Table 2.

Pharmacological studies on antiviral effects of cinnamon.

No	Extract /Main component	Part used	Model	Design	Dosage/ Duration of treatment	Mechanism/outcome	Ref.
1	water extract /cinnzeylanine	Bark	in vitro and in vivo	By Vero cells and silkworm infection model	0.5 m/ Once	Cinnzeylanine inhibits the proliferation of herpes simplex virus type 1	[22]
2	NM	bark	In vitro	?	–	1.Pepsin enzymatic activity was inhibited. 2.The activity of HIV protease was also inhibited.	[39]
3	Type-A procyanidin polyphenol (IND02)	bark	In vitro	HIV-1 primary patient isolates	–	1.HIV-1 Replication was blocked. 2.HIV-1 was inhibited, and T cell exhaustion markers, Tim-3, and PD-1 were down-modulated.	[40]
4	procyanidin type A (IND02)	NM	In vitro	Cell culture-derived HCV	–	1.No effect on HCV replication 2.blockade of HCV entry, dose-dependently, occurring at a post binding step 3.Inhibiting HCV entry demonstrates the functional impact in the most physiological cell-based system for studying HCV–host interactions.	[41]
5	hydroalcoholic extract	wood	in vitro	HSV-1	–	1.Attachment of HSV-1 onto host cells was inhibited. 2.The viral titer of herpes simplex type 1 was reduced before, during, and after inoculation of herpes virus	[42]
6	essential oil	Bark and leaf	In vitro	cytopathic effect reduction method for anti-influenza (A/WS/33 virus) activity	–	No significant effect on influenza A/WS/33 virus activity	[43]

NM: not mentioned, HCV: hepatitis C virus, HIV: human immunodeficiency virus, HSV: hepatitis simplex virus, Tim-3: T cell immunoglobulin mucin domain 3, PD-1: programmed death-1