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Viruses
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Coronaviruses Pathogenesis, Immunity, and Antivirals
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Coronaviruses Pathogenesis, Immunity, and Antivirals

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Coronaviruses".

Deadline for manuscript submissions: 25 January 2025 | Viewed by 2661

Special Issue Editors

Prof. Dr. Wentao Li

grade E-Mail Website
Guest Editor
1. National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
2. The Cooperative Innovation Center for Sustainable Pig Production, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
Interests: virology; ASFV; viral entry; emerging viruses; virus discovery; infectious diseases; coronavirus
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Fei Yu

E-Mail Website
Guest Editor
Hebei Key Laboratory of Analysis and Control of Zoonotic Pathogenic Microorganism, College of Life Sciences, Hebei Agricultural University, Baoding 071001, China
Interests: influenza; COVID-19; HIV; antivirals

Special Issue Information

Dear Colleagues,

The Coronaviridae family includes a large number of viruses affecting humans, farm animals, pets, wildlife, and birds. Since coronaviruses have a broad host range and tropism, there is a continuous emergence of new coronaviruses, new serotypes, and new variants of the currently known coronaviruses. Some of them might cross the species barrier and infect humans, such as in the ongoing SARS-CoV-2 epidemic. Thus, it is important to study the pathogenesis and immunity of coronaviruses to better develop antiviral drugs and vaccines. In this Special Issue of Viruses, we invite the submission of original research papers and review articles spanning all aspects of coronaviruses, including molecular mechanisms mediating virus virulence, the molecular basis of virus replication, virus pathogenesis, virus diagnosis, animal models, host immune responses involved in protection against infection, the development of vaccines and antiviral drugs, and coronaviruses in wildlife.

Prof. Dr. Wentao Li
Prof. Dr. Fei Yu
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

  • coronaviruses
  • virus pathogenesis
  • animal models
  • immune response
  • development of vaccines and antiviral drugs

Published Papers (4 papers)

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Research

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17 pages, 3087 KiB  
Article
Protein C Pretreatment Protects Endothelial Cells from SARS-CoV-2-Induced Activation
by Bruna Rafaela dos Santos Silva, Davi Sidarta-Oliveira, Joseane Morari, Bruna Bombassaro, Carlos Poblete Jara, Camila Lopes Simeoni, Pierina Lorencini Parise, José Luiz Proenca-Modena, Licio A. Velloso, William H. Velander and Eliana P. Araújo
Viruses 2024, 16(7), 1049; https://doi.org/10.3390/v16071049 - 28 Jun 2024
Viewed by 428
Abstract
SARS-CoV-2 can induce vascular dysfunction and thrombotic events in patients with severe COVID-19; however, the cellular and molecular mechanisms behind these effects remain largely unknown. In this study, we used a combination of experimental and in silico approaches to investigate the role of [...] Read more.
SARS-CoV-2 can induce vascular dysfunction and thrombotic events in patients with severe COVID-19; however, the cellular and molecular mechanisms behind these effects remain largely unknown. In this study, we used a combination of experimental and in silico approaches to investigate the role of PC in vascular and thrombotic events in COVID-19. Single-cell RNA-sequencing data from patients with COVID-19 and healthy subjects were obtained from the publicly available Gene Expression Omnibus (GEO) repository. In addition, HUVECs were treated with inactive protein C before exposure to SARS-CoV-2 infection or a severe COVID-19 serum. An RT-qPCR array containing 84 related genes was used, and the candidate genes obtained were evaluated. Activated protein C levels were measured using an ELISA kit. We identified at the single-cell level the expression of several pro-inflammatory and pro-coagulation genes in endothelial cells from the patients with COVID-19. Furthermore, we demonstrated that exposure to SARS-CoV-2 promoted transcriptional changes in HUVECs that were partly reversed by the activated protein C pretreatment. We also observed that the serum of severe COVID-19 had a significant amount of activated protein C that could protect endothelial cells from serum-induced activation. In conclusion, activated protein C protects endothelial cells from pro-inflammatory and pro-coagulant effects during exposure to the SARS-CoV-2 virus. Full article
(This article belongs to the Special Issue Coronaviruses Pathogenesis, Immunity, and Antivirals)
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16 pages, 7293 KiB  
Article
SARS-CoV-2 Accessory Protein ORF8 Targets the Dimeric IgA Receptor pIgR
by Frederique Laprise, Ariana Arduini, Mathew Duguay, Qinghua Pan and Chen Liang
Viruses 2024, 16(7), 1008; https://doi.org/10.3390/v16071008 - 22 Jun 2024
Viewed by 589
Abstract
SARS-CoV-2 is a highly pathogenic respiratory virus that successfully initiates and establishes its infection at the respiratory mucosa. However, little is known about how SARS-CoV-2 antagonizes the host’s mucosal immunity. Recent findings have shown a marked reduction in the expression of the polymeric [...] Read more.
SARS-CoV-2 is a highly pathogenic respiratory virus that successfully initiates and establishes its infection at the respiratory mucosa. However, little is known about how SARS-CoV-2 antagonizes the host’s mucosal immunity. Recent findings have shown a marked reduction in the expression of the polymeric Ig receptor (pIgR) in COVID-19 patients. This receptor maintains mucosal homeostasis by transporting the dimeric IgA (dIgA) and pentameric IgM (pIgM) across mucosal epithelial cells to neutralize the invading respiratory pathogens. By studying the interaction between pIgR and SARS-CoV-2 proteins, we discovered that the viral accessory protein Open Reading Frame 8 (ORF8) potently downregulates pIgR expression and that this downregulation activity of ORF8 correlates with its ability to interact with pIgR. Importantly, the ORF8-mediated downregulation of pIgR diminishes the binding of dIgA or pIgM, and the ORF8 proteins of the variants of concern of SARS-CoV-2 preserve the function of downregulating pIgR, indicating the importance of this conserved activity of ORF8 in SARS-CoV-2 pathogenesis. We further observed that the secreted ORF8 binds to cell surface pIgR, but that this interaction does not trigger the cellular internalization of ORF8, which requires the binding of dIgA to pIgR. These findings suggest the role of ORF8 in SARS-CoV-2 mucosal immune evasion. Full article
(This article belongs to the Special Issue Coronaviruses Pathogenesis, Immunity, and Antivirals)
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21 pages, 1658 KiB  
Article
T-Cell Epitope Mapping of SARS-CoV-2 Reveals Coordinated IFN-γ Production and Clonal Expansion of T Cells Facilitates Recovery from COVID-19
by Xing Fan, Jin-Wen Song, Wen-Jing Cao, Ming-Ju Zhou, Tao Yang, Jing Wang, Fan-Ping Meng, Ming Shi, Chao Zhang and Fu-Sheng Wang
Viruses 2024, 16(7), 1006; https://doi.org/10.3390/v16071006 - 22 Jun 2024
Viewed by 538
Abstract
Background: T-cell responses can be protective or detrimental during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; however, the underlying mechanism is poorly understood. Methods: In this study, we screened 144 15-mer peptides spanning the SARS-CoV-2 spike, nucleocapsid (NP), M, ORF8, ORF10, and [...] Read more.
Background: T-cell responses can be protective or detrimental during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; however, the underlying mechanism is poorly understood. Methods: In this study, we screened 144 15-mer peptides spanning the SARS-CoV-2 spike, nucleocapsid (NP), M, ORF8, ORF10, and ORF3a proteins and 39 reported SARS-CoV-1 peptides in peripheral blood mononuclear cells (PBMCs) from nine laboratory-confirmed coronavirus disease 2019 (COVID-19) patients (five moderate and four severe cases) and nine healthy donors (HDs) collected before the COVID-19 pandemic. T-cell responses were monitored by IFN-γ and IL-17A production using ELISA, and the positive samples were sequenced for the T cell receptor (TCR) β chain. The positive T-cell responses to individual SARS-CoV-2 peptides were validated by flow cytometry. Results: COVID-19 patients with moderate disease produced more IFN-γ than HDs and patients with severe disease (moderate vs. HDs, p < 0.0001; moderate vs. severe, p < 0.0001) but less IL-17A than those with severe disease (p < 0.0001). A positive correlation was observed between IFN-γ production and T-cell clonal expansion in patients with moderate COVID-19 (r = 0.3370, p = 0.0214) but not in those with severe COVID-19 (r = −0.1700, p = 0.2480). Using flow cytometry, we identified that a conserved peptide of the M protein (Peptide-120, P120) was a dominant epitope recognized by CD8+ T cells in patients with moderate disease. Conclusion: Coordinated IFN-γ production and clonal expansion of SARS-CoV-2-specific T cells are associated with disease resolution in COVID-19. Our findings contribute to a better understanding of T-cell-mediated immunity in COVID-19 and may inform future strategies for managing and preventing severe outcomes of SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Coronaviruses Pathogenesis, Immunity, and Antivirals)
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Review

