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Pathogens
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Host-Pathogen Interactions during Pathogenic Human Coronavirus Infection
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Host-Pathogen Interactions during Pathogenic Human Coronavirus Infection

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

Deadline for manuscript submissions: closed (25 September 2023) | Viewed by 8040

Special Issue Editor

Dr. Masfique Mehedi

E-Mail Website
Guest Editor
School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, USA
Interests: host-pathogen interactions; RSV, SARS-CoV-2, cytoskeletal inflammation, respiratory diseases, live-attenuated vaacine, HMPV, HPIV, IAV, organ-on-chip, air-liquid interface
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, a causative agent of coronavirus disease 2019 (COVID-19)) is an enveloped virus responsible for the current never-ending pandemic. SARS-CoV-2 spreads human to human through aerosol and respiratory droplet-based virus transmission. SARS-CoV-2 contains a nonsegmented, positive-sense, single-strand RNA genome with a few unique features: two-thirds of viral RNA is translated into large polyproteins, and a discontinuous transcription process transcribes the remainder of the viral genome into a nested set of subgenomic mRNAs. Respiratory viruses appear to be diverse in cellular tropism, resulting in differences in virus-induced pathobiology, e.g., respiratory syncytial virus causes bronchiolitis, but SARS-COV-2 primarily causes pneumonia. Unlike many respiratory viruses, SARS-CoV-2 causes a systemic infection resulting in multiorgan infection and severe pathophysiology.

This Special Issue will cover a broad understanding of SARS-CoV-2 infection, including cell tropism, strain and variants, pathophysiology, ARDS, vaccine and therapeutics, vaccine injury, treatment, animal models, viral protein characterization, genome, immune response, cytoskeletal signaling, and the convalescent stage of SARS-CoV-2 infection.

Dr. Masfique Mehedi
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. Pathogens 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 2700 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

  • COVID-19
  • spike
  • mRNA
  • goblet cell
  • viremia
  • pneumonia
  • convalescent
  • antibody
  • transmission

Related Special Issue

Published Papers (4 papers)

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Research

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24 pages, 4867 KiB  
Article
The Therapeutic Monoclonal Antibody Bamlanivimab Does Not Enhance SARS-CoV-2 Infection by FcR-Mediated Mechanisms
by Robert W. Cross, Christopher M. Wiethoff, Patricia Brown-Augsburger, Shawn Berens, Jamie Blackbourne, Ling Liu, Xiaohua Wu, Jonathan Tetreault, Carter Dodd, Ramtin Sina, Derrick R. Witcher, Deanna Newcomb, Denzil Frost, Angela Wilcox, Viktoriya Borisevich, Krystle N. Agans, Courtney Woolsey, Abhishek N. Prasad, Daniel J. Deer, Joan B. Geisbert, Natalie S. Dobias, Karla A. Fenton, Beth Strifler, Philip Ebert, Richard Higgs, Anne Beall, Sumit Chanda, Laura Riva, Xin Yin and Thomas W. Geisbertadd Show full author list remove Hide full author list
Pathogens 2023, 12(12), 1408; https://doi.org/10.3390/pathogens12121408 - 30 Nov 2023
Cited by 1 | Viewed by 1125
Abstract
As part of the non-clinical safety package characterizing bamlanivimab (SARS-CoV-2 neutralizing monoclonal antibody), the risk profile for antibody-dependent enhancement of infection (ADE) was evaluated in vitro and in an African green monkey (AGM) model of COVID-19. In vitro ADE assays in primary human [...] Read more.
As part of the non-clinical safety package characterizing bamlanivimab (SARS-CoV-2 neutralizing monoclonal antibody), the risk profile for antibody-dependent enhancement of infection (ADE) was evaluated in vitro and in an African green monkey (AGM) model of COVID-19. In vitro ADE assays in primary human macrophage, Raji, or THP-1 cells were used to evaluate enhancement of viral infection. Bamlanivimab binding to C1q, FcR, and cell-based effector activity was also assessed. In AGMs, the impact of bamlanivimab pretreatment on viral loads and clinical and histological pathology was assessed to evaluate enhanced SARS-CoV-2 replication or pathology. Bamlanivimab did not increase viral replication in vitro, despite a demonstrated effector function. In vivo, no significant differences were found among the AGM groups for weight, temperature, or food intake. Treatment with bamlanivimab reduced viral loads in nasal and oral swabs and BAL fluid relative to control groups. Viral antigen was not detected in lung tissue from animals treated with the highest dose of bamlanivimab. Bamlanivimab did not induce ADE of SARS-CoV-2 infection in vitro or in an AGM model of infection at any dose evaluated. The findings suggest that high-affinity monoclonal antibodies pose a low risk of mediating ADE in patients and support their safety profile as a treatment of COVID-19 disease. Full article
(This article belongs to the Special Issue Host-Pathogen Interactions during Pathogenic Human Coronavirus Infection)
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10 pages, 1391 KiB  
Communication
Interleukin-6 and Its Soluble Receptor Complex in Intensive Care Unit COVID-19 Patients: An Analysis of Second Wave Patients
by Gaetano Di Spigna, Daniela Spalletti Cernia, Bianca Covelli, Maria Vargas, Valentina Rubino, Carmine Iacovazzo, Filomena Napolitano and Loredana Postiglione
Pathogens 2023, 12(10), 1264; https://doi.org/10.3390/pathogens12101264 - 20 Oct 2023
Viewed by 891
Abstract
In December 2019, a SARS-CoV-2 virus, coined Coronavirus Disease 2019 (COVID-19), discovered in Wuhan, China, affected the global population, causing more than a million and a half deaths. Since then, many studies have shown that the hyperinflammatory response of the most severely affected [...] Read more.
In December 2019, a SARS-CoV-2 virus, coined Coronavirus Disease 2019 (COVID-19), discovered in Wuhan, China, affected the global population, causing more than a million and a half deaths. Since then, many studies have shown that the hyperinflammatory response of the most severely affected patients was primarily related to a higher concentration of the pro-inflammatory cytokine interleukin-6, which directly correlated with disease severity and high mortality. Our study analyzes IL-6 and its soluble receptor complex (sIL-6R and sgp130) in critically ill COVID-19 patients who suffered severe respiratory failure from the perspective of the second COVID wave of 2020. A chemiluminescent immunoassay was performed for the determination of IL6 in serum together with an enzyme-linked immunosorbent assay to detect serum levels of sIL-6R and sgp130, which confirmed that the second wave’s serum levels of IL-6 were significantly elevated in the more severe patients, as with the first 2019 COVID-19 wave, resulting in adverse clinical outcomes. At present, considering that no specific treatment for severe COVID-19 cases in its later stages exists, these molecules could be considered promising markers for disease progression, illness severity, and risk of mortality. Full article
(This article belongs to the Special Issue Host-Pathogen Interactions during Pathogenic Human Coronavirus Infection)
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11 pages, 1087 KiB  
Article
Synergistic Detrimental Effects of Cigarette Smoke, Alcohol, and SARS-CoV-2 in COPD Bronchial Epithelial Cells
by Abenaya Muralidharan, Christopher D. Bauer, Dawn M. Katafiasz, Heather M. Strah, Aleem Siddique, St Patrick Reid, Kristina L. Bailey and Todd A. Wyatt
Pathogens 2023, 12(3), 498; https://doi.org/10.3390/pathogens12030498 - 22 Mar 2023
Cited by 1 | Viewed by 1658
Abstract
Lung conditions such as COPD, as well as risk factors such as alcohol misuse and cigarette smoking, can exacerbate COVID-19 disease severity. Synergistically, these risk factors can have a significant impact on immunity against pathogens. Here, we studied the effect of a short [...] Read more.
Lung conditions such as COPD, as well as risk factors such as alcohol misuse and cigarette smoking, can exacerbate COVID-19 disease severity. Synergistically, these risk factors can have a significant impact on immunity against pathogens. Here, we studied the effect of a short exposure to alcohol and/or cigarette smoke extract (CSE) in vitro on acute SARS-CoV-2 infection of ciliated human bronchial epithelial cells (HBECs) collected from healthy and COPD donors. We observed an increase in viral titer in CSE- or alcohol-treated COPD HBECs compared to untreated COPD HBECs. Furthermore, we treated healthy HBECs accompanied by enhanced lactate dehydrogenase activity, indicating exacerbated injury. Finally, IL-8 secretion was elevated due to the synergistic damage mediated by alcohol, CSE, and SARS-CoV-2 in COPD HBECs. Together, our data suggest that, with pre-existing COPD, short exposure to alcohol or CSE is sufficient to exacerbate SARS-CoV-2 infection and associated injury, impairing lung defences. Full article
(This article belongs to the Special Issue Host-Pathogen Interactions during Pathogenic Human Coronavirus Infection)
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Review

