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Exploring the Pathogenetic Mechanisms in Respiratory Virus Infections: Recent Advances...
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Exploring the Pathogenetic Mechanisms in Respiratory Virus Infections: Recent Advances and Future Directions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 2950

Special Issue Editor

Dr. Marta De Angelis

E-Mail Website
Guest Editor
Department of Molecular Medicine, “Sapienza” University of Rome, Rome, Italy
Interests: respiratory viruses; molecular mechanisms involved in regulating viral replication and host response; intracellular redox-related pathways

Special Issue Information

Dear Colleagues,

Respiratory viral infections are a major concern for public health, representing the most prevalent causes of human disease worldwide and exerting considerable impact from epidemiological, clinical and economic perspectives. Among respiratory viruses, Influenza A and B viruses, respiratory syncytial virus, rhinovirus, adenovirus, parainfluenza virus as well as SARS-CoV-2 are the main agents causing mild upper respiratory tract infections or lower respiratory tract infections which can progress in serious complications for both pediatric and adult populations. Understanding the molecular mechanisms underlying virus-host interactions, pathogenesis, and immune evasion is crucial for developing effective preventive and therapeutic strategies.

The aim of this Special Issue is to highlight recent advances in the characterization of pathogenic mechanisms of respiratory virus infections.

The main themes of interest include:

  • interactions between viral and host components;
  • identification of cellular factors involved in regulating virus-life cycle;
  • viral proteins modulating host-cell pathways;
  • dysregulation of immune response upon infections.

Additionally, this issue aims to present new research on innovative therapeutic approaches against respiratory viruses. We welcome submissions of research or review articles that contribute to expand knowledge on the pathogenesis of emerging respiratory viral infections.

Dr. Marta De Angelis
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • respiratory viruses
  • virus-host interactions
  • inflammation
  • metabolic pathways

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Published Papers (2 papers)

