Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses

We have previously shown that the infection of cell cultures with the arenaviruses Junín (JUNV), Tacaribe (TCRV), and Pichindé promotes the phosphorylation of mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinases 1 and 2 (ERK1/2) and that this activation is required for th...

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Publicado:	2018
Materias:	Arenavirus Cell signaling ERK Junín virus Replication Tacaribe virus 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene chlorpromazine messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 ribavirin small interfering RNA viral protein 1,3 butadiene enzyme inhibitor nitrile virus RNA animal cell Article cell proliferation cell viability controlled study gene expression genetic transfection immunofluorescence test Junin virus nonhuman phosphorylation protein expression real time polymerase chain reaction reverse transcription polymerase chain reaction signal transduction virus entry virus infectivity virus replication Western blotting animal biosynthesis cell line host pathogen interaction MAPK signaling metabolism New World arenavirus physiology Animals Arenaviruses, New World Butadienes Cell Line Enzyme Inhibitors Host-Pathogen Interactions MAP Kinase Signaling System Nitriles RNA, Viral Viral Proteins Virus Replication
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19994915_v10_n4_p_Brunetti http://hdl.handle.net/20.500.12110/paper_19994915_v10_n4_p_Brunetti
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_19994915_v10_n4_p_Brunetti
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spelling	paper:paper_19994915_v10_n4_p_Brunetti2023-06-08T16:32:55Z Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses Arenavirus Cell signaling ERK Junín virus Replication Tacaribe virus 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene chlorpromazine messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 ribavirin small interfering RNA viral protein 1,3 butadiene enzyme inhibitor nitrile viral protein virus RNA animal cell Article cell proliferation cell viability controlled study gene expression genetic transfection immunofluorescence test Junin virus nonhuman phosphorylation protein expression real time polymerase chain reaction reverse transcription polymerase chain reaction signal transduction Tacaribe virus virus entry virus infectivity virus replication Western blotting animal biosynthesis cell line host pathogen interaction MAPK signaling metabolism New World arenavirus physiology Animals Arenaviruses, New World Butadienes Cell Line Enzyme Inhibitors Host-Pathogen Interactions MAP Kinase Signaling System Nitriles RNA, Viral Viral Proteins Virus Replication We have previously shown that the infection of cell cultures with the arenaviruses Junín (JUNV), Tacaribe (TCRV), and Pichindé promotes the phosphorylation of mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinases 1 and 2 (ERK1/2) and that this activation is required for the achievement of a productive infection. Here we examined the contribution of ERK1/2 in early steps of JUNV and TCRV multiplication. JUNV adsorption, internalization, and uncoating were not affected by treatment of cultured cells with U0126, an inhibitor of the ERK1/2 signaling pathway. In contrast, U0126 caused a marked reduction in viral protein expression and RNA synthesis, while JUNV RNA synthesis was significantly augmented in the presence of an activator of the ERK1/2 pathway. Moreover, U0126 impaired the expression of a reporter gene in a TCRV-based replicon system, confirming the ability of the compound to hinder arenavirus macromolecular synthesis. By using a cell-based assay, we determined that the inhibitor did not affect the translation of a synthetic TCRV-like mRNA. No changes in the phosphorylation pattern of the translation factor eIF2α were found in U0126-treated cells. Our results indicate that U0126 impairs viral RNA synthesis, thereby leading to a subsequent reduction in viral protein expression. Thus, we conclude that ERK1/2 signaling activation is required for an efficient arenavirus RNA synthesis. © 2018 by the authors. Licensee MDPI, Basel, Switzerland. 2018 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19994915_v10_n4_p_Brunetti http://hdl.handle.net/20.500.12110/paper_19994915_v10_n4_p_Brunetti
