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Abstract:

In this paper we demonstrate that infection of cell cultures with the arenavirus Junín (JUNV), agent of the argentine haemorrhagic fever, leads to the activation of PI3K/Akt signalling pathway. Phosphorylation of Akt occurs early during JUNV infection of Vero cells and is blocked by the PI3K inhibitor, Ly294002. Infection of cells with UV-irradiated JUNV redeemed the pattern of stimulation observed for infectious virus indicating that an early stage of multiplication cycle would be enough to trigger activation. Treatment of cells with chlorpromazine abrogated phosphorylation of Akt upon JUNV infection suggesting virus internalization as responsible for activation. Inhibition of Akt phosphorylation by Ly294002 impaired viral protein synthesis and expression leading to a reduced infectious virus yield without blocking the onset of persistent stage of infection. This impairment is linked to a reduced amount of virus bound to cells probably due to a blockage on the recycling of transferrin cell-receptor, employed by the virus to adsorb to the cell surface. Early Akt activation was also observed in BHK-21 and A549 JUNV infected cells suggesting an important role of PI3K/Akt signalling in JUNV multiplication in vitro. © 2009 Elsevier B.V. All rights reserved.

Registro:

Documento: Artículo
Título:Participation of the phosphatidylinositol 3-kinase/Akt pathway in Junín virus replication in vitro
Autor:Linero, F.N.; Scolaro, L.A.
Filiación:Laboratorio de Virología, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Ciudad Universitaria, Pab II, 4 Piso, C1428BGA Buenos Aires, Argentina
Palabras clave:Akt; Argentine hemorrhagic fever; Junín virus; Ly294002; Phosphatidylinositol 3-kinase; cell receptor; phosphatidylinositol 3 kinase; protein kinase B; transferrin receptor; animal cell; article; cell surface; controlled study; enzyme activation; enzyme inhibition; enzyme phosphorylation; human; human cell; in vitro study; Junin virus; nonhuman; persistent virus infection; priority journal; protein expression; protein synthesis; ultraviolet radiation; Vero cell; virus activation; virus cell interaction; virus entry; virus infection; virus replication; 1-Phosphatidylinositol 3-Kinase; Animals; Cercopithecus aethiops; Chromones; Cricetinae; Enzyme Inhibitors; Hemorrhagic Fever, American; Host-Pathogen Interactions; Humans; Junin virus; Morpholines; Phosphorylation; Proto-Oncogene Proteins c-akt; Signal Transduction; Vero Cells; Virus Internalization; Virus Replication; Arenavirus; Junin virus
Año:2009
Volumen:145
Número:1
Página de inicio:166
Página de fin:170
DOI: http://dx.doi.org/10.1016/j.virusres.2009.07.004
Título revista:Virus Research
Título revista abreviado:Virus Res.
ISSN:01681702
CODEN:VIRED
CAS:phosphatidylinositol 3 kinase, 115926-52-8; protein kinase B, 148640-14-6; 1-Phosphatidylinositol 3-Kinase, 2.7.1.137; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, 154447-36-6; Chromones; Enzyme Inhibitors; Morpholines; Proto-Oncogene Proteins c-akt, 2.7.1.37
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01681702_v145_n1_p166_Linero

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Citas:

---------- APA ----------
Linero, F.N. & Scolaro, L.A. (2009) . Participation of the phosphatidylinositol 3-kinase/Akt pathway in Junín virus replication in vitro. Virus Research, 145(1), 166-170.
http://dx.doi.org/10.1016/j.virusres.2009.07.004
---------- CHICAGO ----------
Linero, F.N., Scolaro, L.A. "Participation of the phosphatidylinositol 3-kinase/Akt pathway in Junín virus replication in vitro" . Virus Research 145, no. 1 (2009) : 166-170.
http://dx.doi.org/10.1016/j.virusres.2009.07.004
---------- MLA ----------
Linero, F.N., Scolaro, L.A. "Participation of the phosphatidylinositol 3-kinase/Akt pathway in Junín virus replication in vitro" . Virus Research, vol. 145, no. 1, 2009, pp. 166-170.
http://dx.doi.org/10.1016/j.virusres.2009.07.004
---------- VANCOUVER ----------
Linero, F.N., Scolaro, L.A. Participation of the phosphatidylinositol 3-kinase/Akt pathway in Junín virus replication in vitro. Virus Res. 2009;145(1):166-170.
http://dx.doi.org/10.1016/j.virusres.2009.07.004