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Research

23 pages, 12194 KiB  
Article
Characterization of Neutrophil Functional Responses to SARS-CoV-2 Infection in a Translational Feline Model for COVID-19
by Sachithra Gunasekara, Miruthula Tamil Selvan, Chelsea L. Murphy, Shoroq Shatnawi, Shannon Cowan, Sunil More, Jerry Ritchey, Craig A. Miller and Jennifer M. Rudd
Int. J. Mol. Sci. 2024, 25(18), 10054; https://doi.org/10.3390/ijms251810054 - 19 Sep 2024
Viewed by 1331
Abstract
There is a complex interplay between viral infection and host innate immune response regarding disease severity and outcomes. Neutrophil hyperactivation, including excessive release of neutrophil extracellular traps (NETs), is linked to exacerbated disease in acute COVID-19, notably in hospitalized patients. Delineating protective versus [...] Read more.
There is a complex interplay between viral infection and host innate immune response regarding disease severity and outcomes. Neutrophil hyperactivation, including excessive release of neutrophil extracellular traps (NETs), is linked to exacerbated disease in acute COVID-19, notably in hospitalized patients. Delineating protective versus detrimental neutrophil responses is essential to developing targeted COVID-19 therapies and relies on high-quality translational animal models. In this study, we utilize a previously established feline model for COVID-19 to investigate neutrophil dysfunction in which experimentally infected cats develop clinical disease that mimics acute COVID-19. Specific pathogen-free cats were inoculated with SARS-CoV-2 (B.1.617.2; Delta variant) (n = 24) or vehicle (n = 6). Plasma, bronchoalveolar lavage fluid, and lung tissues were collected at various time points over 12 days post-inoculation. Systematic and temporal evaluation of the kinetics of neutrophil activation was conducted by measuring markers of activation including myeloperoxidase (MPO), neutrophil elastase (NE), and citrullinated histone H3 (citH3) in SARS-CoV-2-infected cats at 4 and 12 days post-inoculation (dpi) and compared to vehicle-inoculated controls. Cytokine profiling supported elevated innate inflammatory responses with specific upregulation of neutrophil activation and NET formation-related markers, namely IL-8, IL-18, CXCL1, and SDF-1, in infected cats. An increase in MPO-DNA complexes and cell-free dsDNA in infected cats compared to vehicle-inoculated was noted and supported by histopathologic severity in respiratory tissues. Immunofluorescence analyses further supported correlation of NET markers with tissue damage, especially 4 dpi. Differential gene expression analyses indicated an upregulation of genes associated with innate immune and neutrophil activation pathways. Transcripts involved in activation and NETosis pathways were upregulated by 4 dpi and downregulated by 12 dpi, suggesting peak activation of neutrophils and NET-associated markers in the early acute stages of infection. Correlation analyses conducted between NET-specific markers and clinical scores as well as histopathologic scores support association between neutrophil activation and disease severity during SARS-CoV-2 infection in this model. Overall, this study emphasizes the effect of neutrophil activation and NET release in SARS-CoV-2 infection in a feline model, prompting further investigation into therapeutic strategies aimed at mitigating excessive innate inflammatory responses in COVID-19. Full article
(This article belongs to the Special Issue Exploring the Pathogenetic Mechanisms in Respiratory Virus Infections: Recent Advances and Future Directions)
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9 pages, 250 KiB  
Communication
TAS2R38 Genotype Does Not Affect SARS-CoV-2 Infection in Primary Ciliary Dyskinesia
by Gioia Piatti, Giorgia Girotto, Maria Pina Concas, Leonardo Braga, Umberto Ambrosetti and Mirko Aldè
Int. J. Mol. Sci. 2024, 25(16), 8635; https://doi.org/10.3390/ijms25168635 - 8 Aug 2024
Viewed by 872
Abstract
Several chronic respiratory diseases could be risk factors for acquiring SARS-CoV-2 infection: among them, Primary Ciliary Dyskinesia (PCD) is a rare (about 1:10.000) inherited ciliopathy (MIM 242650) characterized by recurrent upper and lower respiratory tract infections due to a dysfunction of the respiratory [...] Read more.
Several chronic respiratory diseases could be risk factors for acquiring SARS-CoV-2 infection: among them, Primary Ciliary Dyskinesia (PCD) is a rare (about 1:10.000) inherited ciliopathy (MIM 242650) characterized by recurrent upper and lower respiratory tract infections due to a dysfunction of the respiratory cilia. In this study, we aimed to investigate whether PCD subjects are more susceptible to infection by SARS-CoV-2 and whether some polymorphisms of the TAS2R38 bitter taste receptor correlate with an increased prevalence of SARS-CoV-2 infection and severity of symptoms. Patients answered several questions about possible SARS-CoV-2 infection, experienced symptoms, and vaccinations; in the case of infection, they also filled out a SNOT-22 questionnaire and ARTIQ. Forty PCD adult patients (mean age, 36.6 ± 16.7 years; 23 females, 17 males) participated in this study, out of which 30% had tested positive for COVID-19 during the last four years; most of them reported a mildly symptomatic disease. We found no differences in age or sex, but a statistically significant difference (p = 0.03) was observed in body mass index (BMI), which was higher in the COVID-acquired group (23.2 ± 3.3 vs. 20.1 ± 4.1 kg/m2). Genotyping for TAS2R38 polymorphisms showed a prevalence of 28.6% PAV/PAV, 48.6% PAV/AVI, and 22.8% AVI/AVI individuals in our cohort. In contrast to our hypothesis, we did not observe a protective role of the PAV allele towards SARS-CoV-2 infection. Conclusions: Our findings suggest that subjects with PCD may not be at increased risk of severe outcomes from COVID-19 and the TAS2R38 bitter taste receptor genotype does not affect SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Exploring the Pathogenetic Mechanisms in Respiratory Virus Infections: Recent Advances and Future Directions)
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