{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T02:44:41Z","timestamp":1790304281634,"version":"4.1.0"},"reference-count":66,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2024,1,22]],"date-time":"2024-01-22T00:00:00Z","timestamp":1705881600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL148184"],"award-info":[{"award-number":["HL148184"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Ross Mossier CF Research Laboratories Fund","award":["HL148184"],"award-info":[{"award-number":["HL148184"]}]},{"name":"NSF Graduate Research Fellowship Program","award":["HL148184"],"award-info":[{"award-number":["HL148184"]}]},{"name":"Stanford Gabilan Graduate Fellowship","award":["HL148184"],"award-info":[{"award-number":["HL148184"]}]},{"name":"Cystic Fibrosis Foundation","award":["HL148184"],"award-info":[{"award-number":["HL148184"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Background: The inovirus Pf4 is a lysogenic bacteriophage of Pseudomonas aeruginosa (Pa). People with Cystic Fibrosis (pwCF) experience chronic airway infection with Pa and a significant proportion have high numbers of Pf4 in their airway secretions. Given the known severe damage in the airways of Pa-infected pwCF, we hypothesized a high Pf4 burden can affect airway healing and inflammatory responses. In the airway, basal epithelial cells (BCs) are a multipotent stem cell population critical to epithelium homeostasis and repair. We sought to investigate the transcriptional responses of BCs under conditions that emulate infection with Pa and exposure to high Pf4 burden. Methods: Primary BCs isolated from pwCF and wild-type (WT) donors were cultured in vitro and exposed to Pf4 or bacterial Lipopolysaccharide (LPS) followed by transcriptomic and functional assays. Results: We found that BCs internalized Pf4 and this elicits a strong antiviral response as well as neutrophil chemokine production. Further, we found that BCs that take up Pf4 demonstrate defective migration and proliferation. Conclusions: Our findings are highly suggestive of Pf4 playing a role in the pathogenicity of Pa in the airways. These findings provide additional evidence for the ability of inoviruses to interact with mammalian cells and disrupt cell function.<\/jats:p>","DOI":"10.3390\/v16010165","type":"journal-article","created":{"date-parts":[[2024,1,22]],"date-time":"2024-01-22T11:36:41Z","timestamp":1705923401000},"page":"165","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["The Inovirus Pf4 Triggers Antiviral Responses and Disrupts the Proliferation of Airway Basal Epithelial Cells"],"prefix":"10.3390","volume":"16","author":[{"given":"Medeea C.","family":"Popescu","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases, Stanford University, Stanford, CA 94305, USA"},{"name":"Immunology Program, Stanford University, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naomi L.","family":"Haddock","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, Stanford University, Stanford, CA 94305, USA"},{"name":"Immunology Program, Stanford University, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8969-6232","authenticated-orcid":false,"given":"Elizabeth B.","family":"Burgener","sequence":"additional","affiliation":[{"name":"Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura S.","family":"Rojas-Hernandez","sequence":"additional","affiliation":[{"name":"Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gernot","family":"Kaber","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, Stanford University, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aviv","family":"Hargil","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, Stanford University, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul L.","family":"Bollyky","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, Stanford University, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5515-3053","authenticated-orcid":false,"given":"Carlos E.","family":"Milla","sequence":"additional","affiliation":[{"name":"Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,1,22]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Fauquet, C.M. 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