Transcriptomic Changes in the Human Airway Epithelium during Respiratory Viral Infection

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 2316

Special Issue Editor

Temasek Life Sciences Laboratory, National University of Singapore, Singapore, Singapore
Interests: broadly protective vaccines; therapeutics against infectious human and animal viral diseases; molecular pathogenesis of emerging and zoonotic infectious viruses including influenza A viruses

Special Issue Information

Dear Colleagues,

The current era of science is influenced by two paradoxical events—one being emerging and re-emerging respiratory RNA viruses such as influenza and SARS-CoV, which are major global health threats, and the other the revolutionary technology of whole-transcriptome analysis with total RNA sequencing, resulting in a deeper understanding of the transcriptional regulations of gene expressions in health and disease. The human nasal epithelium is a primary site of exposure to respiratory viral pathogens and is ideal for understanding the dynamics of host responses against respiratory viral infection. Reports have shown that transcriptional upregulation in the nasal epithelium during experimental infections with respiratory viruses, i.e., influenza, SARS-CoV-2, SARS-CoV, and MERS-CoV, was induced by these viruses in the early stages of infection and that it altered host genes, with increased cytokine production and virus-specific host antiviral responses. These molecular events, which are initiated in the infected nasal epithelium, may adversely impact the airway, and the associated genes identified could provide new therapeutic perspectives regarding the targeting of host factors that viruses depend on.

This Special Issue on “Transcriptomic Changes in the Human Airway Epithelium during Respiratory Viral Infection” welcomes study reports and review articles in the form of human airway epithelial cell model-based thematic approaches, extended hypothetical models, collective real-time patient dataset outcomes of single, extensive, or multiple respiratory viral infections with analyses, experimentally established transcriptional signatures serving as biomarkers, regional tissue-specific or systemic therapeutic approaches based on these transcriptional dynamics, and future directions regarding prophylactic measures.

Dr. Mookkan Prabakaran
Guest Editor

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Keywords

  • respiratory viral infections
  • transcriptional signatures
  • virus–host interactions
  • human airway epithelium
  • extended models

Published Papers (1 paper)

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Research

24 pages, 5404 KiB  
Article
Early Transcriptional Responses of Human Nasal Epithelial Cells to Infection with Influenza A and SARS-CoV-2 Virus Differ and Are Influenced by Physiological Temperature
by Jessica D. Resnick, Michael A. Beer and Andrew Pekosz
Pathogens 2023, 12(3), 480; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens12030480 - 18 Mar 2023
Cited by 3 | Viewed by 1691
Abstract
Influenza A (IAV) and SARS-CoV-2 (SCV2) viruses represent an ongoing threat to public health. Both viruses target the respiratory tract, which consists of a gradient of cell types, receptor expression, and temperature. Environmental temperature has been an understudied contributor to infection susceptibility and [...] Read more.
Influenza A (IAV) and SARS-CoV-2 (SCV2) viruses represent an ongoing threat to public health. Both viruses target the respiratory tract, which consists of a gradient of cell types, receptor expression, and temperature. Environmental temperature has been an understudied contributor to infection susceptibility and understanding its impact on host responses to infection could help uncover new insight into severe disease risk factors. As the nasal passageways are the initial site of respiratory virus infection, in this study we investigated the effect of temperature on host responses in human nasal epithelial cells (hNECs) utilizing IAV and SCV2 in vitro infection models. We demonstrate that temperature affected SCV2, but not IAV, viral replicative fitness and that SCV2-infected cultures were slower to mount an infection-induced response, likely due to suppression by the virus. Additionally, we show that that temperature not only changed the basal transcriptomic landscape of epithelial cells, but that it also impacted the response to infection. The induction of interferon and other innate immune responses was not drastically affected by temperature, suggesting that while the baseline antiviral response at different temperatures remained consistent, there may be metabolic or signaling changes that affect how well the cultures were able to adapt to new pressures, such as infection. Finally, we show that hNECs responded differently to IAV and SCV2 infection in ways that give insight into how the virus is able to manipulate the cell to allow for replication and release. Taken together, these data give new insight into the innate immune response to respiratory infections and can assist in identifying new treatment strategies for respiratory infections. Full article
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