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Host Responses to Virus Infection

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

Deadline for manuscript submissions: 20 October 2025 | Viewed by 1400

Special Issue Editors


E-Mail Website
Guest Editor
Center for Medical Innovation, Nagasaki University, Sakamoto 1-7-1, Nagasaki 852-8588, Japan
Interests: interferon signaling; viral infection; T cell receptor

E-Mail Website
Guest Editor
Department of Clinical Medicine, Institute of Tropical Medicine, Nagasaki University, Nagasaki 852-8523, Japan
Interests: viral infection; retrovirus; interferon gamma

Special Issue Information

Dear Colleagues,

Virus infections, especially those caused by unknown pathogens, pose a significant threat to our society. Learning from the COVID-19 pandemic, we aim to understand how to cope with emerging infectious diseases. This discussion focuses on the responses of host cells to viral infections, particularly the role of cytokines. While cytokines can have beneficial effects in preventing viral spread and expelling the virus, inappropriate responses can lead to devastating consequences for the host. Type I interferons (IFNs), such as IFN-alpha and IFN-beta, type II IFN (IFN-gamma), and other cytokines play crucial roles in activating the intracellular molecules that inhibit viral replication within the cells. Additionally, these cytokines are secreted extracellularly to recruit immune cells. Proper immunological responses to viruses are regulated not only by primary immune cells, such as dendritic cells, T cells, and B cells, but also by the local cytokine environment created by infected cells and immune cells. We will discuss how to harness host reactions to viral infections for effective vaccination and possible preventive measures against fatal cytokine storms.

This Special Issue seeks manuscripts that enhance our understanding of host reactions to viral infections and contribute to the development of efficacious vaccination methods and potential preventive measures against fatal cytokine storms.

Dr. Hideki Hayashi
Dr. Yoshinao Kubo
Guest Editors

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Keywords

  • viral infection
  • host reactions
  • interferon alpha and beta
  • interferon gamma
  • cytokines
  • vaccine
  • cytokine storm

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Published Papers (2 papers)

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Research

16 pages, 3376 KiB  
Article
High Glucose Reduces Influenza and Parainfluenza Virus Productivity by Altering Glycolytic Pattern in A549 Cells
by Kareem Awad, Maha Abdelhadi and Ahmed M. Awad
Int. J. Mol. Sci. 2025, 26(7), 2975; https://doi.org/10.3390/ijms26072975 - 25 Mar 2025
Viewed by 254
Abstract
Influenza A virus is responsible for annual epidemics and occasional pandemics leading to significant mortality and morbidity in human populations. Parainfluenza viruses also contribute to lung infections and chronic lung disease. In this study, we investigated the effect of high glucose on the [...] Read more.
Influenza A virus is responsible for annual epidemics and occasional pandemics leading to significant mortality and morbidity in human populations. Parainfluenza viruses also contribute to lung infections and chronic lung disease. In this study, we investigated the effect of high glucose on the productivity of influenza A and Sendai (murine parainfluenza type 1) viruses in A549 immortalized cells. A glycolytic pattern of infection was determined by monitoring the release of lactate and phosphofructokinase (PFK) activity in infected and uninfected cells. qRT-PCR was used to analyze the expression of viral and cellular cytokine mRNA levels in cultured cells. The data show that the productivity of both influenza and Sendai viruses was reduced in A549 cells cultured in high-glucose conditions. This was accompanied by increased lactate production and altered PFK activity profile. Endogenous or virus infection-induced interferon β (IFN-β) mRNA expression was significantly decreased in high glucose compared to normal glucose status during early times of infection. Unlike in Sendai virus-infected cells, H1N1 virus reversed the significant increase in transforming growth factor β1 (TGF-β1) mRNA expression due to increased glucose concentration during early infection times. In conclusion, high glucose may have a negative effect on influenza and parainfluenza productivity in vitro. This effect may be considered when evaluating personalized therapeutic/diagnostic markers in infection-accompanied hyperglycemic status. Full article
(This article belongs to the Special Issue Host Responses to Virus Infection)
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19 pages, 2253 KiB  
Article
Characterization of the Temporal Dynamics of the Endothelial–Mesenchymal-like Transition Induced by Soluble Factors from Dengue Virus Infection in Microvascular Endothelial Cells
by Jenny Paola Alfaro-García, Carlos Alberto Orozco-Castaño, Julián Andrés Sánchez-Rendón, Herley Fernando Casanova-Yépes, Miguel Vicente-Manzanares and Juan Carlos Gallego-Gómez
Int. J. Mol. Sci. 2025, 26(5), 2139; https://doi.org/10.3390/ijms26052139 - 27 Feb 2025
Viewed by 888
Abstract
Dengue virus (DV) infection poses a severe life-threatening risk in certain cases. This is mainly due to endothelial dysregulation, which causes plasma leakage and hemorrhage. However, the etiology of DV-induced endothelial dysregulation remains incompletely understood. To identify the potential mechanisms of endothelial dysregulation [...] Read more.
Dengue virus (DV) infection poses a severe life-threatening risk in certain cases. This is mainly due to endothelial dysregulation, which causes plasma leakage and hemorrhage. However, the etiology of DV-induced endothelial dysregulation remains incompletely understood. To identify the potential mechanisms of endothelial dysregulation caused by DV, the effects of conditioned media from Dengue virus (CMDV) on the mechanics and transcriptional profile of the endothelial cells were examined using permeability assays, atomic force microscopy, In-Cell Western blot and in silico transcriptomics. Exposure of HMEC-1 cells to the CMDV increased endothelial permeability and cellular stiffness. It also induced the expression of the key proteins associated with endothelial-to-mesenchymal transition (EndMT). These data support the notion that the DV promotes endothelial dysfunction by triggering transcriptional programs that compromise the endothelial barrier function. Understanding the molecular mechanisms underlying DV-induced endothelial dysregulation is crucial for developing targeted therapeutic strategies to mitigate the severe outcomes associated with dengue infection. Full article
(This article belongs to the Special Issue Host Responses to Virus Infection)
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