Use este identificador para citar ou linkar para este item: http://www.repositorio.ufop.br/jspui/handle/123456789/9201
Título: Oxidative stress in Mayaro virus infection.
Autor(es): Camini, Fernanda Caetano
Caetano, Camila Carla da Silva
Almeida, Letícia Trindade
Guerra, Joyce Ferreira da Costa
Silva, Breno de Mello
Silva, Silvana de Queiroz
Magalhães, José Carlos de
Magalhães, Cíntia Lopes de Brito
Palavras-chave: Antioxidant defences
Data do documento: 2017
Referência: CAMINI, F. C. et al. Oxidative stress in Mayaro virus infection. Virus Research, v. 236, p. 1-8, 2017. Disponível em: <http://www.sciencedirect.com/science/article/pii/S0168170216307122?via%3Dihub>. Acesso em: 15 set. 2017.
Resumo: Mayaro virus (MAYV) is a neglected tropical arbovirus that causes a febrile syndrome that is sometimes accompanied by incapacitating arthritis/arthralgia. The pathogenesis of MAYV has not been completely defined and oxidative stress mediated by an increase in reactive oxygen species (ROS) and/or depletion of antioxidant defences has been found to contribute to several aspects of viral disease. To investigate whether MAYV induced oxidative stress in host cells, we monitored ROS production, oxidative stress markers and antioxidant defences at different time points after infection. Our results show that MAYV induced significant oxidative stress in infected HepG2 cells, as indicated by the increase of malondialdehyde (MDA) and protein carbonyl levels, and by a significant decrease of the reduced versus oxidized glutathione (GSH/GSSG) ratio. Generally, MAYV-infected HepG2 cells also showed an increase in antioxidant defences. We observed an increase in the superoxide dismutase (SOD) and catalase (CAT) activities and the total glutathione content. To determine whether similar effects occurred in other cell types, we evaluated the ROS, MDA and SOD activity levels in J774 cells after MAYV infection. Similar to our observations in HepG2 cells, the J774 cells showed an increase in ROS, MDA and total SOD activity following MAYV infection. Thus, since the cellular redox environment is influenced by the production and removal of ROS, we hypothesize that the overproduction of ROS was responsible for the oxidative stress in response to the MAYV infection despite the increase in the antioxidant status. This study is the first report on the involvement of oxidative stress during MAYV infection. Collectively, our data shed light on some mechanisms that are operational in host cells following exposure to MAYV.
URI: http://www.repositorio.ufop.br/handle/123456789/9201
DOI: https://doi.org/10.1016/j.virusres.2017.04.017
ISSN: 0168-1702
Licença: O periódico Virus Research concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 4210820568169.
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