International Immunology, Vol. 11, No. 2, 143-150,
February 1999
© 1999 Japanese Society for Immunology
Anti-rheumatic compound aurothioglucose inhibits tumor necrosis factor-
-induced HIV-1 replication in latently infected OM10.1 and Ach2 cells
1 Departments of Molecular Genetics and
2 Anatomy, Nagoya City University Medical School,Nagoya 467-8601, Japan
3 Division of Human Retroviruses, Center for Chronic Viral Diseases, Faculty of Medicine, Kagoshima University, Kagoshima 890-0075, Japan
4 Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA
Correspondence to: T. Okamoto
NF-
B is a potent cellular activator of HIV-1 gene expression. Down-regulation of NF-B activation is known to inhibit HIV replication from the latently infected cells. Gold compounds have been effectively used for many decades in the treatment of rheumatoid arthritis. We previously reported that gold compounds, especially aurothioglucose (AuTG) containing monovalent gold ion, inhibited the DNA-binding of NF-B in vitro. In this report we have examined the efficacy of the gold compound AuTG as an inhibitor of HIV replication in latently infected OM10.1 and Ach2 cells. Tumor necrosis factor (TNF)-
-induced HIV-1 replication in OM10.1 or Ach2 cells was significantly inhibited by non-cytotoxic doses of AuTG (>10 µM in OM10.1 cells and >25 µM in Ach2 cells), while 25 µM of the counter-anion thioglucose (TG) or gold compound containing divalent gold ion, HAuCl3, had no effect. The effect of AuTG on NF-B-dependent gene expression was confirmed by a transient CAT assay. Specific staining as well as electron microscopic examinations revealed the accumulation of metal gold in the cells, supporting our previous hypothesis that gold ions could block NF-B–DNA binding by a redox mechanism. These observations indicate that the monovalent gold compound AuTG is a potentially useful drug for the treatment of patients infected with HIV.
Keywords: AIDS, antiviral, NF-B, rheumatoid arthritis, viral latency
Transmitting editor: K. Okumura
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