201; https://doi.org/10.3390/v16020201 - 28 Jan 2024

Viewed by 834

Abstract

Severe COVID-19 is characterized by systematic hyper-inflammation and subsequent damage to various organs. Therefore, it is critical to trace this cascade of hyper-inflammation. Blood transcriptome has been routinely utilized in the interrogation of host immune response in COVID-19 and other infectious conditions. In this study, consensus gene dysregulation in the blood was obtained from 13 independent transcriptome studies on COVID-19. Among the up-regulated genes, the most prominent functional categories were neutrophil degranulation and cell cycle, which is clearly different from the classical activation of interferon signaling pathway in seasonal flu. As for the potential upstream causal factors of the atypical gene dysregulation, systemic hypoxia was further examined because it is much more widely reported in COVID-19 than that in seasonal flu. It was found that both physiological and pathological hypoxia can induce activation of neutrophil degranulation-related genes in the blood. Furthermore, COVID-19 patients with different requirement for oxygen intervention showed distinctive levels of gene expression related to neutrophil degranulation in the whole blood, which was validated in isolated neutrophils. Thus, activation of neutrophil degranulation-related genes in the blood of COVID-19 could be partially attributed to hypoxia. Interestingly, similar pattern was also observed in H1N1 infection (the cause of Spanish flu) and several other severe respiratory viral infections. As for the molecular mechanism, both HIF-dependent and HIF-independent pathways have been examined. Since the activation of neutrophil degranulation-related genes is highly correlated with disease severity in COVID-19, early detection of hypoxia and active intervention may prevent further activation of neutrophil degranulation-related genes and other harmful downstream hyper-inflammation. This common mechanism is applicable to current and future pandemic as well as the severe form of common respiratory infection. Full article

(This article belongs to the Special Issue Viral Strategies to Regulate Host Immunity or Signal Pathways)

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14 pages, 2456 KiB

Open AccessArticle

Naringenin Improves Innate Immune Suppression after PRRSV Infection by Reactivating the RIG-I-MAVS Signaling Pathway, Promoting the Production of IFN-I

by Jiaying Yu, Haitao Shi, Ke Song, Yuxin Yang, Xinmiao Li, Luyuan Peng, Bendong Fu and Pengfei Yi

Viruses 2023, 15(11), 2172; https://doi.org/10.3390/v15112172 - 29 Oct 2023

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Abstract

Porcine reproductive and respiratory syndrome (PRRS) has been prevalent for nearly forty years since it was first reported. It has been one of the major diseases jeopardizing the healthy development of the world swine industry, as well as causing great economic losses to the industry’s economic development. Furthermore, no way has been found to combat the disease due to the immunosuppressive properties of its pathogen porcine reproductive and respiratory syndrome virus (PRRSV) infection. We previously examined the mRNA expression of IFN-I in PRRSV-infected Marc-145 cells at different time periods using qRT-PCR, and found that the mRNA expression of IFN-I in the late stage of PRRSV infection showed suppression. Naringenin is a flavonoid found in citrus fruits and has a very wide range of pharmacological activities. Therefore, the aim of the present study was to investigate the modulatory effect of naringenin on the suppressed innate immune response after PRRSV infection. The expression of IFN-I, IL-10, and ISGs in the late stage of PRRSV infection was examined using qRT-PCR, and the results showed that naringenin improved the expression of antiviral cytokines suppressed by PRRSV infection. Further results showed that naringenin treatment significantly up-regulated the expression of proteins related to the RIG-I-MAV immune signaling pathway, and that naringenin could not significantly activate the RIG-I-MAVS signaling pathway after the addition of the RIG-I inhibitor Cyclo. Overall, these data demonstrated that naringenin could improve the innate immune response suppressed by PRRSV infection by modulating the RIG-I-MAVS signaling pathway. Therefore, our study will provide a theoretical basis for the development of naringenin as a drug against immunosuppressive viral infectious disease infections. Full article

(This article belongs to the Special Issue Viral Strategies to Regulate Host Immunity or Signal Pathways)

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Review

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24 pages, 6549 KiB

Open AccessReview

Molecular Mechanisms of Ferroptosis and Its Role in Viral Pathogenesis

by Riwei Huang, Jiang Wu, Yaodan Ma and Kai Kang

Viruses 2023, 15(12), 2373; https://doi.org/10.3390/v15122373 - 01 Dec 2023

Viewed by 1516

Abstract

Ferroptosis is a novelty form of regulated cell death, and it is mainly characterized by iron accumulation and lipid peroxidation in the cells. Its underlying mechanism is related to the amino acid, iron, and lipid metabolisms. During viral infection, pathogenic microorganisms have evolved to interfere with ferroptosis, and ferroptosis is often manipulated by viruses to regulate host cell servicing for viral reproduction. Therefore, this review provides a comprehensive overview of the mechanisms underlying ferroptosis, elucidates the intricate signaling pathways involved, and explores the pivotal role of ferroptosis in the pathogenesis of viral infections. By enhancing our understanding of ferroptosis, novel therapeutic strategies can be devised to effectively prevent and treat diseases associated with this process. Furthermore, unraveling the developmental mechanisms through which viral infections exploit ferroptosis will facilitate development of innovative antiviral agents. Full article

(This article belongs to the Special Issue Viral Strategies to Regulate Host Immunity or Signal Pathways)

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12 pages, 1159 KiB

Open AccessReview

Protective versus Pathogenic Type I Interferon Responses during Virus Infections

by Kwang Il Jung, Savannah McKenna, Vijayamahantesh Vijayamahantesh, Ying He and Bumsuk Hahm

Viruses 2023, 15(9), 1916; https://doi.org/10.3390/v15091916 - 13 Sep 2023

Viewed by 1323

Abstract

Following virus infections, type I interferons are synthesized to induce the expression of antiviral molecules and interfere with virus replication. The importance of early antiviral type I IFN response against virus invasion has been emphasized during COVID-19 as well as in studies on the microbiome. Further, type I IFNs can directly act on various immune cells to enhance protective host immune responses to viral infections. However, accumulating data indicate that IFN responses can be harmful to the host by instigating inflammatory responses or inducing T cell suppression during virus infections. Also, inhibition of lymphocyte and dendritic cell development can be caused by type I IFN, which is independent of the traditional signal transducer and activator of transcription 1 signaling. Additionally, IFNs were shown to impair airway epithelial cell proliferation, which may affect late-stage lung tissue recovery from the infection. As such, type I IFN–virus interaction research is diverse, including host antiviral innate immune mechanisms in cells, viral strategies of IFN evasion, protective immunity, excessive inflammation, immune suppression, and regulation of tissue repair. In this report, these IFN activities are summarized with an emphasis placed on the functions of type I IFNs recently observed during acute or chronic virus infections. Full article

(This article belongs to the Special Issue Viral Strategies to Regulate Host Immunity or Signal Pathways)

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