{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T21:05:27Z","timestamp":1791320727905,"version":"4.3.1"},"reference-count":73,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2010,8,1]],"date-time":"2010-08-01T00:00:00Z","timestamp":1280620800000},"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":[[2010,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>HIV-1 replication within macrophages of the CNS often results in cognitive and motor impairment, which is known as HIV-associated dementia (HAD) in its most severe form. IFN-\u03b2 suppresses viral replication within these cells during early CNS infection, but the effect is transient. HIV-1 eventually overcomes this protective innate immune response to resume replication through an unknown mechanism, initiating the progression toward HAD. In this article, we show that Suppressor of Cytokine Signaling (SOCS)3, a molecular inhibitor of IFN signaling, may allow HIV-1 to evade innate immunity within the CNS. We found that SOCS3 is elevated in an in vivo SIV\/macaque model of HAD and that the pattern of expression correlates with recurrence of viral replication and onset of CNS disease. In vitro, the HIV-1 regulatory protein transactivator of transcription induces SOCS3 in human and murine macrophages in a NF-\u03baB\u2013dependent manner. SOCS3 expression attenuates the response of macrophages to IFN-\u03b2 at proximal levels of pathway activation and downstream antiviral gene expression and consequently overcomes the inhibitory effect of IFN-\u03b2 on HIV-1 replication. These studies indicate that SOCS3 expression, induced by stimuli present in the HIV-1\u2013infected brain, such as transactivator of transcription, inhibits antiviral IFN-\u03b2 signaling to enhance HIV-1 replication in macrophages. This consequence of SOCS3 expression in vitro, supported by a correlation with increased viral load and onset of CNS disease in vivo, suggests that SOCS3 may allow HIV-1 to evade the protective innate immune response within the CNS, allowing the recurrence of viral replication and, ultimately, promoting progression toward HAD.<\/jats:p>","DOI":"10.4049\/jimmunol.0903563","type":"journal-article","created":{"date-parts":[[2010,7,14]],"date-time":"2010-07-14T20:02:01Z","timestamp":1279137721000},"page":"2393-2404","source":"Crossref","is-referenced-by-count":89,"title":["Suppressor of Cytokine Signaling 3 Inhibits Antiviral IFN-\u03b2 Signaling To Enhance HIV-1 Replication in Macrophages"],"prefix":"10.1093","volume":"185","author":[{"given":"Lisa Nowoslawski","family":"Akhtar","sequence":"first","affiliation":[{"name":"Department of Cell Biology, University of Alabama at Birmingham , Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongwei","family":"Qin","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Alabama at Birmingham , Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle T","family":"Muldowney","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Alabama at Birmingham , Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lora L","family":"Yanagisawa","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Alabama at Birmingham , Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olaf","family":"Kutsch","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, University of Alabama at Birmingham , Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janice E","family":"Clements","sequence":"additional","affiliation":[{"name":"Department of Molecular and Comparative Pathobiology, The Johns Hopkins University , Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Etty N","family":"Benveniste","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Alabama at Birmingham , Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,8,15]]},"reference":[{"key":"2025032411474223600_r1","doi-asserted-by":"crossref","first-page":"33","DOI":"10.1038\/nrn2040","article-title":"HIV and antiretroviral therapy in the brain: neuronal injury and repair","volume":"8","author":"Ellis","year":"2007","journal-title":"Nat. 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