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Although JQKD82 has been studied in latent HIV infection of T cell models, its effects on HIV infection in macrophages remain unclear. Here, we investigated the impact of JQKD82 on HIV infection of primary human monocyte\u2010derived macrophages (MDMs). We observed that treatment of MDMs with non\u2010cytotoxic concentrations of JQKD82 dose\u2010dependently inhibited HIV replication, as evidenced by reduced virus\u2010induced syncytium formation, decreased viral Gag mRNA expression, and lower p24 protein levels. Pretreatment of cells with JQKD82 was more effective than post\u2010infection treatment, suggesting inhibition at the viral entry stage, which was confirmed using pseudotyped HIV NL4\u20103\u2010\u0394Env\u2010eGFP\u2010Bal. Mechanistically, JQKD82 downregulated CD4 and CCR5 expression while inducing the CCR5 ligand RANTES in MDMs. In addition, JQKD82 enhanced interferon\u2010stimulated gene (ISG) expression in HIV\u2010infected macrophages. Together, these findings demonstrate that JQKD82 inhibits HIV infection through dual mechanisms\u2014blocking viral entry and enhancing antiviral ISG responses\u2014supporting further evaluation of KDM5 inhibition as a potential therapeutic strategy against HIV.<\/jats:p>","DOI":"10.1002\/jmv.71043","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T08:31:13Z","timestamp":1783326673000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["JQKD82 Inhibits HIV Infection of Macrophages Through Blocking Viral Entry and Enhancing Antiviral ISG Responses"],"prefix":"10.1002","volume":"98","author":[{"given":"Jie","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Temple University Lewis Katz School of Medicine Philadelphia Pennsylvania 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