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. 2021 Jan 31;9(2):292. doi: 10.3390/microorganisms9020292

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.