{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T13:51:03Z","timestamp":1787061063047,"version":"build-2736575974"},"update-to":[{"DOI":"10.1371\/journal.ppat.1012317","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2024,7,8]],"date-time":"2024-07-08T00:00:00Z","timestamp":1720396800000}}],"reference-count":58,"publisher":"Public Library of Science (PLoS)","issue":"6","license":[{"start":{"date-parts":[[2024,6,20]],"date-time":"2024-06-20T00:00:00Z","timestamp":1718841600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI104920"],"award-info":[{"award-number":["R01 AI104920"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000052","name":"NIH Office of the Director","doi-asserted-by":"publisher","award":["S10 OD026741"],"award-info":[{"award-number":["S10 OD026741"]}],"id":[{"id":"10.13039\/100000052","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1 TR000423"],"award-info":[{"award-number":["UL1 TR000423"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["P30 CA015704"],"award-info":[{"award-number":["P30 CA015704"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>\n                    Mammalian \u03b1-defensins are a family of abundant effector peptides of the mucosal innate immune system. Although primarily considered to be antimicrobial, \u03b1-defensins can increase rather than block infection by certain prominent bacterial and viral pathogens in cell culture and\n                    <jats:italic>in vivo<\/jats:italic>\n                    . We have shown previously that exposure of mouse and human adenoviruses (HAdVs) to \u03b1-defensins is able to overcome competitive inhibitors that block cell binding, leading us to hypothesize a defensin-mediated binding mechanism that is independent of known viral receptors. To test this hypothesis, we used genetic approaches to demonstrate that none of several primary receptors nor integrin co-receptors are needed for human \u03b1-defensin-mediated binding of HAdV to cells; however, infection remains integrin dependent. Thus, our studies have revealed a novel pathway for HAdV binding to cells that bypasses viral primary receptors. We speculate that this pathway functions in parallel with receptor-mediated entry and contributes to \u03b1-defensin-enhanced infection of susceptible cells. Remarkably, we also found that in the presence of \u03b1-defensins, HAdV tropism is expanded to non-susceptible cells, even when viruses are exposed to a mixture of both susceptible and non-susceptible cells. Therefore, we propose that in the presence of sufficient concentrations of \u03b1-defensins, such as in the lung or gut, integrin expression rather than primary receptor expression will dictate HAdV tropism\n                    <jats:italic>in vivo<\/jats:italic>\n                    . In summary, \u03b1-defensins may contribute to tissue tropism not only through the neutralization of susceptible viruses but also by allowing certain defensin-resistant viruses to bind to cells independently of previously described mechanisms.\n                  <\/jats:p>","DOI":"10.1371\/journal.ppat.1012317","type":"journal-article","created":{"date-parts":[[2024,6,20]],"date-time":"2024-06-20T13:43:51Z","timestamp":1718891031000},"page":"e1012317","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":7,"title":["Alpha-defensin binding expands human adenovirus tropism"],"prefix":"10.1371","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-1526-6532","authenticated-orcid":true,"given":"Cheng","family":"Zhao","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-5298-1881","authenticated-orcid":true,"given":"Jessica M.","family":"Porter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phillip C.","family":"Burke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7069-6678","authenticated-orcid":true,"given":"Niklas","family":"Arnberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6727-5269","authenticated-orcid":true,"given":"Jason G.","family":"Smith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2024,6,20]]},"reference":[{"issue":"1","key":"ppat.1012317.ref001","doi-asserted-by":"crossref","first-page":"84","DOI":"10.1111\/j.1600-065X.2011.01082.x","article-title":"alpha-Defensins in human innate immunity","volume":"245","author":"RI 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