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spelling todo:paper_03048608_v160_n2_p469_Linero2023-10-03T15:21:01Z Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells Linero, F.N. Fernández Bell-Fano, P.M. Cuervo, E. Castilla, V. Scolaro, L.A. Junín virus LY294002 Persistence PI3K/AKT 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one chromone derivative enzyme inhibitor morpholine derivative phosphatidylinositol 3 kinase protein kinase B virus protein animal antagonists and inhibitors apoptosis biosynthesis cell line Chlorocebus aethiops drug effects growth, development and aging Hemorrhagic Fever, American Junin virus physiology Vero cell line virology virus entry virus replication Animals Apoptosis Cell Line Cercopithecus aethiops Chromones Enzyme Inhibitors Hemorrhagic Fever, American Junin virus Morpholines Phosphatidylinositol 3-Kinases Proto-Oncogene Proteins c-akt Vero Cells Viral Proteins Virus Internalization Virus Replication In previous work, we demonstrated that the arenavirus Junín virus (JUNV) is able to activate Akt by means of the phosphatidylinositol-3-kinase (PI3K) survival pathway during virus entry. This work extends our study, emphasizing the relevance of this pathway in the establishment and maintenance of persistent infection in vitro. During the course of infection, JUNV-infected Vero cells showed a typical cytopathic effect that may be ascribed to apoptotic cell death. Treatment of infected cultures with Ly294002, an inhibitor of the PI3K/Akt pathway, produced an apoptotic response similar to that observed for uninfected cells treated with the drug. This result suggests that virus-induced activation of the PI3K/Akt pathway does not deliver a strong enough anti-apoptotic signal to explain the low proportion of apoptotic cells observed during infection. Also, inhibition of the PI3K/Akt pathway during the acute stage of infection did not prevent the establishment of persistence. Furthermore, treatment of persistently JUNV-infected cells with Ly294002 did not alter viral protein expression. These findings indicate that despite the positive modulation of the PI3/Akt pathway during Junín virus entry, this would not play a critical role in the establishment and maintenance of JUNV persistence in Vero cells. © 2014, Springer-Verlag Wien. Fil:Linero, F.N. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Fernández Bell-Fano, P.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Castilla, V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Scolaro, L.A. 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_v160_n2_p469_Linero
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Junín virus
LY294002
Persistence
PI3K/AKT
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
chromone derivative
enzyme inhibitor
morpholine derivative
phosphatidylinositol 3 kinase
protein kinase B
virus protein
animal
antagonists and inhibitors
apoptosis
biosynthesis
cell line
Chlorocebus aethiops
drug effects
growth, development and aging
Hemorrhagic Fever, American
Junin virus
physiology
Vero cell line
virology
virus entry
virus replication
Animals
Apoptosis
Cell Line
Cercopithecus aethiops
Chromones
Enzyme Inhibitors
Hemorrhagic Fever, American
Junin virus
Morpholines
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
Vero Cells
Viral Proteins
Virus Internalization
Virus Replication
spellingShingle Junín virus
LY294002
Persistence
PI3K/AKT
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
chromone derivative
enzyme inhibitor
morpholine derivative
phosphatidylinositol 3 kinase
protein kinase B
virus protein
animal
antagonists and inhibitors
apoptosis
biosynthesis
cell line
Chlorocebus aethiops
drug effects
growth, development and aging
Hemorrhagic Fever, American
Junin virus
physiology
Vero cell line
virology
virus entry
virus replication
Animals
Apoptosis
Cell Line
Cercopithecus aethiops
Chromones
Enzyme Inhibitors
Hemorrhagic Fever, American
Junin virus
Morpholines
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
Vero Cells
Viral Proteins
Virus Internalization
Virus Replication
Linero, F.N.
Fernández Bell-Fano, P.M.
Cuervo, E.
Castilla, V.
Scolaro, L.A.
Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells
topic_facet Junín virus
LY294002
Persistence
PI3K/AKT
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
chromone derivative
enzyme inhibitor
morpholine derivative
phosphatidylinositol 3 kinase
protein kinase B
virus protein
animal
antagonists and inhibitors
apoptosis
biosynthesis
cell line
Chlorocebus aethiops
drug effects
growth, development and aging
Hemorrhagic Fever, American
Junin virus
physiology
Vero cell line
virology
virus entry
virus replication
Animals
Apoptosis
Cell Line
Cercopithecus aethiops
Chromones
Enzyme Inhibitors
Hemorrhagic Fever, American
Junin virus
Morpholines
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
Vero Cells
Viral Proteins
Virus Internalization
Virus Replication
description In previous work, we demonstrated that the arenavirus Junín virus (JUNV) is able to activate Akt by means of the phosphatidylinositol-3-kinase (PI3K) survival pathway during virus entry. This work extends our study, emphasizing the relevance of this pathway in the establishment and maintenance of persistent infection in vitro. During the course of infection, JUNV-infected Vero cells showed a typical cytopathic effect that may be ascribed to apoptotic cell death. Treatment of infected cultures with Ly294002, an inhibitor of the PI3K/Akt pathway, produced an apoptotic response similar to that observed for uninfected cells treated with the drug. This result suggests that virus-induced activation of the PI3K/Akt pathway does not deliver a strong enough anti-apoptotic signal to explain the low proportion of apoptotic cells observed during infection. Also, inhibition of the PI3K/Akt pathway during the acute stage of infection did not prevent the establishment of persistence. Furthermore, treatment of persistently JUNV-infected cells with Ly294002 did not alter viral protein expression. These findings indicate that despite the positive modulation of the PI3/Akt pathway during Junín virus entry, this would not play a critical role in the establishment and maintenance of JUNV persistence in Vero cells. © 2014, Springer-Verlag Wien.
format JOUR
author Linero, F.N.
Fernández Bell-Fano, P.M.
Cuervo, E.
Castilla, V.
Scolaro, L.A.
author_facet Linero, F.N.
Fernández Bell-Fano, P.M.
Cuervo, E.
Castilla, V.
Scolaro, L.A.
author_sort Linero, F.N.
title Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells
title_short Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells
title_full Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells
title_fullStr Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells
title_full_unstemmed Inhibition of the PI3K/Akt pathway by Ly294002 does not prevent establishment of persistent Junín virus infection in Vero cells
title_sort inhibition of the pi3k/akt pathway by ly294002 does not prevent establishment of persistent junín virus infection in vero cells
url http://hdl.handle.net/20.500.12110/paper_03048608_v160_n2_p469_Linero
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