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Viruses
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Virus-Induced Cytokine Storms
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Virus-Induced Cytokine Storms

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 (15 June 2021) | Viewed by 27818

Special Issue Editor

Dr. Byram W. Bridle

E-Mail Website
Guest Editor
Ontario Veterinary College, University of Guelph, Guelph, ON N1G 2W1, Canada
Interests: viral immunology; virus-vectored vaccines; oncolytic viruses

Special Issue Information

Dear Colleagues,

Cytokines are critical for cell-to-cell communication within the immune system. Their induction after sensing virus-associated molecular patterns by pattern recognition receptors in or on sentinel cells is essential to the resolution of infectious diseases. However, excessive production of pro-inflammatory cytokines are a major clinical issue due to their association with a number of pathologies, including lung damage after infection with severe acute respiratory syndrome-coronavirus-2 (the causative agent of the coronavirus disease identified in 2019 [COVID-19]), related coronaviruses, influenza viruses and others. Indeed, many deaths associated with influenza, Ebola, dengue viruses, and coronaviruses are caused by grossly excessive cytokine responses that lead to severe inflammatory response syndrome and a state of shock with acute loss of blood pressure. Biological factors such as age and sex can influence the severity and outcomes of these virus-induced cytokine storms.

The aim of this Special Issue of Viruses is to publish original research articles and timely reviews to facilitate a better understanding of mechanisms behind dysregulated cytokine responses to viruses, with an emphasis on identifying novel treatment strategies for these challenging clinical scenarios.

Dr. Byram W. Bridle
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

  • viruses
  • infectious diseases
  • cytokine storm
  • cytokines
  • chemokines
  • immune response
  • host response
  • leukocytes
  • severe acute respiratory syndrome (SARS)
  • COVID-19
  • influenza virus
  • ebola virus
  • dengue virus
  • sex as a biological variable
  • Age as a variable

Published Papers (5 papers)

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Research

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10 pages, 772 KiB  
Communication
Population Difference in Allele Frequency of HLA-C*05 and Its Correlation with COVID-19 Mortality
by Atsushi Sakuraba, Haider Haider and Toshiro Sato
Viruses 2020, 12(11), 1333; https://0-doi-org.brum.beds.ac.uk/10.3390/v12111333 - 20 Nov 2020
Cited by 40 | Viewed by 3867
Abstract
Background: coronavirus disease 2019 (COVID-19) causes severe illness including cytokine storms, but mortality among countries differs largely. In the present study, we investigated the association between human leukocyte antigen (HLA) class I, which plays a major role in susceptibility to viral infections, and [...] Read more.
Background: coronavirus disease 2019 (COVID-19) causes severe illness including cytokine storms, but mortality among countries differs largely. In the present study, we investigated the association between human leukocyte antigen (HLA) class I, which plays a major role in susceptibility to viral infections, and the mortality of COVID-19. Methods: data of allele frequencies of HLA-A, -B and -C and COVID-19 mortality were obtained for 74 countries from the Allele Frequency Net Database and worldometer.info. Association between allele frequency of each HLA and mortality was assessed by linear regression followed by multivariable regression. Subsequently, association of HLA-C*05 to its receptor KIR2DS4fl, expressed on natural killer (NK) cells, and differential mortality to historic pandemics were analyzed. Results: HLA-A*01, -B*07, -B*08, -B*44 and -C*05 were significantly associated with the risk of deaths (adjusted p = 0.040, 0.00081, 0.047, 0.0022, 0.00032, respectively), but only HLA-C*05 remained statistically significant (p = 0.000027) after multivariable regression. A 1% increase in the allele frequency of HLA-C*05 was associated with an increase of 44 deaths/million. Countries with different mortality could be categorized by the distribution of HLA-C*05 and its receptor KIR2DS4fl, which in combination cause NK cell-induced hyperactive immune response. Countries with similar ethnic and/or geographic background responded in a similar pattern to each pandemic. Conclusions: we demonstrated that allele frequency of HLA-C*05 and the distribution pattern with its receptor KIR2DS4fl strongly correlated with COVID-19 mortality. Host genetic variance of innate immunity may contribute to the difference in mortality among various countries and further investigation using patient samples is warranted. Full article
(This article belongs to the Special Issue Virus-Induced Cytokine Storms)
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Review

