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Advanced Research on Immune Response to Viral Infection
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Advanced Research on Immune Response to Viral Infection

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: 30 April 2024 | Viewed by 1919

Special Issue Editor

Prof. Dr. Tatiana Betáková

E-Mail Website
Guest Editor
Department of Microbiology and Virology, Faculty of Natural Sciences, Comenius University, 842 15 Bratislava, Slovakia
Interests: virus; infection; immunity

Special Issue Information

Dear Colleagues,

Over the past twenty years, a number of new viruses have emerged and entered the human population. Annual epidemics and occasional pandemics result in considerable morbidity and mortality worldwide. Native and adaptive immunity plays an important role in host defense against viral infection. Viruses encode proteins which are able to suppress the host immune response, and some use immune cells for replication. On the other hand, many infected people die not because of robust virus replication, but because of acute respiratory distress syndrome (ARDS) triggered by the cytokine storm.

In this Special Issue for IJMS, we will focus on the induction/inhibition of metabolic and signaling pathways, cytokines, proteins, and populations and subpopulations of immune cells involved in the regulation of immune response against viruses. The discovery of molecular profiles and mechanisms that are responsible for pathogenicity could provide new insights into controlling viral infections and/or immune responses and contribute to the development of new antivirals. Eligible submissions include original research papers and up-to-date review articles.

Prof. Dr. Tatiana Betáková
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

  • virus
  • infection
  • immunity
  • signaling pathways
  • cytokine
  • antibody
  • pathology

Published Papers (2 papers)

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Research

22 pages, 4809 KiB  
Article
Changes in the Expression of Proteins Associated with Neurodegeneration in the Brains of Mice after Infection with Influenza A Virus with Wild Type and Truncated NS1
by Karin Donátová, Miriam Mladá, Katarína Lopušná, Filip Baran and Tatiana Betáková
Int. J. Mol. Sci. 2024, 25(5), 2460; https://doi.org/10.3390/ijms25052460 - 20 Feb 2024
Viewed by 767
Abstract
Influenza type A virus (IAV) infection is a major cause of morbidity and mortality during influenza epidemics. Recently, a specific link between IAV infection and neurodegenerative disease progression has been established. The non-structural NS1 protein of IAV regulates viral replication during infection and [...] Read more.
Influenza type A virus (IAV) infection is a major cause of morbidity and mortality during influenza epidemics. Recently, a specific link between IAV infection and neurodegenerative disease progression has been established. The non-structural NS1 protein of IAV regulates viral replication during infection and antagonizes host antiviral responses, contributing to influenza virulence. In the present study, we have prepared a mouse lung-to-lung adapted to the NS1-truncated virus (NS80ad). Transcriptome analysis of the gene expression in the lungs revealed that infection with wild-type A/WSN/33 (WSN), NS80, and NS80ad viruses resulted in different regulation of genes involved in signaling pathways associated with the cell proliferation, inflammatory response, and development of neurodegenerative diseases. NS1 protein did not influence the genes involved in the RIG-I-like receptor signaling pathway in the brains. Lethal infection with IAVs dysregulated expression of proteins associated with the development of neurodegenerative diseases (CX3CL1/Fractalkine, Coagulation factor III, and CD105/Endoglin, CD54/ICAM-1, insulin-like growth factor-binding protein (IGFBP)-2, IGFBP-5, IGFBP-6, chitinase 3-like 1 (CHI3L1), Myeloperoxidase (MPO), Osteopontin (OPN), cystatin C, and LDL R). Transcription of GATA3 mRNA was decreased, and expression of MPO was inhibited in the brain infected with NS80 and NS80ad viruses. In addition, the truncation of NS1 protein led to reduced expression of IGFBP-2, CHI3L1, MPO, and LDL-R proteins in the brains. Our results indicate that the influenza virus influences the expression of proteins involved in brain function, and this might occur mostly through the NS1 protein. These findings suggest that the abovementioned proteins represent a promising target for the development of potentially effective immunotherapy against neurodegeneration. Full article
(This article belongs to the Special Issue Advanced Research on Immune Response to Viral Infection)
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15 pages, 4087 KiB  
Article
Mitochondrial Reactive Oxygen Species in TRIF-Dependent Toll-like Receptor 3 Signaling in Bronchial Epithelial Cells against Viral Infection
by Ga Eul Chu, Jun Young Park, Chan Ho Park and Won Gil Cho
Int. J. Mol. Sci. 2024, 25(1), 226; https://doi.org/10.3390/ijms25010226 - 22 Dec 2023
Viewed by 797
Abstract
Toll-like receptor 3 (TLR3) plays an important role in double-stranded RNA recognition and triggers the innate immune response by acting as a key receptor against viral infections. Intracellular reactive oxygen species (ROS) are involved in TLR3-induced inflammatory responses during viral infections; however, their [...] Read more.
Toll-like receptor 3 (TLR3) plays an important role in double-stranded RNA recognition and triggers the innate immune response by acting as a key receptor against viral infections. Intracellular reactive oxygen species (ROS) are involved in TLR3-induced inflammatory responses during viral infections; however, their relationship with mitochondrial ROS (mtROS) remains largely unknown. In this study, we show that polyinosinic–polycytidylic acid (poly(I:C)), a mimic of viral RNA, induced TLR3-mediated nuclear factor-kappa B (NF-κB) signaling pathway activation and enhanced mtROS generation, leading to inflammatory cytokine production. TLR3-targeted small interfering RNA (siRNA) and Mito-TEMPO inhibited inflammatory cytokine production in poly(I:C)-treated BEAS-2B cells. Poly(I:C) recruited the TLR3 adaptor molecule Toll/IL-1R domain-containing adaptor, inducing IFN (TRIF) and activated NF-κB signaling. Additionally, TLR3-induced mtROS generation suppression and siRNA-mediated TRIF downregulation attenuated mitochondrial antiviral signaling protein (MAVS) degradation. Our findings provide insights into the TLR3-TRIF signaling pathway and MAVS in viral infections, and suggest TLR3-mtROS as a therapeutic target for the treatment of airway inflammatory and viral infectious diseases. Full article
(This article belongs to the Special Issue Advanced Research on Immune Response to Viral Infection)
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