Table 1.
Antiviral activities of curcumin, curcumin metal complexes, and curcumin formulations against herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2) infections.
Type of Study, Test Performed, Virus, and Cells/Animal Model | Results | Mechanism of Action and Pathway | Reference |
---|---|---|---|
In vitro. Plaque assays, ChIP assay, and western blot analysis. HSV-1. HeLa and Vero cells. |
Inhibition of HSV-1 replication and suppression of IE gene expression. | Curcumin was observed to utilize the mechanism independent of the transcriptional coactivator proteins p300/CBP histone acetyltransferase activity to affect the viral transactivator protein VP16-mediated enlistment of RNA polymerase II to IE gene promoters, leading to suppressing gene expression and blocking viral infection. | [50] |
In vitro and in vivo. Plaque reduction assay. HSV-2. Primary rabbit kidney cells (in vitro). Guinea pig model (in vivo). |
In an in vitro plaque reduction assay, curcumin suppressed the replication of HSV-2 with an ED50 value of 0.32 mg/mL, while at a concentration of 100 mg/mL, the in vivo inhibitory activity was confirmed using a mouse model of genital HSV-2 infection. | The mechanism is unknown. | [51] |
In vitro. Plaque assay. HSV-2. Human genital epithelial cells. |
In primary human genital epithelial cells, pre-treatment of cells with curcumin (5 µM) decreased HSV-2 shedding by 1000-fold and at a concentration of 50 µM, entirely blocked HSV-2 production. | Investigation of the cellular pathways known to be regulated by curcumin involving the transcription factor NF-κB. | [52] |
In vitro. Plaque assay and virus adsorption assay. HSV-1 and HSV-2. Vero cells. |
At a concentration of 30 µM, curcumin inhibited the replication of HSV-1 and HSV-2. | Inhibition of adsorption and replication of HSV-1 and HSV-2. | [53] |
In vivo. Plaque assay. HSV-2. Genital epithelial cells of female C57BL/6 mice. |
Nanoparticle-containing curcumin (0.5 mg) reduced tissue inflammation and the severity of HSV-2 infection in an animal model. | The mechanism of action was detected to be correlated with the anti-inflammatory properties of curcumin. | [54] |
In vitro. Cytopathic inhibition assay. HSV-1. Vero cells. |
Curcumin, gallium-curcumin, and copper-curcumin inhibited the replication of HSV-1 with IC50 values of 33.0, 13.9, and 23.1 µg/mL, respectively. | The mechanisms of action of both gallium-curcumin and copper-curcumin have been suggested to be investigated in further studies. | [55] |
CBP, CREB-binding protein; ChIP, chromatin immunoprecipitation; ED50, the concentration of drug that decreased the plaque number by 50%; HSV-1, herpes simplex virus 1; HSV-2, herpes simplex virus 2; IC50, 50% inhibitory concentration; IE gene, immediate early gene; NF-κB, nuclear factor kappa B.