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20 pages, 880 KiB  
Review
The Roles of Neutrophils in Cytokine Storms
by Lily Chan, Negar Karimi, Solmaz Morovati, Kasra Alizadeh, Julia E. Kakish, Sierra Vanderkamp, Fatemeh Fazel, Christina Napoleoni, Kimia Alizadeh, Yeganeh Mehrani, Jessica A. Minott, Byram W. Bridle and Khalil Karimi
Viruses 2021, 13(11), 2318; https://0-doi-org.brum.beds.ac.uk/10.3390/v13112318 - 21 Nov 2021
Cited by 29 | Viewed by 5300
Abstract
A cytokine storm is an abnormal discharge of soluble mediators following an inappropriate inflammatory response that leads to immunopathological events. Cytokine storms can occur after severe infections as well as in non-infectious situations where inflammatory cytokine responses are initiated, then exaggerated, but fail [...] Read more.
A cytokine storm is an abnormal discharge of soluble mediators following an inappropriate inflammatory response that leads to immunopathological events. Cytokine storms can occur after severe infections as well as in non-infectious situations where inflammatory cytokine responses are initiated, then exaggerated, but fail to return to homeostasis. Neutrophils, macrophages, mast cells, and natural killer cells are among the innate leukocytes that contribute to the pathogenesis of cytokine storms. Neutrophils participate as mediators of inflammation and have roles in promoting homeostatic conditions following pathological inflammation. This review highlights the advances in understanding the mechanisms governing neutrophilic inflammation against viral and bacterial pathogens, in cancers, and in autoimmune diseases, and how neutrophils could influence the development of cytokine storm syndromes. Evidence for the destructive potential of neutrophils in their capacity to contribute to the onset of cytokine storm syndromes is presented across a multitude of clinical scenarios. Further, a variety of potential therapeutic strategies that target neutrophils are discussed in the context of suppressing multiple inflammatory conditions. Full article
(This article belongs to the Special Issue Virus-Induced Cytokine Storms)
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27 pages, 484 KiB  
Review
Human Coronaviruses: Counteracting the Damage by Storm
by Dewald Schoeman and Burtram C. Fielding
Viruses 2021, 13(8), 1457; https://0-doi-org.brum.beds.ac.uk/10.3390/v13081457 - 27 Jul 2021
Cited by 5 | Viewed by 4509
Abstract
Over the past 18 years, three highly pathogenic human (h) coronaviruses (CoVs) have caused severe outbreaks, the most recent causative agent, SARS-CoV-2, being the first to cause a pandemic. Although much progress has been made since the COVID-19 pandemic started, much about SARS-CoV-2 [...] Read more.
Over the past 18 years, three highly pathogenic human (h) coronaviruses (CoVs) have caused severe outbreaks, the most recent causative agent, SARS-CoV-2, being the first to cause a pandemic. Although much progress has been made since the COVID-19 pandemic started, much about SARS-CoV-2 and its disease, COVID-19, is still poorly understood. The highly pathogenic hCoVs differ in some respects, but also share some similarities in clinical presentation, the risk factors associated with severe disease, and the characteristic immunopathology associated with the progression to severe disease. This review aims to highlight these overlapping aspects of the highly pathogenic hCoVs—SARS-CoV, MERS-CoV, and SARS-CoV-2—briefly discussing the importance of an appropriately regulated immune response; how the immune response to these highly pathogenic hCoVs might be dysregulated through interferon (IFN) inhibition, antibody-dependent enhancement (ADE), and long non-coding RNA (lncRNA); and how these could link to the ensuing cytokine storm. The treatment approaches to highly pathogenic hCoV infections are discussed and it is suggested that a greater focus be placed on T-cell vaccines that elicit a cell-mediated immune response, using rapamycin as a potential agent to improve vaccine responses in the elderly and obese, and the potential of stapled peptides as antiviral agents. Full article
