Chemical sympathectomy further increases muscle protein degradation of acutely diabetic rats

The present work investigated the role of the sympathetic nervous system (SINS) in the control of protein degradation in skeletal muscles from rats with streptozotocin (STZ)-induced diabetes. Diabetes (1, 3, and 5 days after STZ) induced a significant increase in the norepinephrine content of soleus and EDL muscles, but it did not affect plasma catecholamine levels. Chemical sympathectomy induced by guanethidine (100 mg/kg body weight, for 1 or 2 days) reduced muscle norepinephrine content to negligible levels (less than 5%), decreased plasma epinephrine concentration, and further increased the high rate of protein degradation in muscles from acutely diabetic rats. The rise in the rate of proteolysis (nmol.mg wet wt(-1).2h(-1)) in soleus from 1-day diabetic sympathectomized rats was associated with increased activities of lysosomal (0.127 +/- 0.008 vs. 0.086 +/- 0.013 in diabetic control) and ubiquitin (Ub)-proteasome-dependent proteolytic pathways (0.154 +/- 0,007 vs. 0.121 +/- 0.006 in diabetic control). Increases in Ca2+-depenclent (0.180 +/- 0.007 vs. 0.121 +/- 0.011 in diabetic control) and Ub-proteasome-dependent proteolytic systems (0.092 +/- 0.003 vs. 0.060 +/- 0.002 in diabetic control) were observed in EDL from 1-day diabetic sympathectomized rats. The lower phosphorylation levels of AKT and Foxo3a in EDL muscles from 3-day diabetic rats were further decreased by sympathectomy. The data suggest that the SNS exerts acute inhibitory control of skeletal muscle proteolysis during the early stages of diabetes in rats, probably involving the AKT/Foxo signaling pathway

Insulin/IGF1 signalling mediates the effects of β2‐adrenergic agonist on muscle proteostasis and growth

Abstract Background Stimulation of β2‐adrenoceptors can promote muscle hypertrophy and fibre type shift, and it can counteract atrophy and weakness. The underlying mechanisms remain elusive. Methods Fed wild type (WT), 2‐day fasted WT, muscle‐specific insulin (INS) receptor (IR) knockout (M‐IR−/−), and MKR mice were studied with regard to acute effects of the β2‐agonist formoterol (FOR) on protein metabolism and signalling events. MKR mice express a dominant negative IGF1 receptor, which blocks both INS/IGF1 signalling. All received one injection of FOR (300 μg kg−1 subcutaneously) or saline. Skeletal muscles and serum samples were analysed from 30 to 240 min. For the study of chronic effects of FOR on muscle plasticity and function as well as intracellular signalling pathways, fed WT and MKR mice were treated with formoterol (300 μg kg−1 day−1) for 30 days. Results In fed and fasted mice, one injection of FOR inhibited autophagosome formation (LC3‐II content, 65%, P ≤ 0.05) that was paralleled by an increase in serum INS levels (4‐fold to 25‐fold, P ≤ 0.05) and the phosphorylation of Akt (4.4‐fold to 6.5‐fold, P ≤ 0.05) and ERK1/2 (50% to two‐fold, P ≤ 0.05). This led to the suppression (40–70%, P ≤ 0.05) of the master regulators of atrophy, FoxOs, and the mRNA levels of their target genes. FOR enhanced (41%, P ≤ 0.05) protein synthesis only in fed condition and stimulated (4.4‐fold to 35‐fold, P ≤ 0.05) the prosynthetic Akt/mTOR/p70S6K pathway in both fed and fasted states. FOR effects on Akt signalling during fasting were blunted in both M‐IR−/− and MKR mice. Inhibition of proteolysis markers by FOR was prevented only in MKR mice. Blockade of PI3K/Akt axis and mTORC1, but not ERK1/2, in fasted mice also suppressed the acute FOR effects on proteolysis and autophagy. Chronic stimulation of β2‐adrenoceptors in fed WT mice increased body (11%, P ≤ 0.05) and muscle (15%, P ≤ 0.05) growth and downregulated atrophy‐related genes (30–40%, P ≤ 0.05), but these effects were abolished in MKR mice. Increases in muscle force caused by FOR (WT, 24%, P ≤ 0.05) were only partially impaired in MKR mice (12%, P ≤ 0.05), and FOR‐induced slow‐to‐fast fibre type shift was not blocked at all in these animals. In MKR mice, FOR also restored the lower levels of muscle SDH activity to basal WT values and caused a marked reduction (57%, P ≤ 0.05) in the number of centrally nucleated fibers. Conclusions NS/IGF1 signalling is necessary for the anti‐proteolytic and hypertrophic effects of in vivo β2‐adrenergic stimulation and appears to mediate FOR‐induced enhancement of protein synthesis. INS/IGF1 signalling only partially contributes to gain in strength and does not mediate fibre type transition induced by FOR