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20 pages, 2140 KiB  
Review
Towards Understanding Long COVID: SARS-CoV-2 Strikes the Host Cell Nucleus
by Laura Lafon-Hughes
Pathogens 2023, 12(6), 806; https://doi.org/10.3390/pathogens12060806 - 06 Jun 2023
Cited by 1 | Viewed by 3556
Abstract
Despite what its name suggests, the effects of the COVID-19 pandemic causative agent “Severe Acute Respiratory Syndrome Coronavirus-2” (SARS-CoV-2) were not always confined, neither temporarily (being long-term rather than acute, referred to as Long COVID) nor spatially (affecting several body systems). Moreover, the [...] Read more.
Despite what its name suggests, the effects of the COVID-19 pandemic causative agent “Severe Acute Respiratory Syndrome Coronavirus-2” (SARS-CoV-2) were not always confined, neither temporarily (being long-term rather than acute, referred to as Long COVID) nor spatially (affecting several body systems). Moreover, the in-depth study of this ss(+) RNA virus is defying the established scheme according to which it just had a lytic cycle taking place confined to cell membranes and the cytoplasm, leaving the nucleus basically “untouched”. Cumulative evidence shows that SARS-CoV-2 components disturb the transport of certain proteins through the nuclear pores. Some SARS-CoV-2 structural proteins such as Spike (S) and Nucleocapsid (N), most non-structural proteins (remarkably, Nsp1 and Nsp3), as well as some accessory proteins (ORF3d, ORF6, ORF9a) can reach the nucleoplasm either due to their nuclear localization signals (NLS) or taking a shuttle with other proteins. A percentage of SARS-CoV-2 RNA can also reach the nucleoplasm. Remarkably, controversy has recently been raised by proving that-at least under certain conditions-, SARS-CoV-2 sequences can be retrotranscribed and inserted as DNA in the host genome, giving rise to chimeric genes. In turn, the expression of viral-host chimeric proteins could potentially create neo-antigens, activate autoimmunity and promote a chronic pro-inflammatory state. Full article
(This article belongs to the Special Issue Host-Pathogen Interactions during Pathogenic Human Coronavirus Infection)
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