(This article belongs to the Special Issue Virus-Induced Cytokine Storms)
16 pages, 1310 KiB  
Review
The Mechanism behind Influenza Virus Cytokine Storm
by Yinuo Gu, Xu Zuo, Siyu Zhang, Zhuoer Ouyang, Shengyu Jiang, Fang Wang and Guoqiang Wang
Viruses 2021, 13(7), 1362; https://0-doi-org.brum.beds.ac.uk/10.3390/v13071362 - 14 Jul 2021
Cited by 69 | Viewed by 7430
Abstract
Influenza viruses are still a serious threat to human health. Cytokines are essential for cell-to-cell communication and viral clearance in the immune system, but excessive cytokines can cause serious immune pathology. Deaths caused by severe influenza are usually related to cytokine storms. The [...] Read more.
Influenza viruses are still a serious threat to human health. Cytokines are essential for cell-to-cell communication and viral clearance in the immune system, but excessive cytokines can cause serious immune pathology. Deaths caused by severe influenza are usually related to cytokine storms. The recent literature has described the mechanism behind the cytokine–storm network and how it can exacerbate host pathological damage. Biological factors such as sex, age, and obesity may cause biological differences between different individuals, which affects cytokine storms induced by the influenza virus. In this review, we summarize the mechanism behind influenza virus cytokine storms and the differences in cytokine storms of different ages and sexes, and in obesity. Full article
(This article belongs to the Special Issue Virus-Induced Cytokine Storms)
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24 pages, 1986 KiB  
Review
Demystifying Excess Immune Response in COVID-19 to Reposition an Orphan Drug for Down-Regulation of NF-κB: A Systematic Review
by Apparao Peddapalli, Manish Gehani, Arunasree M. Kalle, Siva R. Peddapalli, Angela E. Peter and Shashwat Sharad
Viruses 2021, 13(3), 378; https://0-doi-org.brum.beds.ac.uk/10.3390/v13030378 - 27 Feb 2021
Cited by 13 | Viewed by 5574
Abstract
The immunological findings from autopsies, biopsies, and various studies in COVID-19 patients show that the major cause of morbidity and mortality in COVID-19 is excess immune response resulting in hyper-inflammation. With the objective to review various mechanisms of excess immune response in adult [...] Read more.
The immunological findings from autopsies, biopsies, and various studies in COVID-19 patients show that the major cause of morbidity and mortality in COVID-19 is excess immune response resulting in hyper-inflammation. With the objective to review various mechanisms of excess immune response in adult COVID-19 patients, Pubmed was searched for free full articles not related to therapeutics or co-morbid sub-groups, published in English until 27 October 2020, irrespective of type of article, country, or region. Joanna Briggs Institute’s design-specific checklists were used to assess the risk of bias. Out of 122 records screened for eligibility, 42 articles were included in the final review. The review found that eventually, most mechanisms result in cytokine excess and up-regulation of Nuclear Factor-κB (NF-κB) signaling as a common pathway of excess immune response. Molecules blocking NF-κB or targeting downstream effectors like Tumour Necrosis Factor α (TNFα) are either undergoing clinical trials or lack specificity and cause unwanted side effects. Neutralization of upstream histamine by histamine-conjugated normal human immunoglobulin has been demonstrated to inhibit the nuclear translocation of NF-κB, thereby preventing the release of pro-inflammatory cytokines Interleukin (IL) 1β, TNF-α, and IL-6 and IL-10 in a safer manner. The authors recommend repositioning it in COVID-19. Full article
(This article belongs to the Special Issue Virus-Induced Cytokine Storms)
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