Special Issue "Viral Immune Modulation"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 30 September 2021.

Special Issue Editor

Prof. Dr. Bernd Lepenies
E-Mail Website
Guest Editor
University of Veterinary Medicine Hannover Institute for Immunology & Research Center for Emerging Infections and Zoonoses Bünteweg 17, 30559 Hannover, Germany
Interests: infection immunology; innate immunity; glycobiology; C-type lectin receptors; vaccination; adjuvants; targeted antigen delivery
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Special Issue Information

Dear Colleagues,

The host immune system is crucial to combat viral infections, but viruses may escape the host immune response and/or overshoot immune responses, therefore significantly contributing to pathology. Due to the current COVID-19 pandemic, it is well known that organ damage during viral infections may (at least partially) be caused by a dysregulated immune response. In addition, viruses have evolved intricate strategies to modulate host immune responses to enable persistence or viral spreading. There are numerous targets in the host immune system that can be exploited and/or manipulated by viruses, such as recognition of viruses by pattern recognition receptors, type-I interferon induction and signaling, viral antigen presentation, or cytokine responses, to just name a few examples.

Thus, two major topics will be considered for this Special Issue: on the one hand, viral immune evasion strategies targeting viral recognition by host innate immunity and antiviral adaptive immune responses. On the other hand, this Special Issue also welcomes submissions focusing on dysregulated immune responses during viral infections and strategies to cope with such overshooting immune responses, i.e. novel therapies. Studies on immune modulation during infection with the novel SARS-CoV-2 coronavirus are also particularly welcome.

Prof. Dr. Bernd Lepenies
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 papers will be 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 2200 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

  • virus
  • immune modulation
  • immune escape
  • host–pathogen interactions
  • host–antiviral responses

Published Papers (1 paper)

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Research

Article
Influenza Virus-Induced Novel miRNAs Regulate the STAT Pathway
Viruses 2021, 13(6), 967; https://doi.org/10.3390/v13060967 - 23 May 2021
Viewed by 844
Abstract
MicroRNAs (miRNAs) are essential regulators of gene expression in humans and can control pathogenesis and host–virus interactions. Notably, the role of specific host miRNAs during influenza virus infections are still ill-defined. The central goal of this study was to identify novel miRNAs and [...] Read more.
MicroRNAs (miRNAs) are essential regulators of gene expression in humans and can control pathogenesis and host–virus interactions. Notably, the role of specific host miRNAs during influenza virus infections are still ill-defined. The central goal of this study was to identify novel miRNAs and their target genes in response to influenza virus infections in airway epithelium. Human airway epithelial cells exposed to influenza A virus (IAV) induced several novel miRNAs that were identified using next-generation sequencing (NGS) and their target genes by biochemical methods. NGS analysis predicted forty-two RNA sequences as possible miRNAs based on computational algorithms. The expression patterns of these putative miRNAs were further confirmed using RT-PCR in human bronchial epithelial cells exposed to H1N1, H9N1(1P10), and H9N1 (1WF10) strains of influenza virus. A time-course study showed significant downregulation of put-miR-34 in H1N1 and put-miR-35 in H9N1(1P10)-infected cells, which is consistent with the NGS data. Additionally, put-miR-34 and put-miR-35 showed a high fold enrichment in an argonaute-immunoprecipitation assay compared to the controls, indicating their ability to form a complex with argonaute protein and RNA-induced silencing complex (RISC), which is a typical mode of action found with miRNAs. Our earlier studies have shown that the replication and survival of influenza virus is modulated by certain transcription factors such as NF-ĸB. To identify the target(s) of these putative miRNAs, we screened 84 transcription factors that have a role in viral pathogenesis. Cells transfected with mimic of the put-miR-34 showed a significant decrease in the expression of Signal Transducers and Activators of Transcription 3 (STAT3), whereas the inhibitor of put-miR-34 showed a significant increase in STAT3 expression and its phosphorylation. In addition, put-miR-34 had 76% homology to the untranslated region of STAT3. NGS and PCR array data submitted to the Gene Ontology project also predicted the role of transcription factors modulated by put-miR-34. Our data suggest that put-miR-34 may be a good target for antiviral therapy. Full article
(This article belongs to the Special Issue Viral Immune Modulation)
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