Effect of fatty acids on arenavirus replication : inhibition of virus production by lauric acid

• Published in: Archives of virology Vol. 146; no. 4; pp. 777 - 790
• Main Authors: BARTOLOTTA, S, GARCIA, C. C, CANDURRA, N. A, DAMONTE, E. B
• Format: Journal Article
• Language: English
• Published: Wien Springer 01.01.2001; New York, NY Springer Nature B.V
• Subjects: Animal viral diseases; Animals; Biological and medical sciences; Cell Line; Cell membranes; Cell viability; Cercopithecus aethiops; Dose-Response Relationship, Drug; Epidemiology; Fatty acids; Fatty Acids - pharmacology; Fundamental and applied biological sciences. Psychology; Glycoproteins; Infectious diseases; Infectivity; Inhibitory Concentration 50; Insertion; Junin virus; Junin virus - drug effects; Junin virus - genetics; Junin virus - metabolism; Lauric acid; Lauric Acids - pharmacology; Medical sciences; Membrane Glycoproteins - metabolism; Microbial Sensitivity Tests; Microbiology; Protein biosynthesis; Triglycerides - metabolism; Vero Cells; Viral diseases; Viral Proteins - metabolism; Virion - drug effects; Virions; Virology; Virus Replication - drug effects; Viruses; Virus multiplication; Lipids; Fatty acids; Junin virus; Arenavirus; Virus; Infection; Pathogenicity; Saturated fatty acid; Pathogenic; Viral disease; Attenuation; Replication; Inhibitor; Yield; Inhibition; Cell; Arenaviridae
• ISSN: 0304-8608; 1432-8798
• DOI: 10.1007/s007050170146

To study the functional involvement of cellular membrane properties on arenavirus infection, saturated fatty acids of variable chain length (C10-C18) were evaluated for their inhibitory activity against the multiplication of Junin virus (JUNV). The most active inhibitor was lauric acid (C12), which reduced virus yields of several attenuated and pathogenic strains of JUNV in a dose dependent manner, without affecting cell viability. Fatty acids with shorter or longer chain length had a reduced or negligible anti-JUNV activity. Lauric acid did not inactivate virion infectivity neither interacted with the cell to induce a state refractory to virus infection. From mechanistic studies, it can be concluded that lauric acid inhibited a late maturation stage in the replicative cycle of JUNV. Viral protein synthesis was not affected by the compound, but the expression of glycoproteins in the plasma membrane was diminished. A direct correlation between the inhibition of JUNV production and the stimulation of triacylglycerol cell content was demonstrated, and both lauric-acid induced effects were dependent on the continued presence of the fatty acid. Thus, the decreased insertion of viral glycoproteins into the plasma membrane, apparently due to the increased incorporation of triacylglycerols, seems to cause an inhibition of JUNV maturation and release.