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Viral Infections and Immune Responses
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Viral Infections and Immune Responses

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 3122

Special Issue Editors

Dr. Alessandra Ruggiero

E-Mail Website
Guest Editor
Department Neurosciences, Biomedicine and Movement Sciences, School of Medicine, University of Verona, Strada le Grazie 8, 37134 Verona, Italy
Interests: virology; immunology; HIV-1; SARS-CoV2; HIV and SARS-CoV-2 immunology; T and B cellular response; humoral response; quantification of virus reservoir; HIV persistence; neurovirology; neutralization assay; vaccinology
Special Issues, Collections and Topics in MDPI journals
Dr. Marco Iannetta

E-Mail Website
Guest Editor
Department of System Medicine, Tor Vergata University of Rome, 00133 Roma, RM, Italy
Interests: infectious diseases; viral infections; emerging infectious diseases; innate immunity; HIV; dendritic cells; flow cytometry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pathogen–host interplay includes a fine molecular stream of pathways. These interactions determine whether a pathogen will overcome the host immune response driving the emergence of the symptoms associated with the disease and with different possible clinical outcomes. It should be noted that there are different gaps in our knowledge on the virus–host immune response relationship and it is fundamental to fill these gaps in order to design efficient vaccines and therapies. The present Special Issue seeks to improve the current body of literature by accepting all works exploring the virus–host interaction spanning from human to animal viruses that potentially represent a global health threat. All papers including in vitro infection systems, characterisation of the anti-viral immune responses and molecular characterisation of the virus–host interactions will be considered for publication in this Special Issue.

Dr. Alessandra Ruggiero
Dr. Marco Iannetta
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. 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

  • virus
  • infections
  • immune response
  • T-cells
  • B-cells
  • antibodies
  • neutralizing activity

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Published Papers (3 papers)

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Research

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14 pages, 4707 KiB  
Article
Cross-Reactive Immune Response of Bovine Coronavirus Spike Glycoprotein to SARS-CoV-2 Variants of Concern
by Chiara Cossu, Valentina Franceschi, Antonino Di Lorenzo, Elisabetta Bolli, Sergio Minesso, Camilla Cotti, Laura Conti and Gaetano Donofrio
Int. J. Mol. Sci. 2024, 25(21), 11509; https://doi.org/10.3390/ijms252111509 - 26 Oct 2024
Viewed by 1060
Abstract
The high variability observed in the clinical symptoms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections has been attributed to the presence, in a proportion of infection-naive subjects, of pre-existing cross-reactive immune responses. Here, we demonstrate that the bovine coronavirus spike protein [...] Read more.
The high variability observed in the clinical symptoms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections has been attributed to the presence, in a proportion of infection-naive subjects, of pre-existing cross-reactive immune responses. Here, we demonstrate that the bovine coronavirus spike protein (BoS) may represent a source of protective immunity to SARS-CoV-2. Indeed, vaccination of BALB/c mice with a Bovine herpesvirus 4 (BoHV-4)-based vector expressing BoS induced both cell-mediated and humoral immune responses that cross-react with SARS-CoV-2 spike protein. Although the spike-specific antibodies induced by BoS did not neutralize SARS-CoV-2, the T lymphocytes activated by BoS were able to induce cytotoxicity of cells expressing spike proteins derived from several SARS-CoV-2 variants. These results demonstrate that immunization with BoS may represent a source of cross-reactive immunity to SARS-CoV-2, and that these cross-reactive immune responses may exert protective functions. These results contribute to deciphering the mechanisms responsible for lack or mildness of symptoms observed in many individuals upon SARS-CoV-2 infection and may open new ways for the development of new vaccines for coronaviruses. Full article
(This article belongs to the Special Issue Viral Infections and Immune Responses)
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18 pages, 3681 KiB  
Article
Post-Transcriptional Induction of the Antiviral Host Factor GILT/IFI30 by Interferon Gamma
by Taisuke Nakamura, Mai Izumida, Manya Bakatumana Hans, Shuichi Suzuki, Kensuke Takahashi, Hideki Hayashi, Koya Ariyoshi and Yoshinao Kubo
Int. J. Mol. Sci. 2024, 25(17), 9663; https://doi.org/10.3390/ijms25179663 - 6 Sep 2024
Cited by 1 | Viewed by 735
Abstract
Gamma-interferon-inducible lysosomal thiol reductase (GILT) plays pivotal roles in both adaptive and innate immunities. GILT exhibits constitutive expression within antigen-presenting cells, whereas in other cell types, its expression is induced by interferon gamma (IFN-γ). Gaining insights into the precise molecular mechanism governing the [...] Read more.
Gamma-interferon-inducible lysosomal thiol reductase (GILT) plays pivotal roles in both adaptive and innate immunities. GILT exhibits constitutive expression within antigen-presenting cells, whereas in other cell types, its expression is induced by interferon gamma (IFN-γ). Gaining insights into the precise molecular mechanism governing the induction of GILT protein by IFN-γ is of paramount importance for adaptive and innate immunities. In this study, we found that the 5′ segment of GILT mRNA inhibited GILT protein expression regardless of the presence of IFN-γ. Conversely, the 3′ segment of GILT mRNA suppressed GILT protein expression in the absence of IFN-γ, but it loses this inhibitory effect in its presence. Although the mTOR inhibitor rapamycin suppressed the induction of GILT protein expression by IFN-γ, the expression from luciferase sequence containing the 3′ segment of GILT mRNA was resistant to rapamycin in the presence of IFN-γ, but not in its absence. Collectively, this study elucidates the mechanism behind GILT induction by IFN-γ: in the absence of IFN-γ, GILT mRNA is constitutively transcribed, but the translation process is hindered by both the 5′ and 3′ segments. Upon exposure to IFN-γ, a translation inhibitor bound to the 3′ segment is liberated, and a translation activator interacts with the 3′ segment to trigger the initiation of GILT translation. Full article
(This article belongs to the Special Issue Viral Infections and Immune Responses)
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Review