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 signaling ERK Junín virus Replication Tacaribe virus 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene chlorpromazine messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 ribavirin small interfering RNA viral protein 1,3 butadiene enzyme inhibitor nitrile viral protein virus RNA animal cell Article cell proliferation cell viability controlled study gene expression genetic transfection immunofluorescence test Junin virus nonhuman phosphorylation protein expression real time polymerase chain reaction reverse transcription polymerase chain reaction signal transduction Tacaribe virus virus entry virus infectivity virus replication Western blotting animal biosynthesis cell line host pathogen interaction MAPK signaling metabolism New World arenavirus physiology Animals Arenaviruses, New World Butadienes Cell Line Enzyme Inhibitors Host-Pathogen Interactions MAP Kinase Signaling System Nitriles RNA, Viral Viral Proteins Virus Replication
spellingShingle	Arenavirus Cell signaling ERK Junín virus Replication Tacaribe virus 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene chlorpromazine messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 ribavirin small interfering RNA viral protein 1,3 butadiene enzyme inhibitor nitrile viral protein virus RNA animal cell Article cell proliferation cell viability controlled study gene expression genetic transfection immunofluorescence test Junin virus nonhuman phosphorylation protein expression real time polymerase chain reaction reverse transcription polymerase chain reaction signal transduction Tacaribe virus virus entry virus infectivity virus replication Western blotting animal biosynthesis cell line host pathogen interaction MAPK signaling metabolism New World arenavirus physiology Animals Arenaviruses, New World Butadienes Cell Line Enzyme Inhibitors Host-Pathogen Interactions MAP Kinase Signaling System Nitriles RNA, Viral Viral Proteins Virus Replication Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses
topic_facet	Arenavirus Cell signaling ERK Junín virus Replication Tacaribe virus 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene chlorpromazine messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 ribavirin small interfering RNA viral protein 1,3 butadiene enzyme inhibitor nitrile viral protein virus RNA animal cell Article cell proliferation cell viability controlled study gene expression genetic transfection immunofluorescence test Junin virus nonhuman phosphorylation protein expression real time polymerase chain reaction reverse transcription polymerase chain reaction signal transduction Tacaribe virus virus entry virus infectivity virus replication Western blotting animal biosynthesis cell line host pathogen interaction MAPK signaling metabolism New World arenavirus physiology Animals Arenaviruses, New World Butadienes Cell Line Enzyme Inhibitors Host-Pathogen Interactions MAP Kinase Signaling System Nitriles RNA, Viral Viral Proteins Virus Replication
description	We have previously shown that the infection of cell cultures with the arenaviruses Junín (JUNV), Tacaribe (TCRV), and Pichindé promotes the phosphorylation of mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinases 1 and 2 (ERK1/2) and that this activation is required for the achievement of a productive infection. Here we examined the contribution of ERK1/2 in early steps of JUNV and TCRV multiplication. JUNV adsorption, internalization, and uncoating were not affected by treatment of cultured cells with U0126, an inhibitor of the ERK1/2 signaling pathway. In contrast, U0126 caused a marked reduction in viral protein expression and RNA synthesis, while JUNV RNA synthesis was significantly augmented in the presence of an activator of the ERK1/2 pathway. Moreover, U0126 impaired the expression of a reporter gene in a TCRV-based replicon system, confirming the ability of the compound to hinder arenavirus macromolecular synthesis. By using a cell-based assay, we determined that the inhibitor did not affect the translation of a synthetic TCRV-like mRNA. No changes in the phosphorylation pattern of the translation factor eIF2α were found in U0126-treated cells. Our results indicate that U0126 impairs viral RNA synthesis, thereby leading to a subsequent reduction in viral protein expression. Thus, we conclude that ERK1/2 signaling activation is required for an efficient arenavirus RNA synthesis. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
title	Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses
title_short	Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses
title_full	Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses
title_fullStr	Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses
title_full_unstemmed	Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses
title_sort	role of the erk1/2 signaling pathway in the replication of junín and tacaribe viruses
publishDate	2018
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19994915_v10_n4_p_Brunetti http://hdl.handle.net/20.500.12110/paper_19994915_v10_n4_p_Brunetti
_version_	1768543298205515776

Role of the ERK1/2 signaling pathway in the replication of junín and tacaribe viruses

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