Decreased rate of protein synthesis, caspase-3 activity, and ubiquitin-proteasome proteolysis in soleus muscles from growing rats fed a low-protein, high-carbohydrate diet

The aim of this study was to investigate the changes in the rates of both protein synthesis and breakdown, and the activation of intracellular effectors that control these processes in soleus muscles from growing rats fed a low-protein, high-carbohydrate (LPHC) diet for 15 days. The mass and the protein content, as well as the rate of protein synthesis, were decreased in the soleus from LPHC-fed rats. The availability of amino acids was diminished, since the levels of various essential amino acids were decreased in the plasma of LPHC-fed rats. Overall rate of proteolysis was also decreased, explained by reductions in the mRNA levels of atrogin-1 and MuRF-1, ubiquitin conjugates, proteasome activity, and in the activity of caspase-3. Soleus muscles from LPHC-fed rats showed increased insulin sensitivity, with increased levels of insulin receptor and phosphorylation levels of AKT, which probably explains the inhibition of both the caspase-3 activity and the ubiquitin-proteasome system. The fall of muscle proteolysis seems to represent an adaptive response that contributes to spare proteins in a condition of diminished availability of dietary amino acids. Furthermore, the decreased rate of protein synthesis may be the driving factor to the lower muscle mass gain in growing rats fed the LPHC diet.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES

Dietary Protein Restriction Improves Metabolic Dysfunction in Patients with Metabolic Syndrome in a Randomized, Controlled Trial

Dietary restriction (DR) reduces adiposity and improves metabolism in patients with one or more symptoms of metabolic syndrome. Nonetheless, it remains elusive whether the benefits of DR in humans are mediated by calorie or nutrient restriction. This study was conducted to determine whether isocaloric dietary protein restriction is sufficient to confer the beneficial effects of dietary restriction in patients with metabolic syndrome. We performed a prospective, randomized controlled dietary intervention under constant nutritional and medical supervision. Twenty-one individuals diagnosed with metabolic syndrome were randomly assigned for caloric restriction (CR; n = 11, diet of 5941 ± 686 KJ per day) or isocaloric dietary protein restriction (PR; n = 10, diet of 8409 ± 2360 KJ per day) and followed for 27 days. Like CR, PR promoted weight loss due to a reduction in adiposity, which was associated with reductions in blood glucose, lipid levels, and blood pressure. More strikingly, both CR and PR improved insulin sensitivity by 62.3% and 93.2%, respectively, after treatment. Fecal microbiome diversity was not affected by the interventions. Adipose tissue bulk RNA-Seq data revealed minor changes elicited by the interventions. After PR, terms related to leukocyte proliferation were enriched among the upregulated genes. Protein restriction is sufficient to confer almost the same clinical outcomes as calorie restriction without the need for a reduction in calorie intake. The isocaloric characteristic of the PR intervention makes this approach a more attractive and less drastic dietary strategy in clinical settings and has more significant potential to be used as adjuvant therapy for people with metabolic syndrome

Replacement of the Gamma by the Delta variant in Brazil: Impact of lineage displacement on the ongoing pandemic

