Three inhibitors of type 1 human immunodeficiency virus long terminal repeat-directed gene expression and virus replication.

Abstract

Transcription of type 1 human immunodeficiency virus (HIV-1) provirus is governed by the viral long terminal repeat (LTR). Drugs can block HIV-1 replication by inhibiting activity of its LTR. We report that topotecan, beta-lapachone, and curcumin are potent and selective inhibitors of HIV-1 LTR-directed gene expression, at concentrations that have minor effects on cells. At these concentrations, each drug inhibited p24 antigen production in cells either acutely or chronically infected with HIV-1. Their target is transcriptional function of the LTR.

Mood‐Enhancing Antidepressant St. John's Wort Inhibits the Activation of Human Immunodeficiency Virus Gene Expression by Ultraviolet Light

“…Thus, compounds that block activation of HIV-1 are of therapeutic potential for extension of latency or inhibition of progressive HIV-1 infection (41). Additionally, for the first time, we have shown here the activation of p38 MAP kinase and JNK1 and -2 by SJW.…”

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“…[137] One study showed curcumin to be an effective compound to inhibit the HIV-1 LTR-directed gene expression without any major effects on cell viability. [138] It was also found that curcumin and its derivatives, specifically, reduced curcumin, allyl-curcumin, and tocopheryl-curcumin, discovered 70-85% inhibition in Tat protein transactivation of HIV-1 LTR measured by β-galactosidase activities of HeLa cells which in HIV-1 LTR was fused to the indictor of lac Z gene. [139] Furthermore, curcumin reserved the acetylation of Tat protein of HIV significantly by p300 related with invasion of HIV-1 multiplication.…”

Effect of Antioxidant (Turmeric, Turmerin and Curcumin) on Human Immunodeficiency Virus

“…Curcumin (diferuloylmethane), the yellow pigments in T that is widely used as a food coloring (curry) and preservative has been extensively studied. In particular, Cu inhibited purified human immunodeficiency virus type 1 (HIV-1) integrase [5,6], HIV-1 and HIV-2 proteases [7], and HIV-1 long terminal repeatdirected gene expression of acutely or chronically infected HIV-1 cells [8]. Cu also inhibited lipopolysaccharide (LPS)-induced activation of nuclear factor kappa B, a factor involved in the activation and replication of HIV-1 [9].…”