Oxidative stress influences positive strand RNA virus genome synthesis and capping.
TLDR
It is found that antioxidant treatment reduced virus production, reduced the viral positive-to-negative strand RNA ratio, and resulted in the accumulation of uncapped positive-sense viral RNAs, suggesting that RNA viruses may utilize oxidative stress induced during infection to help temporally control genome RNA capping and genome replication.About:
This article is published in Virology.The article was published on 2015-01-15 and is currently open access. It has received 75 citations till now. The article focuses on the topics: RNA-dependent RNA polymerase & RNA.read more
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Implications of oxidative stress on viral pathogenesis.
Fernanda Caetano Camini,Camila Carla da Silva Caetano,Letícia Trindade Almeida,Cintia Lopes de Brito Magalhães +3 more
TL;DR: The modulation of reactive species production and oxidative stress potentially represents a novel pharmacological approach for reducing the consequences of viral pathogenesis.
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SARS-CoV-2 infection, COVID-19 pathogenesis, and exposure to air pollution: What is the connection?
TL;DR: Air pollution exposure may affect different stages of the viral life cycle, including inhibition of mucociliary clearance, alteration of viral receptors and proteases required for entry, changes to antiviral interferon production and viral replication, changes in viral assembly mediated by autophagy, prevention of uptake by macrophages, and promotion of viral spread by increasing epithelial permeability.
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Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes
Pítia Flores Ledur,Karina Karmirian,Carolina da S. G. Pedrosa,Leticia R. Q. Souza,Gabriela Assis-de-Lemos,Thiago Martino Martins,Jéssica de Cassia Cavalheiro Gomes Ferreira,Gabriel Ferreira de Azevedo Reis,Eduardo Santos Silva,Débora Pedroza Guedes da Silva,José Alexandre Salerno,Isis M. Ornelas,Sylvie Devalle,Rodrigo Madeiro da Costa,Livia Goto-Silva,Luiza M. Higa,Adriana Suely de Oliveira Melo,Amilcar Tanuri,Leila Chimelli,Marcos Massao Murata,Patricia P. Garcez,Eduardo C. Filippi-Chiela,Antonio Galina,Helena L. Borges,Stevens K. Rehen +24 more
TL;DR: The results show ROS imbalance, mitochondrial defects and DNA breakage, which have been previously linked to neurological disorders, and may help to explain the observed effects in congenital Zika syndrome related to neuronal loss and motor deficit.
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Dance with the Devil: Stress Granules and Signaling in Antiviral Responses
TL;DR: This review summarizes the current understanding of how stress and innate immune signaling act in concert to mount an effective response against virus infection, with a particular focus on the potential role of stress granules in the coordination of antiviral signaling cascades.
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Flaviviridae Viruses and Oxidative Stress: Implications for Viral Pathogenesis
TL;DR: The current understanding of the pathogenic mechanisms of oxidative stress induced by Flaviviridae viruses are discussed and the relevance of autophagy and DNA damage in the life cycle of viruses is highlighted.
References
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TL;DR: The present research attacked the Flavivirus infection through two mechanisms: Membrane Reorganization and the Compartmentalization and Assembly and Release of Particles from Flaviv virus-infected Cells and Host Resistance to Flaviviral Infection.
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Dengue: a continuing global threat
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TL;DR: A global strategy aimed at increasing the capacity for surveillance and outbreak response, changing behaviours and reducing the disease burden using integrated vector management in conjunction with early and accurate diagnosis has been advocated.
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ATM Activation by Oxidative Stress
TL;DR: It is shown that oxidation of ATM directly induces ATM activation in the absence of DNA DSBs and the MRN complex, and that ATM is an important sensor of reactive oxygen species in human cells.
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Inhibition of interferon signaling by dengue virus
TL;DR: It is found that expression in human A549 cells of the dengue virus nonstructural proteins NS2A, NS4A, or NS4B enhances replication of an IFN-sensitive virus.