Abstract
PERMISSIVENESS to replication of human immunodeficiency virus (HIV) differs in T lymphocytes and macrophages. In T cells, HIV transcription is poorly detected in vivo1. Cloned, normal T lymphocytes show very little, if any, basal activity of the HIV enhancer and low nuclear expression of NF-κB2, a potent tran-scriptional activator of the HIV enhancer3–5. In contrast, fixed tissue macrophages express detectable HIV proteins, indicating permanent virus transcription6. One explanation for the perpetuation of virus infection in macrophages could be sustained nuclear NF-κB expression. However, the U937 monocytic cell line, which is fully permissive to HIV replication, is known to express only low levels of nuclear NF-κB7. We show here that chronic HIV infection results in both induction of a nuclear factor with antigenic properties indistinguishable from those of NF-κB and permanently increased HIV enhancer activity. This phenomenon, which is independent of tumour necrosis factor, is associated with HIV replication, and is thus likely to explain at least in part the perpetuation of HIV infection in monocytes.
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Bachelerie, F., Alcami, J., Arenzana-Seisdedos, F. et al. HIV enhancer activity perpetuated by NF-κB induction on infection of monocytes. Nature 350, 709–712 (1991). https://doi.org/10.1038/350709a0
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DOI: https://doi.org/10.1038/350709a0
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