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Age Matters: Key Contributors to Interferon Toxicity in Infants During Influenza Virus Infection
Journal article   Open access   Peer reviewed

Age Matters: Key Contributors to Interferon Toxicity in Infants During Influenza Virus Infection

Alison J Carey and Abigail Onufer
Viruses, v 17(7), 1002
17 Jul 2025
PMID: 40733618
Featured in Collection :   Research Supported by Drexel Libraries' OA Programs
url
https://doi.org/10.3390/v17071002View
Published, Version of Record (VoR)Open Access Discount via Drexel Libraries Read and Publish Program 2025CC BY V4.0 Open

Abstract

interferon (IFN) influenza virus (IV) lung neonate repair barrier reactive oxygen species (ROS)
Respiratory viral infections are a leading cause of early childhood hospitalizations in the United States. Neonatal immune responses are reliant on innate mechanisms during the first few months of life. Interferons (IFNs) are a key component of this response. These antiviral cytokines are produced early in infection and aid in viral control and clearance. Although generally considered protective in the setting of respiratory viral infections, the recent literature has suggested that IFNs may exacerbate disease. In the process of promoting an antiviral environment, IFNs impede cell proliferation, contribute to pulmonary barrier disruption, and generate reactive oxygen species. This is not tolerated in the rapidly developing neonatal lung. Therefore, IFNs contribute to pathogenesis in the influenza-infected neonate. This review focuses on the potential mechanisms that drive IFN-induced toxicity in neonates and prospective therapeutics to mitigate this toxicity.

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Web of Science research areas
Virology
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