Implications Using Coconut oil a bit in regular use is certainly helpful —but it needs further studies as to how to effectively increase its effectiveness. This blog is based on our preliminary understanding and shall be followed by various updates in the field.
Lauric acid (C12) and monolaurin, its derivative, have been known for many years to have significant antiviral activity. Lauric acid is a medium-chain fatty acid which makes up about 50% of coconut oil; monolaurin is a metabolite that is naturally produced by the body’s own enzymes upon ingestion of coconut oil and is also available in pure form as a supplement. Sodium lauryl sulphate, a common surfactant that is made from lauric acid, has been shown to have potent antiviral properties. Lauric acid, monolaurin, and sodium lauryl sulphate (which is also known as sodium dodecyl sulphate) are used in a wide range of products for their antiviral properties.
MECHANISM OF ACTIONS
Three mechanisms have be disintegration of the virus envelope; second, they can inhibit late maturation stage in the virus replicative cycle; and third, they can prevent the binding of viral proteins to the host cell membrane.
- Disintegration of the virus membrane. The antiviral activities of lauric acid and monolaurin were first noted by Sands and co-workers (1979) and later by Hierholzer & Kabara (1982). In particular, Hierholzer & Kabara showed that monolaurin was able to reduce infectivity of 14 human RNA and DNA enveloped viruses in cell culture by >99.9%, and that monolaurin acted by disintegrating the virus envelope. Thormar and co-workers (1987) confirmed the ability of lauric acid and monolaurin to inactivate viruses by disintegration of the cell membrane. Sodium lauryl sulfate has been shown to be able to solubilize and denature the viral envelope (Piret 2000, 2002).
- Inhibits virus maturation. The Junin virus (JUNV) is the causative agent of Argentine hemorrhagic fever. In a comparison among the saturated fatty acids from C10 to C18 against JUNV infection, Bartolotta and co-workers (2001) showed that lauric acid was the most active inhibitor. From mechanistic studies, it was concluded that lauric acid inhibited a late maturation stage in the replicative cycle of JUNV. From transmission electron microscope images, JUNV is an enveloped virus featuring glycoproteins that are embedded in the lipid bilayer forming viral spikes (Grant et al., 2012); this is similar to nCoV-2019.
- Prevents binding of viral proteins to the host cell membrane. Hornung and co-workers (1994) showed that in the presence of lauric acid, the production of infectious vesicular stomatitis virus was inhibited in a dose-dependent and reversible manner: after removal of lauric acid, the antiviral effect disappeared. They observed that lauric acid did not influence viral membrane (M) protein synthesis, but prevented the binding of viral M proteins to the host cell membrane.Although lauric acid accounts for much of the reported antiviral activity of coconut oil, capric acid (C10) and monocaprin have also shown promising activity against other viruses, such as HIV-1 (Kristmundsdóttir et al., 1999). Capric acid accounts for about 7% of coconut oil. Thus, at least two fatty acids in coconut oil, and their monoglycerides, have antiviral properties. Hilarsson and co-workers (2007) tested virucidal activities of fatty acids, monoglycerides and fatty alcohols against respiratory syncytial virus (RSV) and human parainfluenza virus type 2 (HPIV2) at different concentrations, times and pH levels. They reported the most active compound tested was monocaprin (C10), which also showed activity against influenza A virus and significant virucidal activities even at a concentration as low as 0.06-0.12%
