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. 2015 Jul 25:12:108.
doi: 10.1186/s12985-015-0339-8.

The Chinese herb-derived Sparstolonin B suppresses HIV-1 transcription

Xin Deng  1 , Yaping Zhang  2 , Feng Jiang  3 , Ran Chen  4 , Peichun Peng  5 , Bin Wen  6 , Jian Liang  7
Affiliations

The Chinese herb-derived Sparstolonin B suppresses HIV-1 transcription

Xin Deng et al. Virol J. .

Abstract

Background: The Chines herb derived Sparstolonin B, (SsnB), is a recently identified natural compound that selectively blocks TLR2- and TLR4-mediated inflammatory signaling. But it is unknown whether this compound has any effect on HIV infection.

Findings: We found that SsnB treatment blocked HIV-1 transcription via a novel mechanism that requires the TAR region. Treatment of human T cell lines or peripheral blood mononuclear cells with SsnB at 1 μM significantly inhibited HIV production. Lastly, SsnB was able to inhibit HIV in synergy with AZT.

Conclusions: These data suggest that SsnB is a novel natural compound that inhibits HIV-1 transcription and may be a new drug in the treatment of HIV infection.

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Figures

Fig. 1
Fig. 1
SsnB inhibits HIV production. a CEM-SS cells were infected with HIV pNL4.3 (MOI 0.01) and then treated with SsnB at indicated concentrations for 12 h. Newly released virus in the supernatants was collected 24 h after exposure to SsnB and then titered on the TZM-Bl cells. *p < 0.01, n = 4. b PHA activated PMBCs were infected with pNL4.3 (MOI 0.1) for 5 h followed by SsnB treatment for 12 h. After an additional 24 h, the HIV p24 concentrations in the supernatants were determined by ELISA. *p < 0.01, n = 3
Fig. 2
Fig. 2
SsnB inhibited HIV LTR promoter activity. a 293T cells were transfected with HIV LTR plasmid together with pGL4.74 [hRluc/TK]. Cells were either left unstimulated or stimulated with PMA (50 ng/ml) for 12 h followed by mock or SsnB (1 μg/ml, ~3.7 μM) treatment for another 12 h. Luciferase assay was performed. Normalized HIV LTR promoter activity was presented. b CEM-SS cells were treated with SsnB at various concentrations for 12 h and cell viability was determined by CellTiter Glo kit (Promega) 24 h after the initial exposure
Fig. 3
Fig. 3
SsnB inhibition of HIV requires TAR region. a Illustration of successive deletion constructs that were used in this experiment. The TAR-deleted LTR was created by restriction digest to remove nucleotides downstream of +24 relative to the transcription start site. b 0.1 μg of the reporter constructs in (a) were transfected into 293T cells in the presence or absence of SsnB (1 μg/ml) for 12 h. Luciferase assays were done 48 h after transfection. *p < 0.01, n = 3. c 0.1 μg of the minimal TAR-LTR (−31 to +83) construct was transfected into 293T cells alone or with 5 or 10 ng Tat expressing plasmid. Twenty four hours post-transfection, two samples were treated with SsnB (1 μg/ml) for 12 h. Luciferase assay was done 24 h thereafter. Notably, this construct does not respond to PMA treatment (50 ng/ml)
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