{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T06:55:29Z","timestamp":1790060129295,"version":"4.0.1"},"reference-count":71,"publisher":"American Society for Clinical Investigation","issue":"20","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,12,8]]},"abstract":"<jats:p>\n                    IFN-\u03b5 is a unique type I IFN that is not induced by pattern recognition response elements. IFN-\u03b5 is constitutively expressed in mucosal tissues, including the female genital mucosa. Although the direct antiviral activity of IFN-\u03b5 was thought to be weak compared with IFN-\u03b1, IFN-\u03b5 controls\n                    <jats:italic>Chlamydia muridarum<\/jats:italic>\n                    and herpes simplex virus 2 in mice, possibly through modulation of immune response. We show here that IFN-\u03b5 induces an antiviral state in human macrophages that blocks HIV-1 replication. IFN-\u03b5 had little or no protective effect in activated CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells or transformed cell lines unless activated CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells were infected with replication-competent HIV-1 at a low MOI. The block to HIV infection of macrophages was maximal after 24 hours of treatment and was reversible. IFN-\u03b5 acted on early stages of the HIV life cycle, including viral entry, reverse transcription, and nuclear import. The protection did not appear to operate through known type I IFN-induced HIV host restriction factors, such as APOBEC3A and SAMHD1. IFN-\u03b5\u2013stimulated immune mediators and pathways had the signature of type I IFNs but were distinct from IFN-\u03b1 in macrophages. IFN-\u03b5 induced significant phagocytosis and ROS, which contributed to the block to HIV replication. These findings indicate that IFN-\u03b5 induces an antiviral state in macrophages that is mediated by different factors than those induced by IFN-\u03b1. Understanding the mechanism of IFN-\u03b5\u2013mediated HIV inhibition through immune modulation has implications for prevention.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.88255","type":"journal-article","created":{"date-parts":[[2016,12,7]],"date-time":"2016-12-07T11:00:58Z","timestamp":1481108458000},"source":"Crossref","is-referenced-by-count":37,"title":["IFN-\u03b5 protects primary macrophages against HIV infection"],"prefix":"10.1172","volume":"1","author":[{"given":"Carley","family":"Tasker","sequence":"first","affiliation":[{"name":"Department of Microbiology, Biochemistry and Molecular Genetics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Selvakumar","family":"Subbian","sequence":"additional","affiliation":[{"name":"Public Health Research Institute, Rutgers University, New Jersey Medical School, Newark, New Jersey, 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