Table 2.
Summary of the main studies related to the antiviral activity of Eucalyptus essential oil or its monoterpenes.
| Treatment | Type of Study | Active against | Main Findings | IC50/IC100 | Mechanism of Action/Viral Target | Reference |
|---|---|---|---|---|---|---|
| 1,8-cineole | In vivo (murine model (females) of genital infection) | HSV-2 | At an absolute concentration (100%), 1,8-cineole produced a 44% reduction in viral infection. | - | Protection prior to the viral infection challenge | [36] |
| Essential oil (E. caesia) | In vitro (plaque reduction assay in RC-37 cells) | HSV-1 and HSV-2 | At a concentration of 0.03% in medium, E. caesia essential oil reduced virus titers by 57.9% for HSV-1 and 75.4% for HSV-2. Significant inhibitory effect on the HSV-1 and HSV-2 plaque formation. |
IC50 of 0.009% for HSV-1 and 0.008% for HSV-2. | Direct binding to free virus | [37] * |
| Essential oil (E. globulus) | In vitro (plaque reduction assay in Vero cells) | HSV-1 | Significant inhibitory effect on the HSV-1 plaque formation. | IC100 of 1%. | Direct binding to free virus | [38] * |
| Essential oil (E. globulus) and individual monoterpenes (1,8-cineole, α-pinene, p-cymene, γ-terpinene, α-terpineol, and terpinen-4-ol) | In vitro (plaque reduction assay in RC-37 cells) | HSV-1 (cepa KOS) | Significant inhibitory effect on the HSV-1 plaque formation. | IC50: E. globulus essential oil (55 μg/mL), 1,8-cineole (1.20 mg/mL), α-pinene (4.5 μg/mL), γ-terpinene (7.0 μg/mL), p-cymene. (16.0 μg/mL), α-terpineol (22.0 μg/mL), terpinen-4-ol (60.0 μg/mL). | Direct binding to free virus | [39] * |
| Essential oil (E. caesia) | In vitro (plaque reduction assay in Vero cells) | HSV-1 | Significant inhibitory effect on the HSV-1 plaque formation. | IC50 of 0.004%. | Direct binding to free virus | [31] * |
| Essential oil (E. polybractea) | In vitro (plaque reduction assay in MDCK cells) | Influenza virus A (NWS/G70C/H11N9) | Exposure to the aerosol (15 s; 125 μg/L of air) achieved 100% inactivation of IFV-A in the air. One day of exposure to oil vapor (saturated) reduced viral infection by IFV-A by 86%. |
- | Direct binding to free virus | [40] |
| Essential oil (E. globulus) | In vitro (plaque reduction assay in MDCK cells and hemagglutinin and neuraminidase inhibition assays) | Influenza virus A (Denver/1/57/H1N1) | Significant inhibitory effect on the Influenza virus A plaque formation. Exposure to steam (250 µL of essential oil at 100%) for 10 min produced a 94% reduction in viral infection. Exposure to steam (1/160 dilution of essential oil) for 10 min inhibited hemagglutinin activity but not neuraminidase activity. |
IC100 of 50 μL/mL. | Binding with the virus surface hemagglutinin protein (responsible for the binding of the virus to the host cell) | [41] * |
| 1,8-cineole | In vivo (murine model of influenza infection) | Influenza virus A (FM/47/H1N1) | Treatments of 60 and 120 mg/kg prolonged the survival time of the mice. Treatment decreased IL-4, IL-5, IL-10, and MCP-1 levels in nasal lavage fluids and IL-1β, IL-6, TNF-α, and IFN-γ levels in lung tissue of mice infected with the virus. The expression of NF-kB p65, ICAM-1, and VCAM)-1 decreased. |
- | Attenuate pulmonary inflammatory responses caused by IFV-A | [42] |
| 1,8-cineole | In vivo (murine model immunized and then challenged with the virus) | Influenza virus A (FM/47/H1N1) | The coadministration of the vaccine with 1,8-cineole (12.5 mg/kg) increased the serum production of specific antibodies against influenza (IgG2a), the secretory response of IgA in the nasal cavity mucosa, the expression of intraepithelial lymphocytes in the upper respiratory tract, the maturation of dendritic cells and the expression of costimulatory molecules cluster of differentiation (CD) 40, CD80 and CD86 in peripheral blood. | - | Cross-protection against influenza virus | [23] |
| 1,8-cineole | In silico (molecular docking: Mpro -1,8-cineole interaction) | SARS-CoV-2 | The free energy of binding was −6.04 kcal/mol within the amino acids of the active site of Mpro. The interaction of 1,8-cineole in the binding pocket of the active site of Mpro was mediated by two hydrophobic interactions through MET6, PHE8, ASP295, and ARG298. |
- | Interaction with the active site of Mpro | [43] |
| 1,8-cineole, α-pinene α-terpineol, limonene and o-cymene | In silico (molecular docking: Mpro -monoterpene interaction) | SARS-CoV-2 | The binding of monoterpenes to the active site of Mpro was investigated. The following binding free energies were obtained: 1,8-cineole (−5.86 kcal/mol) > α-pinene (−5.6 kcal/mol) > α-terpineol (−5.43 kcal/mol), > limonene (−5.18 kcal/mol), >o-cymene (−4.99 kcal/mol). |
- | Interaction with the active site of Mpro | [13] |
| Essential oil (E. globulus) | In vitro (plaque reduction assay in Vero cells) | Mumps virus | Treatment with 0.25 μg/mL reduced virus plaque formation by nearly 33%. | - | Direct binding to free virus | [44] |
| Essential oil (E. maidenii, E. cinerea, and E. bicostata) | In vitro (Vero cell protection assay) | Coxsackievirus B3 strain Nancy | Significant reduction in viral infectivity. | IC50: E. bicostata (0.7 µg/µL), E. cinerea (102.0 µg/µL), E. maidenii (136.5 µg/µL). | Direct binding to free virus | [18] * |
| Essential oil (E. camaldulensis) | In vitro (plaque reduction assay in MA104, BGM, and Vero cells) | Rotavirus strain Wa, Coxsackievirus B4, and HSV-1 | A 1/10 dilution of 100 μL of oil reduced Rotavirus strain Wa, Coxsackievirus B4, and HSV-1 plaque formation by 50%, 53.3%, and 90%, respectively. | - | Direct binding to free virus | [45] |
* Studies that have reported the half-maximal inhibitory concentration (IC50) or the maximal inhibitory concentration (IC100) of Eucalyptus essential oil or its monoterpenes.