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Microorganisms
Special Issues
Innate Antimicrobial Immunity and Virus–Bacteria Interactions
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Innate Antimicrobial Immunity and Virus–Bacteria Interactions

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Antimicrobial Agents and Resistance".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 5364

Special Issue Editor

Dr. Carolina Scagnolari

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Guest Editor
Laboratory of Virology, Department of Molecular Medicine, Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, 00185 Roma, Italy
Interests: virus-host interaction; antiviral immunity; virus interferon resistance; flavivirus, HIV; respiratory infectious diseases; cystic fibrosis; COVID-19 pathogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The outcome of microbial infections depends on the interplay between host factors and the environment. Host factors, like the activation of the type I-III interferon (IFN) innate immune responses, are involved in tuning antimicrobial and inflammation responses as well as emerging negative modifiers of many viral infections. However, the role of these antiviral genes in the context of bacterial infections has been not well characterized. Of note, bacteria and viruses often occupy the same niches, but their potential roles in promoting wellness or disease states as well as in modifying the innate immunity response has only recently gained traction. Hence, the scope of this Special Issue will be as follows:  I) to delineate the presence and demonstrate the clinical value of the IFN-signature and innate immunity in different bacteria or viral infections; ii) to better understand the dynamics between bacteria and viruses; and iii) to ascertain whether the virus–bacteria coinfection compromises the IFN and inflammatory response.

This Special Issue will provide some key examples of the importance of the innate immune response in the control of microbial infections as well as how virus–bacteria interactions can impact the infection process and the activation of host defenses.

Dr. Carolina Scagnolari
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. Microorganisms 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.

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Published Papers (2 papers)

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Research

11 pages, 736 KiB  
Communication
Distribution of Interferon Lambda 4 Single Nucleotide Polymorphism rs11322783 Genotypes in Patients with COVID-19
by Leonardo Sorrentino, Valentina Silvestri, Giuseppe Oliveto, Mirko Scordio, Federica Frasca, Matteo Fracella, Camilla Bitossi, Alessandra D’Auria, Letizia Santinelli, Lucia Gabriele, Alessandra Pierangeli, Claudio Maria Mastroianni, Gabriella d’Ettorre, Guido Antonelli, Antonio Caruz, Laura Ottini and Carolina Scagnolari
Microorganisms 2022, 10(2), 363; https://doi.org/10.3390/microorganisms10020363 - 4 Feb 2022
Cited by 4 | Viewed by 2272
Abstract
Type III interferons (IFN-III), also known as IFN-Lambda, have a pivotal role during SARS-CoV-2 infection. IFN-Lambda response among individuals is heterogeneous and its association with COVID-19 symptoms severity needs to be further clarified. We analyzed the genotype frequencies of IFNL4 single nucleotide polymorphism [...] Read more.
Type III interferons (IFN-III), also known as IFN-Lambda, have a pivotal role during SARS-CoV-2 infection. IFN-Lambda response among individuals is heterogeneous and its association with COVID-19 symptoms severity needs to be further clarified. We analyzed the genotype frequencies of IFNL4 single nucleotide polymorphism (SNP) rs11322783 in patients with COVID-19 (n = 128), in comparison with a validated data set of European healthy controls (n = 14152). The IFNL4 SNP was also analyzed according to the haematological and clinical parameters of patients with COVID-19. The distributions of IFNL4 genotypes among SARS-CoV-2 positive patients [TT/TT 41.4% (n = 53), TT/ΔG 47.7% (n = 61) and ΔG/ΔG 10.9% (n = 14)] and healthy controls were comparable. Different levels of white blood cells (p = 0.036) and neutrophils (p = 0.042) were found in the IFNL4 different genotypes in patients with COVID-19; the ΔG/ΔG genotype was more represented in the groups with low white blood cells and neutrophils. There were no differences in major inflammation parameters (C-reactive protein, D-dimer, Albumin, and Lactate-dehydrogenase (LDH)] and survival rate according to the IFNL4 genotypes. In conclusion, although patients with COVID-19 did not exhibit a different distribution of the IFNL4 SNP, the ΔG/ΔG genotype was associated with a lower count of immune cell populations. These findings need to be confirmed in larger groups of patients with COVID-19 and the role of IFNL4 SNP needs to be also investigated in other respiratory viral infections. Full article
(This article belongs to the Special Issue Innate Antimicrobial Immunity and Virus–Bacteria Interactions)
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8 pages, 918 KiB  
Communication
SARS-CoV-2 Entry Genes Expression in Relation with Interferon Response in Cystic Fibrosis Patients
by Camilla Bitossi, Federica Frasca, Agnese Viscido, Giuseppe Oliveto, Mirko Scordio, Laura Belloni, Giuseppe Cimino, Valeria Pietropaolo, Massimo Gentile, Gabriella d’Ettorre, Fabio Midulla, Maria Trancassini, Guido Antonelli, Alessandra Pierangeli and Carolina Scagnolari
Microorganisms 2021, 9(1), 93; https://doi.org/10.3390/microorganisms9010093 - 3 Jan 2021
Cited by 5 | Viewed by 2625
Abstract
The expression rate of SARS-CoV-2 entry genes, angiotensin-converting enzyme 2 (ACE2), the main viral receptor and the proteases, furin and transmembrane serine protease 2 (TMPRSS2) in cystic fibrosis (CF) individuals is poorly known. Hence, we examined their levels in upper respiratory samples of [...] Read more.
The expression rate of SARS-CoV-2 entry genes, angiotensin-converting enzyme 2 (ACE2), the main viral receptor and the proteases, furin and transmembrane serine protease 2 (TMPRSS2) in cystic fibrosis (CF) individuals is poorly known. Hence, we examined their levels in upper respiratory samples of CF patients (n = 46) and healthy controls (n = 45). Moreover, we sought to understand the interplay of type I interferon (IFN-I) with ACE2, furin and TMPRSS2 by evaluating their gene expression with respect to ISG15, a well-known marker of IFN activation, in upper respiratory samples and after ex vivo IFNβ exposure. Lower ACE2 levels and trends toward the reduction of furin and TMPRSS2 were found in CF patients compared with the healthy controls; decreased ACE2 amounts were also detected in CF individuals with pancreatic insufficiency and in those receiving inhaled antibiotics. Moreover, there was a strong positive correlation between ISG15 and ACE2 levels. However, after ex vivo IFNβ stimulation of nasopharyngeal cells, the truncated isoform (dACE2), recently demonstrated as the IFN stimulated one with respect to the full-length isoform (flACE2), slightly augmented in cells from CF patients whereas in those from healthy donors, dACE2 levels showed variable levels of upregulation. An altered expression of SARS-COV-2 entry genes and a poor responsiveness of dACE2 to IFN-I stimulation might be crucial in the diffusion of SARS-CoV-2 infection in CF. Full article
(This article belongs to the Special Issue Innate Antimicrobial Immunity and Virus–Bacteria Interactions)
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