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21 pages, 1708 KiB  
Review
Exploring the Contrasts and Similarities of Dengue and SARS-CoV-2 Infections During the COVID-19 Era
by Alexis Hipólito García and Juan Bautista De Sanctis
Int. J. Mol. Sci. 2024, 25(21), 11624; https://doi.org/10.3390/ijms252111624 - 29 Oct 2024
Viewed by 964
Abstract
Extensive research has been conducted on the SARS-CoV-2 virus in association with various infectious diseases to understand the pathophysiology of the infection and potential co-infections. In tropical countries, exposure to local viruses may alter the course of SARS-CoV-2 infection and coinfection. Notably, only [...] Read more.
Extensive research has been conducted on the SARS-CoV-2 virus in association with various infectious diseases to understand the pathophysiology of the infection and potential co-infections. In tropical countries, exposure to local viruses may alter the course of SARS-CoV-2 infection and coinfection. Notably, only a portion of the antibodies produced against SARS-CoV-2 proteins demonstrate neutralizing properties, and the immune response following natural infection tends to be temporary. In contrast, long-lasting IgG antibodies are common after dengue virus infections. In cases where preexisting antibodies from an initial dengue virus infection bind to a different dengue serotype during a subsequent infection, there is a potential for antibody-dependent enhancement (ADE) and the formation of immune complexes associated with disease severity. Both SARS-CoV-2 and dengue infections can result in immunodeficiency. Viral proteins of both viruses interfere with the host’s IFN-I signaling. Additionally, a cytokine storm can occur after viral infection, impairing a proper response, and autoantibodies against a wide array of proteins can appear during convalescence. Most of the reported autoantibodies are typically short-lived. Vaccines against both viruses alter the immune response, affecting the course of viral infection and enhancing clearance. A comprehensive analysis of both viral infections and pathogenicity is revisited to prevent infection, severity, and mortality. Full article
(This article belongs to the Special Issue Viral Infections and Immune Responses)
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