BackgroundIn Brazil, dengue epidemics erupt sporadically throughout the country and it is unclear if outbreaks may initiate a sustainable transmission cycle. There are few studies evaluating the ability of Brazilian Aedes aegypti populations to transmit dengue virus (DENV). The aim of this study was to compare DENV susceptibility of field-captured Ae. aegypti populations from nine distinct geographic areas of the city of Belo Horizonte in 2009 and 2011. Infection Rate (IR), Vector Competence (VC) and Disseminated Infection Rate (DIR) were determined.MethodsAedes aegypti eggs from each region were collected and reared separately in an insectary. Adult females were experimentally infected with DENV-2 and the virus was detected by qPCR in body and head samples. Data were analyzed with the Statistical Package for the Social Sciences version 17.ResultsIR varied from 40.0% to 82.5% in 2009 and 60.0% to 100.0% in 2011. VC ranged from 25.0% to 77.5% in 2009 and 25.0% to 80.0% in 2011. DIR oscillated from 68.7% to 100.0% in 2009 and 38.4% to 86.8 in 2011. When the results were evaluated by a logistic model using IR as covariate, North, Barreiro, South-Central and Venda Nova showed the strongest association in 2009. In 2011, a similar association was observed for South-Central, Venda Nova, West and Northeast regions. Using VC as covariate, South-Central and Venda Nova showed the most relevant association in 2009. In 2011, South-Central, Venda Nova and Barreiro presented the greatest revelation associations. When DIR data were analyzed by logistic regression models, Pampulha, South-Central, Venda Nova, West, Northeast and East (2009) as well as South-Central, Venda Nova and West (2011) were the districts showing the strongest associations.ConclusionsWe conclude that Ae. aegypti populations from Belo Horizonte exhibit wide variation in vector competence to transmit dengue. Therefore, vector control strategies should be adapted to the available data for each region. Further analysis should be conducted to better understand the reasons for this large variability in vector competence and how these parameters correlate with epidemiological findings in subsequent years.

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.

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Dengue virus nonstructural protein 1 (NS1) is a glycoprotein involved in viral RNA replication. NS1 associates with host cell proteins and can be found in lipid raft domains on the host cell surface, suggesting an involvement in signal transduction events. In this work, we observed that NS1 expression in HepG2 cells increases nuclear translocation of NF-κB p65 protein, which was paralleled by DNA-protein complex formation. Luciferase assays showed an increase in NF-κB transcriptional activities in NS1-expressing cells when compared to parental cells. NS1 may enhance NF-κB function in host cells and contribute to the pathogenesis of dengue.