{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T03:11:06Z","timestamp":1773803466588,"version":"3.50.1"},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[1995,11,1]],"date-time":"1995-11-01T00:00:00Z","timestamp":815184000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1995,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Although human eosinophils express low concentrations of CD4, the capacity of mature, non-replicating eosinophils to be infected with human immunodeficiency virus-1 (HIV-1) has not been established. Using peripheral blood eosinophils isolated free of contaminating lymphocytes and mononuclear leukocytes, we evaluated eosinophil infection with HIV-1. Eosinophils could be infected with strains of HIV-1 as evidenced by HIV-induced cytolytic effects, progressive release of p24 antigen in cultures of infected eosinophils, recovery of HIV from infected eosinophils by co-cultivation, and detection of HIV-1 gag viral DNA from infected eosinophils by polymerase chain reaction (PCR) amplification. Greater p24 antigen release from infected eosinophils was elicited by the phorbol ester, PMA; and eosinophil killing by HIV-1 was enhanced by the cytokine GM-CSF. By light and electron microscopy, HIV-infected eosinophils demonstrated apoptosis and necrosis. Apoptotic subdiploid nuclear staining was detected by flow cytometric analyses of propidium iodide-stained nuclei from HIV-infected eosinophils, and DNA isolated from HIV-infected eosinophils showed both nucleosomal fragmentation and diffuse degradation. Thus, mature eosinophils, non-replicating terminally differentiated leukocytes, can be infected with HIV-1. HIV-1 expression in eosinophils is promoted by increased granulocyte-macrophage colony-stimulating factor (GM-CSF) and can cause eosinophils to undergo death due to apoptosis and necrosis.<\/jats:p>","DOI":"10.1165\/ajrcmb.13.5.7576698","type":"journal-article","created":{"date-parts":[[2013,4,3]],"date-time":"2013-04-03T22:29:14Z","timestamp":1365028154000},"page":"610-620","source":"Crossref","is-referenced-by-count":31,"title":["Infection, Apoptosis, and Killing of Mature Human Eosinophils by Human Immunodeficiency Virus-1"],"prefix":"10.1093","volume":"13","author":[{"given":"P F","family":"Weller","sequence":"first","affiliation":[{"name":"Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W L","family":"Marshall","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D R","family":"Lucey","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T H","family":"Rand","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A M","family":"Dvorak","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R W","family":"Finberg","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1995,11,1]]},"container-title":["American Journal of Respiratory Cell and Molecular Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/academic.oup.com\/ajrcmb\/article-pdf\/13\/5\/610\/67384590\/ajrcmb_13_5_610.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/academic.oup.com\/ajrcmb\/article-pdf\/13\/5\/610\/67384590\/ajrcmb_13_5_610.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T01:55:29Z","timestamp":1773798929000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ajrcmb\/article\/13\/5\/610\/8526694"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-online":{"date-parts":[[1995,11,1]]},"published-print":{"date-parts":[[1995,11,1]]}},"URL":"https:\/\/doi.org\/10.1165\/ajrcmb.13.5.7576698","relation":{},"ISSN":["1044-1549","1535-4989"],"issn-type":[{"value":"1044-1549","type":"print"},{"value":"1535-4989","type":"electronic"}],"subject":[],"published-other":{"date-parts":[[1995,11]]},"published":{"date-parts":[[1995,11,1]]}}}