The coronavirus disease 2019 (COVID-19) epidemic in Brazil was driven mainly by the spread of Gamma (P.1), a locally emerged variant of concern (VOC) that was first detected in early January 2021. This variant was estimated to be responsible for more than 96_per cent of cases reported between January and June 2021, being associated with increased transmissibility and disease severity, a reduction in neutralization antibodies and effectiveness of treatments or vaccines, and diagnostic detection failure. Here we show that, following several importations predominantly from the USA, the Delta variant rapidly replaced Gamma after July 2021. However, in contrast to what was seen in other countries, the rapid spread of Delta did not lead to a large increase in the number of cases and deaths reported in Brazil. We suggest that this was likely due to the relatively successful early vaccination campaign coupled with natural immunity acquired following prior infection with Gamma. Our data reinforce reports of the increased transmissibility of the Delta variant and, considering the increasing concern due to the recently identified Omicron variant, argues for the necessity to strengthen genomic monitoring on a national level to quickly detect the emergence and spread of other VOCs that might threaten global health

Genomic epidemiology reveals how restriction measures shaped the SARS-CoV-2 epidemic in Brazil

Abstract Brazil has experienced some of the highest numbers of COVID-19 infections and deaths globally and made Latin America a pandemic epicenter from May 2021. Although SARS-CoV-2 established sustained transmission in Brazil early in the pandemic, important gaps remain in our understanding of local virus transmission dynamics. Here, we describe the genomic epidemiology of SARS-CoV-2 using near-full genomes sampled from 27 Brazilian states and an adjacent country - Paraguay. We show that the early stage of the pandemic in Brazil was characterised by the co-circulation of multiple viral lineages, linked to multiple importations predominantly from Europe, and subsequently characterized by large local transmission clusters. As the epidemic progressed, the absence of effective restriction measures led to the local emergence and international spread of Variants of Concern (VOC) and under monitoring (VUM), including the Gamma (P.1) and Zeta (P.2) variants. In addition, we provide a preliminary genomic overview of the epidemic in Paraguay, showing evidence of importation from Brazil. These data reinforce the need for the implementation of widespread genomic surveillance in South America as a toolkit for pandemic monitoring and providing a means to follow the real-time spread of emerging SARS-CoV-2 variants with possible implications for public health and immunization strategies

Field and classroom initiatives for portable sequence-based monitoring of dengue virus in Brazil