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20 pages, 6148 KiB  
Review
3-Chymotrypsin-like Protease (3CLpro) of SARS-CoV-2: Validation as a Molecular Target, Proposal of a Novel Catalytic Mechanism, and Inhibitors in Preclinical and Clinical Trials
by Vitor Martins de Freitas Amorim, Eduardo Pereira Soares, Anielle Salviano de Almeida Ferrari, Davi Gabriel Salustiano Merighi, Robson Francisco de Souza, Cristiane Rodrigues Guzzo and Anacleto Silva de Souza
Viruses 2024, 16(6), 844; https://doi.org/10.3390/v16060844 - 24 May 2024
Viewed by 774
Abstract
Proteases represent common targets in combating infectious diseases, including COVID-19. The 3-chymotrypsin-like protease (3CLpro) is a validated molecular target for COVID-19, and it is key for developing potent and selective inhibitors for inhibiting viral replication of SARS-CoV-2. In this review, we discuss structural [...] Read more.
Proteases represent common targets in combating infectious diseases, including COVID-19. The 3-chymotrypsin-like protease (3CLpro) is a validated molecular target for COVID-19, and it is key for developing potent and selective inhibitors for inhibiting viral replication of SARS-CoV-2. In this review, we discuss structural relationships and diverse subsites of 3CLpro, shedding light on the pivotal role of dimerization and active site architecture in substrate recognition and catalysis. Our analysis of bioinformatics and other published studies motivated us to investigate a novel catalytic mechanism for the SARS-CoV-2 polyprotein cleavage by 3CLpro, centering on the triad mechanism involving His41-Cys145-Asp187 and its indispensable role in viral replication. Our hypothesis is that Asp187 may participate in modulating the pKa of the His41, in which catalytic histidine may act as an acid and/or a base in the catalytic mechanism. Recognizing Asp187 as a crucial component in the catalytic process underscores its significance as a fundamental pharmacophoric element in drug design. Next, we provide an overview of both covalent and non-covalent inhibitors, elucidating advancements in drug development observed in preclinical and clinical trials. By highlighting various chemical classes and their pharmacokinetic profiles, our review aims to guide future research directions toward the development of highly selective inhibitors, underscore the significance of 3CLpro as a validated therapeutic target, and propel the progression of drug candidates through preclinical and clinical phases. Full article
(This article belongs to the Special Issue Coronaviruses Pathogenesis, Immunity, and Antivirals)
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