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Lung cell fates during influenza
Journal article   Open access   Peer reviewed

Lung cell fates during influenza

Brianna Jarboe, Maria Shubina, Ryan A Langlois, David F Boyd and Siddharth Balachandran
Cell research, v 35(10), pp 707-718
01 Oct 2025
DOI: https://doi.org/10.1038/s41422-025-01163-y
PMID: 40820141
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1038/s41422-025-01163-yView
Published, Version of Record (VoR) Open

Abstract

Animals Humans Influenza A virus - pathogenicity Influenza, Human - immunology Influenza, Human - pathology Influenza, Human - virology Lung - pathology Lung - virology
Roughly 1 billion people are infected by Influenza A viruses (IAVs) worldwide each year, resulting in approximately half a million deaths. Particularly concerning is the threat of IAV spillover from avian and other animal reservoirs. The recent outbreak of highly pathogenic avian influenza H5N1 in US dairy cows highlights this concern. While viruses that enter human populations from such zoonotic transmission typically lack the ability to transmit effectively between humans, they may be only a few mutations from acquiring this capacity. These newly adapted viruses have the potential to be significantly more virulent than seasonal strains. A major contributor to influenza pathology is the over-exuberant immune response to the virus, particularly when the infection is present in distal pulmonary tissues. Maladaptive immune pathway over-activation can drive tissue damage and pathology, often independently of effective viral control. Anti-inflammatories targeting host-initiated pathological processes hold promise, but these avenues require a thorough understanding of virus-triggered lung inflammation before they can be fully exploited. In this review, we will discuss recent advances in our understanding of the cell types that are targeted by IAV, the consequences of IAV infection on the biology of these cells, and their contribution to lung pathology in influenza. We will also discuss how virus-induced hyper-inflammatory responses present new entry-points for therapeutic intervention, showcasing Z-form nucleic acid-binding protein 1 (ZBP1)-initiated necroptosis as an example of one such pathway.

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
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