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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kitano, K. Articles by Golde, D. W. Search for Related Content PubMed PubMed Citation Articles by Kitano, K. Articles by Golde, D. W. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Tumor necrosis factor-dependent production of human immunodeficiency virus 1 in chronically infected HL-60 cells K Kitano, CI Rivas, GC Baldwin, JC Vera and DW Golde Second Department of Internal Medicine, Shinshu University School of Medicine, Nagano-Ken, Japan. Tumor necrosis factor (TNF) may play a central role in proviral activation and release from latency in cells infected with the human immunodeficiency virus (HIV). We studied viral production and its relation to TNF in a HL-60 cell line (J22-HL-60) infected with a monocytotropic strain of HIV-1JR-FL. Viral production was stimulated to similar levels by TNF, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and 1,25-dihydroxyvitamin D3 (1,25[OH]2D3). Production of the virus was not suppressed by 3'-azido-3'-deoxythymidine (AZT), indicating that viral production was not caused by superinfection. Low concentrations of TNF (0.1 ng/mL) induced viral production with a short lag period of 8 hours, and this proviral activation was specifically suppressed by anti- TNF antibodies. However, induction of virus production by 1,25(OH)2D3 showed an extended lag period of 2 to 3 days. The effect of 1,25(OH)2D3 on virus production was also blocked by anti-TNF antibodies, which suggests the direct participation of TNF in this process. TNF accumulated in the culture supernatant of cells stimulated with 1,25(OH)2D3 with a kinetics consistent with its involvement in the action of 1,25(OH)2D3 on viral production. The J22-HL-60 cell line produced low levels of virus when cultured in the absence of an external stimulus; however, this basal viral production was suppressed greater than 80% in the presence of anti-TNF antibodies. Corresponding low levels of TNF were detected in the culture supernatants. Viral production decreased slowly with increasing passage of the cells, and no virus was detected in the supernatants of cells maintained in culture for several months. Concomitantly, TNF was no longer detected in the supernatant of these cells, which suggests that endogenous autocrine production of TNF drives viral production in the unstimulated cells. However, viral production was stimulated in these cells by low concentrations (0.1 ng/mL) of added TNF. These results argue for a central role for TNF in HIV proviral activation in chronically infected myeloid cells. Volume 82, Issue 9, pp. 2742-2748, 11/01/1993 Copyright © 1993 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Solomon, G. Rosenblum, P. E. Gonzales, J. D. Leonard, S. Mobashery, M. E. Milla, and I. Sagi Pronounced Diversity in Electronic and Chemical Properties between the Catalytic Zinc Sites of Tumor Necrosis Factor-{alpha}-converting Enzyme and Matrix Metalloproteinases despite Their High Structural Similarity J. Biol. Chem., July 23, 2004; 279(30): 31646 - 31654. [Abstract] [Full Text] [PDF]

	Copyright © 1993 by American Society of Hematology         Online ISSN: 1528-0020