This work was supported by Decit, SCTIE, Brazilian Ministry of Health, Conselho Nacional de Desenvolvimento Científico - CNPq (440685/ 2016-8, 440856/2016-7 and 421598/2018-2), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES - (88887.130716/2016-00), European Union’s Horizon 2020 Research and Innovation Programme under ZIKAlliance Grant Agreement (734548), STARBIOS (709517), Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro – FAPERJ (E-26/2002.930/2016), International Development Research Centre (IDRC) Canada (108411-001), European Union’s Horizon 2020 under grant agreements ZIKACTION (734857) and ZIKAPLAN (734548).Fundação Ezequiel Dias. Laboratório Central de Saúde Pública do Estado de Minas Gerais. Belo Horizonte, MG, Brazil / Latin American Genomic Surveillance Arboviral Network.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil / Latin American Genomic Surveillance Arboviral Network.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil Latin American Genomic Surveillance Arboviral Network.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Leônidas e Maria Deane. Laboratório de Ecologia de Doenças Transmissíveis na Amazônia. Manaus, AM, Brazil.Secretaria de Saúde do Estado de Mato Grosso do Sul. Laboratório Central de Saúde Pública. Campo Grande, MS, Brazil.Fundação Ezequiel Dias. Laboratório Central de Saúde Pública do Estado de Minas Gerais. Belo Horizonte, MG, Brazil.Laboratório Central de Saúde Pública Dr. Giovanni Cysneiros. Goiânia, GO, Brazil.Laboratório Central de Saúde Pública Professor Gonçalo Moniz. Salvador, BA, Brazil.Secretaria de Saúde do Estado da Bahia. Salvador, BA, Brazil.Laboratório Central de Saúde Pública Dr. Milton Bezerra Sobral. Recife, PE, Brazil.Laboratório Central de Saúde Pública do Estado de Mato Grosso. Cuiabá, MT, Brazil.Laboratório Central de Saúde Pública do Distrito Federal. Brasília, DF, Brazil.Fundação Ezequiel Dias. Laboratório Central de Saúde Pública do Estado de Minas Gerais. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Coordenação Geral dos Laboratórios de Saúde Pública. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Coordenação Geral dos Laboratórios de Saúde Pública. Brasília, DF, Brazil.Organização Pan-Americana da Saúde / Organização Mundial da Saúde. Brasília, DF, Brazil.Organização Pan-Americana da Saúde / Organização Mundial da Saúde. Brasília, DF, Brazil.Organização Pan-Americana da Saúde / Organização Mundial da Saúde. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde Coordenação Geral das Arboviroses. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde Coordenação Geral das Arboviroses. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde Coordenação Geral das Arboviroses. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde Coordenação Geral das Arboviroses. Brasília, DF, Brazil.Fundação Hemocentro de Ribeirão Preto. Ribeirão Preto, SP, Brazil.Gorgas Memorial Institute for Health Studies. Panama, Panama.Universidade Federal da Bahia. Vitória da Conquista, BA, Brazil.Laboratorio Central de Salud Pública. Asunción, Paraguay.Fundação Oswaldo Cruz. Bio-Manguinhos. Rio de Janeiro, RJ, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Coordenação Geral dos Laboratórios de Saúde Pública. Brasília, DF, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, BrazilFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, BrazilMinistério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Laboratório Central de Saúde Pública do Estado de Mato Grosso do Sul. Campo Grande, MS, Brazil.Laboratório Central de Saúde Pública do Estado de Mato Grosso do Sul. Campo Grande, MS, Brazil.Instituto de Investigaciones en Ciencias de la Salud. San Lorenzo, Paraguay.Secretaria de Estado de Saúde de Mato Grosso do Sul. Campo Grande, MS, Brazil.Fundação Oswaldo Cruz. Campo Grande, MS, Brazil.Fundação Hemocentro de Ribeirão Preto. Ribeirão Preto, SP, Brazil.Laboratório Central de Saúde Pública Dr. Giovanni Cysneiros. Goiânia, GO, Brazil.Laboratório Central de Saúde Pública Dr. Giovanni Cysneiros. Goiânia, GO, Brazil.Laboratório Central de Saúde Pública Professor Gonçalo Moniz. Salvador, BA, Brazil.Laboratório Central de Saúde Pública Dr. Milton Bezerra Sobral. Recife, PE, Brazil.Laboratório Central de Saúde Pública do Distrito Federal. Brasília, DF, Brazil.Secretaria de Saúde de Feira de Santana. Feira de Santana, Ba, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Secretaria de Saúde do Estado de Minas Gerais. Belo Horizonte, MG, Brazil.Hospital das Forças Armadas. