{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T08:21:23Z","timestamp":1770711683408,"version":"3.49.0"},"reference-count":0,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[1995,9,1]],"date-time":"1995-09-01T00:00:00Z","timestamp":809913600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Rev"],"published-print":{"date-parts":[[1995,9]]},"abstract":"<jats:p>CD4+ macrophages in tissues such as lung, skin, and lymph nodes, promyelocytic cells in bone marrow, and peripheral blood monocytes serve as important targets and reservoirs for human immunodeficiency virus type 1 (HIV-1) replication. HIV-1-infected myeloid cells are often diminished in their ability to participate in chemotaxis, phagocytosis, and intracellular killing. HIV-1 infection of myeloid cells can lead to the expression of surface receptors associated with cellular activation and\/or differentiation that increase the responsiveness of these cells to cytokines secreted by neighboring cells as well as to bacteria or other pathogens. Enhancement of HIV-1 replication is related in part to increased DNA-binding activity of cellular transcription factors such as NF-kappa B. NF-kappa B binds to the HIV-1 enhancer region of the long terminal repeat and contributes to the inducibility of HIV-1 gene expression in response to multiple activating agents. Phosphorylation and degradation of the cytoplasmic inhibitor I kappa B alpha are crucial regulatory events in the activation of NF-kappa B DNA-binding activity. Both N- and C-terminal residues of I kappa B alpha are required for inducer-mediated degradation. Chronic HIV-1 infection of myeloid cells leads to constitutive NF-kappa B DNA-binding activity and provides an intranuclear environment capable of perpetuating HIV-1 replication. Increased intracellular stores of latent NF-kappa B may also result in rapid inducibility of NF-kappa B-dependent cytokine gene expression. In response to secondary pathogenic infections or antigenic challenge, cytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in HIV-1-infected myeloid cells compared with uninfected cells. Elevated levels of several inflammatory cytokines have been detected in the sera of HIV-1-infected individuals. Secretion of myeloid cell-derived cytokines may both increase virus production and contribute to AIDS-associated disorders.<\/jats:p>","DOI":"10.1128\/mr.59.3.481-505.1995","type":"journal-article","created":{"date-parts":[[2020,12,5]],"date-time":"2020-12-05T05:58:36Z","timestamp":1607147916000},"page":"481-505","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":132,"title":["Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by NF-kappa B\/Rel transcription factors"],"prefix":"10.1128","volume":"59","author":[{"given":"A","family":"Roulston","sequence":"first","affiliation":[{"name":"Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, Sir Mortimer B. 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