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The IFN-\u03b12 subtype is currently in HIV-1 clinical trials, but it has not consistently reduced viral loads in HIV-1 patients and is not the most effective subtype against HIV-1\n                    <jats:italic>in vitro<\/jats:italic>\n                    . We now demonstrate in humanized mice that, when delivered at the same high clinical dose, the human IFN-\u03b114 subtype has very potent anti-HIV-1 activity whereas IFN-\u03b12 does not. In both postexposure prophylaxis and treatment of acute infections, IFN-\u03b114, but not IFN-\u03b12, significantly suppressed HIV-1 replication and proviral loads. Furthermore, HIV-1-induced immune hyperactivation, which is a prognosticator of disease progression, was reduced by IFN-\u03b114 but not IFN-\u03b12. Whereas ineffective IFN-\u03b12 therapy was associated with CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell activation, successful IFN-\u03b114 therapy was associated with increased intrinsic and innate immunity, including significantly higher induction of tetherin and MX2, increased APOBEC3G signature mutations in HIV-1 proviral DNA, and higher frequencies of TRAIL\n                    <jats:sup>+<\/jats:sup>\n                    NK cells. These results identify IFN-\u03b114 as a potent new therapeutic that operates via mechanisms distinct from those of antiretroviral drugs. The ability of IFN-\u03b114 to reduce both viremia and proviral loads\n                    <jats:italic>in vivo<\/jats:italic>\n                    suggests that it has strong potential as a component of a cure strategy for HIV-1 infections. The broad implication of these results is that the antiviral efficacy of each individual IFN-\u03b1 subtype should be evaluated against the specific virus being treated.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>IMPORTANCE<\/jats:bold>\n                    The naturally occurring antiviral protein IFN-\u03b12 is used to treat hepatitis viruses but has proven rather ineffective against HIV in comparison to triple therapy with the antiretroviral (ARV) drugs. Although ARVs suppress the replication of HIV, they fail to completely clear infections. Since IFN-\u03b1 acts by different mechanism than ARVs and has been shown to reduce HIV proviral loads, clinical trials are under way to test whether IFN-\u03b12 combined with ARVs might eradicate HIV-1 infections. IFN-\u03b1 is actually a family of 12 distinct proteins, and each IFN-\u03b1 subtype has different efficacies toward different viruses. Here, we use mice that contain a human immune system, so they can be infected with HIV. With this model, we demonstrate that while IFN-\u03b12 is only weakly effective against HIV, IFN-\u03b114 is extremely potent. This discovery identifies IFN-\u03b114 as a more powerful IFN-\u03b1 subtype for use in combination therapy trials aimed toward an HIV cure.\n                  <\/jats:p>","DOI":"10.1128\/jvi.00451-16","type":"journal-article","created":{"date-parts":[[2016,4,21]],"date-time":"2016-04-21T01:43:51Z","timestamp":1461203031000},"page":"6001-6013","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":129,"title":["Interferon Alpha Subtype-Specific Suppression of HIV-1 Infection\n                    <i>In Vivo<\/i>"],"prefix":"10.1128","volume":"90","author":[{"given":"Kerry J.","family":"Lavender","sequence":"first","affiliation":[{"name":"Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathrin","family":"Gibbert","sequence":"additional","affiliation":[{"name":"Institute for Virology, University Hospital 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