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

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...

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Autores principales: Bartolotta, S., García, C.C., Candurra, N.A., Damonte, E.B.
Formato: JOUR
Materias:
Arenavirus
cell membrane
cell stimulation
Junin virus
lauric acid
saturated fatty acid
triacylglycerol
virion
virus glycoprotein
virus infection
virus protein
virus replication
Animals
Cell Line
Cercopithecus aethiops
Dose-Response Relationship, Drug
Fatty Acids
Inhibitory Concentration 50
Lauric Acids
Membrane Glycoproteins
Microbial Sensitivity Tests
Triglycerides
Vero Cells
Viral Proteins
Virion
Virus Replication
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_03048608_v146_n4_p777_Bartolotta
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
id todo:paper_03048608_v146_n4_p777_Bartolotta
record_format dspace
spelling todo:paper_03048608_v146_n4_p777_Bartolotta2023-10-03T15:20:58Z Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid Bartolotta, S. García, C.C. Candurra, N.A. Damonte, E.B. Arenavirus cell membrane cell stimulation Junin virus lauric acid saturated fatty acid triacylglycerol virion virus glycoprotein virus infection virus protein virus replication Animals Cell Line Cercopithecus aethiops Dose-Response Relationship, Drug Fatty Acids Inhibitory Concentration 50 Junin virus Lauric Acids Membrane Glycoproteins Microbial Sensitivity Tests Triglycerides Vero Cells Viral Proteins Virion Virus Replication Arenavirus Junin virus 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. Fil:García, C.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Candurra, N.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Damonte, E.B. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_03048608_v146_n4_p777_Bartolotta
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Arenavirus
cell membrane
cell stimulation
Junin virus
lauric acid
saturated fatty acid
triacylglycerol
virion
virus glycoprotein
virus infection
virus protein
virus replication
Animals
Cell Line
Cercopithecus aethiops
Dose-Response Relationship, Drug
Fatty Acids
Inhibitory Concentration 50
Junin virus
Lauric Acids
Membrane Glycoproteins
Microbial Sensitivity Tests
Triglycerides
Vero Cells
Viral Proteins
Virion
Virus Replication
Arenavirus
Junin virus
spellingShingle Arenavirus
cell membrane
cell stimulation
Junin virus
lauric acid
saturated fatty acid
triacylglycerol
virion
virus glycoprotein
virus infection
virus protein
virus replication
Animals
Cell Line
Cercopithecus aethiops
Dose-Response Relationship, Drug
Fatty Acids
Inhibitory Concentration 50
Junin virus
Lauric Acids
Membrane Glycoproteins
Microbial Sensitivity Tests
Triglycerides
Vero Cells
Viral Proteins
Virion
Virus Replication
Arenavirus
Junin virus
Bartolotta, S.
García, C.C.
Candurra, N.A.
Damonte, E.B.
Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid
topic_facet Arenavirus
cell membrane
cell stimulation
Junin virus
lauric acid
saturated fatty acid
triacylglycerol
virion
virus glycoprotein
virus infection
virus protein
virus replication
Animals
Cell Line
Cercopithecus aethiops
Dose-Response Relationship, Drug
Fatty Acids
Inhibitory Concentration 50
Junin virus
Lauric Acids
Membrane Glycoproteins
Microbial Sensitivity Tests
Triglycerides
Vero Cells
Viral Proteins
Virion
Virus Replication
Arenavirus
Junin virus
description 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.
format JOUR
author Bartolotta, S.
García, C.C.
Candurra, N.A.
Damonte, E.B.
author_facet Bartolotta, S.
García, C.C.
Candurra, N.A.
Damonte, E.B.
author_sort Bartolotta, S.
title Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid
title_short Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid
title_full Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid
title_fullStr Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid
title_full_unstemmed Effect of fatty acids on arenavirus replication: Inhibition of virus production by lauric acid
title_sort effect of fatty acids on arenavirus replication: inhibition of virus production by lauric acid
url http://hdl.handle.net/20.500.12110/paper_03048608_v146_n4_p777_Bartolotta
work_keys_str_mv AT bartolottas effectoffattyacidsonarenavirusreplicationinhibitionofvirusproductionbylauricacid
AT garciacc effectoffattyacidsonarenavirusreplicationinhibitionofvirusproductionbylauricacid
AT candurrana effectoffattyacidsonarenavirusreplicationinhibitionofvirusproductionbylauricacid
AT damonteeb effectoffattyacidsonarenavirusreplicationinhibitionofvirusproductionbylauricacid
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