Open AccessCD14 is involved in control of human immunodeficiency virus type 1 expression in latently infected cells by lipopolysaccharide.
Author(s) -
Omar Bagasra,
Samuel D. Wright,
Thikkavarapu Seshamma,
Joseph W. Oakes,
Roger J. Pomerantz
Publication year - 1992
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.89.14.6285
Subject(s) - cd14 , biology , lipopolysaccharide , monocyte , virology , cell culture , u937 cell , macrophage , virus , transfection , stimulation , monoclonal antibody , antibody , immunology , in vitro , immune system , biochemistry , genetics , neuroscience
Lipopolysaccharide (LPS) potently stimulates human immunodeficiency virus type 1 (HIV-1) long terminal repeat-directed transcription in transfected monocyte-macrophage cell lines and dramatically increases HIV-1 production in the latently infected monocyte-macrophage-like cell line U1. This response to LPS, however, can only be observed after pretreatment of the U1 cells with granulocyte-macrophage colony-stimulating factor (GM-CSF). CD14, the differentiation antigen that acts as a receptor for complexes of LPS and LPS-binding protein, is now demonstrated to be involved in LPS-induced stimulation of HIV-1 replication. CD14 is shown to be expressed on a subpopulation of U1 cells only after treatment with GM-CSF and correlates with HIV-1 production stimulated by LPS. Importantly, only those U1 cells that express CD14 can be induced by LPS to upregulate HIV-1 production. In addition, a monoclonal antibody directed against CD14 can block LPS-induced stimulation of HIV-1 production from these latently infected cells.