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• W2800268079 abstract "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." @default.
• W2800268079 created "2018-05-17" @default.
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• W2800268079 date "2018-04-17" @default.
• W2800268079 modified "2023-10-14" @default.
• W2800268079 title "Role of the ERK1/2 Signaling Pathway in the Replication of Junín and Tacaribe Viruses" @default.
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• W2800268079 doi "https://doi.org/10.3390/v10040199" @default.
• W2800268079 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5923493" @default.
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• W2800268079 hasPublicationYear "2018" @default.
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