Table 2.

Antiviral properties of curcumin and curcumin formulations against human cytomegalovirus (HCMV), Kaposi’s sarcoma-associated herpesvirus (KSHV), Epstein–Barr virus (EBV), bovine herpesvirus 1 (BoHV-1), and pseudorabies virus (PRV) infections.

Herpesvirus and Type of Study	Results	Mechanism of Action and Pathway	Reference
HCMV (in vitro, in vivo, and in silico).	At various concentrations in micromolar ranges, curcumin was detected with anti-HCMV properties.	Inhibition of IEA and UL83A expressions and downregulation of Hsp90. Determination of anti-inflammatory and antioxidant effects as possible mechanisms underlying the anti-HCMV activity.	[66,67,68]
KSHV (in vitro).	At various concentrations (in µM), curcumin efficiently inhibited KSHV replication and virus-associated pathogenic properties.	Blocking APE1-mediated redox function.	[73]
EBV (in vitro).	Inhibition of EBV reactivation in Raji DR-CAT cells with curcumin treatment (15 µM).	Inhibition of BZLF1 gene transcription.	[77]
BoHV-1 (in vitro).	At a concentration of 10 µM, curcumin reduced BoHV-1 titer, leading to inhibiting viral replication. Co-encapsulation of acyclovir and curcumin into three microparticle formulations noticeably reduced the BoVH-1 plaque formation at a concentration of 75 µg/mL.	Inhibition of virus post-binding entry process by upregulating the lipid raft formation.	[80,81]
PRV (in vitro).	Treatment with curcumin (30 µM) blocked PRV infectivity in PK-15 cells by decreasing the viral plaque formation.	No mechanism of action was revealed.	[84]

APE1, apurinic/apyrimidinic endonuclease 1; BoHV-1, bovine herpesvirus 1; EBV, Epstein–Barr virus; HCMV, human cytomegalovirus; Hsp90, heat shock protein 90; IEA, immediate early antigen; KSHV, Kaposi’s sarcoma-associated herpesvirus; PK, porcine kidney; PRV, pseudorabies virus.