TABLE 8.
Polyphenols | Virus type | Targets/signaling pathways | Mechanism of action | References |
---|---|---|---|---|
Resveratrol | Human herpesvirus 1 and Human herpesvirus 2 | ND | Significantly reduced skin lesions, and the effectiveness of the drug depended on its concentration, the time of initiation of treatment and the number of applications per day | (Docherty et al., 2004), (Docherty et al., 2005) |
Epigallocatechin-3-gallate | Hepatitis C Virus | E1/E2 | Inhibition of virion attachment | Ciesek et al. (2011) |
Epigallocatechin-3-gallate | Hepatitis C Virus | GT3a and NS3 helicase | Binding interaction of virus NS3 helicase active pocket | Fatima et al. (2014) |
Epigallocatechin-3-gallate | Hepatitis B Virus | HBsAg, HBeAg and virus DNA | Strong anti-HBV activity through decreasing the secretion of HBsAg, HBeAg and extracellular HBV DNA, although perhaps in such a way that the mechanism may interfere with the replication cycle of HBV DNA | Pang et al. (2014) |
Resveratrol | Human papillomavirus | p-pRb1, p53, virus E6 and E7 genes | Inhibits cervical cancer development by suppressing the transcription and translation of E6 and E7, and also by promoting the apoptosis and G1/S phase transition arrest. | Sun et al. (2021) |
6-Gingerol | Human papillomavirus | p53, p21, caspase-3 and PARP | Inhibits the chymotrypsin activity of proteasomes; induce reactivation of p53, and DNA damage and G2/M cell cycle arrest; increases levels of p21; and potentiates the cytotoxicity of cisplatin. | Rastogi et al. (2015) |
Resveratrol | Epstein-Barr virus | Rta, Zta, and EA-D | Inhibits virus lytic cycle | Yiu et al. (2010) |
GT3a, genotype 3a; NS3, nonstructural protein 3; HBsAg, hepatitis B surface antigen; HBeAg, hepatitis B e-antigen; p-pRb1, phosphorylated retinoblastoma protein; PARP, Poly (ADP-ribose) polymerase; HBV, Hepatitis B Virus; ND, not mentioned.