Figure 2.

The effects of curcumin on different viruses and multi-site inhibitory effects of curcumin in the life cycle of human viruses. In general, the virus life cycle can be divided into various stages including: (1) attachment of virion, (2) entry, (3) viral genome replication, (4) viral transcription, (5) viral translation, and (6) virion assembly and exit. Hence, these critical steps specific to the viral life cycle have been attractive targets for chemotherapeutic intervention. Pathways and processes are inhibited by curcumin and its analogues, which affect various stages of the virus life cycle. Curcumin blocks viral attachment and entry in several enveloped viruses by abrogating the function of viral envelope proteins. Furthermore, curcumin serves as a veridical agent via attacking and disrupting the integrity of viral membrane envelopes. Additionally, curcumin influences viral replication machinery in two ways: (i) directly targeting the viral replication machinery, and (ii) interrupting viral replication machinery through modulating host cell signaling pathways, for instance, NF-κB, PI3K-AKT, Jab-1, and inflammation, as well as transcription/translation factors, which then cardinally hinder virus replication. The versatile anti-viral effect of curcumin has been demonstrated in numerous viruses as indicated in the boxes. IAV, influenza A virus; PIV-3, parainfluenza virus 3; CHIKV, chikungunya virus; JEV, Japanese encephalitis virus; EV71, enterovirus 71; HCV, hepatitis C virus; VSV, vesicular stomatitis virus; EV, Ebola virus; RSV, respiratory Syncytial virus; HIV, human immunodeficiency virus; HTLV-1, human T-lymphocyte virus; RVFV, Rift Valley fever virus; HuNoV, human norovirus; CVB3, coxsackievirus B3; HBV, hepatitis B virus; HSV, herpes simplex viruses; HCMV, human cytomegalovirus; EBV, Epstein–Barr virus.