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Brasília, DF, Brazil.Universidade Nova de Lisboa. Instituto de Higiene e Medicina Tropical. Lisboa, Portugal.University of Sydney. School of Life and Environmental Sciences and School of Medical Sciences. Marie Bashir Institute for Infectious Diseases and Biosecurity. Sydney, NSW, Australia.University of KwaZulu-Natal. College of Health Sciences. KwaZulu-Natal Research Innovation and Sequencing Platform. Durban, South Africa.University of Oxford. Peter Medawar Building. Department of Zoology. Oxford, UK.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Universidade Estadual de Feira de Santana. Salvador, BA, Brazil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brazil.Universidade de Brasília. Brasília, DF, Brazil.Universidade Salvador. Salvador, BA, Brazil.Fundação Ezequiel Dias. Belo Horizonte, MG, Brazil.Fundação Ezequiel Dias. Belo Horizonte, MG, Brazil.Fundação Ezequiel Dias. Belo Horizonte, MG, Brazil.Fundação Ezequiel Dias. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Flavivírus. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hantaviroses e Rickettsioses. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Leônidas e Maria Deane. Laboratório de Ecologia de Doenças Transmissíveis na Amazônia. Manaus, AM, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Faculdade de Medicina Veterinária. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Faculdade de Medicina Veterinária. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brazil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brazil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brazil.Laboratório Central de Saúde Pública do Estado do Paraná. Curitiba, PR, Brazil.Laboratório Central de Saúde Pública do Estado de Rondônia. Porto Velho, RO, Brazil.Laboratório Central de Saúde Pública do Estado do Amazonas. Manaus, AM, Brazil.Laboratório Central de Saúde Pública do Estado do Rio Grande do Norte. Natal, RN, Brazil.Laboratório Central de Saúde Pública do Estado de Mato Grosso. Cuiabá, MT, Brazil.Laboratório Central de Saúde Pública Professor Gonçalo Moniz. Salvador, BA, Brazil.Laboratório Central de Saúde Pública Professor Gonçalo Moniz. Salvador, BA, Brazil.Laboratório Central de Saúde Pública Noel Nutels. Rio de Janeiro, RJ, Brazil.Instituto Adolfo Lutz. São Paulo, SP, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Universidade de São Paulo. Instituto de Medicina Tropical. São Paulo, SP, Brazil.Universidade de São Paulo. Instituto de Medicina Tropical. São Paulo, SP, Brazil.Universidade de São Paulo. Instituto de Medicina Tropical. São Paulo, SP, Brazil.University of Oxford. Peter Medawar Building. Department of Zoology. Oxford, UK.Instituto Nacional de Enfermedades Virales Humanas Dr. Julio Maiztegui. Pergamino, Argentina.Gorgas Memorial Institute for Health Studies. Panama, Panama.Gorgas Memorial Institute for Health Studies. Panama, Panama.Gorgas Memorial Institute for Health Studies. Panama, Panama.Instituto de Salud Pública de Chile. Santiago, Chile.Instituto de Diagnóstico y Referencia Epidemiológicos Dr. Manuel Martínez Báez. Ciudad de México, México.Instituto Nacional de Enfermedades Infecciosas Dr Carlos G Malbrán. Buenos Aires, Argentina.Ministerio de Salud Pública de Uruguay. Montevideo, Uruguay.Instituto Costarricense de Investigación y Enseñanza em Nutrición y Salud. Tres Ríos, Costa Rica.Instituto Nacional de Investigacion en Salud Publica Dr Leopoldo Izquieta Pérez. Guayaquil, Ecuador.Instituto Nacional de Investigacion en Salud Publica Dr Leopoldo Izquieta Pérez. Guayaquil, Ecuador.Universidade Federal de Pernambuco. Recife, PE, Brazil.Secretaria de Saúde do Estado de Minas Gerais. Belo Horizonte. MG, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Brasília, DF, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Brasília, DF, Brazil.Universidade Federal do Rio de Janeiro. Rio de Janeiro, RJ, Brazil.Universidade Federal do Rio de Janeiro. Rio de Janeiro, RJ, Brazil.Universidade Federal do Rio de Janeiro. Rio de Janeiro, RJ, Brazil.Universidade Federal do Rio de Janeiro. Rio de Janeiro, RJ, Brazil.Universidade Federal de Ouro Preto. Ouro Preto, MG, Brazil.Universidade Federal de Ouro Preto. Ouro Preto, MG, Brazil.Universidade Federal de Ouro Preto. Ouro Preto, MG, Brazil.Universidade Federal de Ouro Preto. Ouro Preto, MG, Brazil.Fundação Hemocentro de Ribeirão Preto. Ribeirão Preto, SP, Brazil.Secretaria de Saúde de Feira de Santana. Feira de Santana, BA, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Belo Horizonte, MG, Brazil.Brazil experienced a large dengue virus (DENV) epidemic in 2019, highlighting a continuous struggle with effective control and public health preparedness. Using Oxford Nanopore sequencing, we led field and classroom initiatives for the monitoring of DENV in Brazil, generating 227 novel genome sequences of DENV1-2 from 85 municipalities (2015–2019). This equated to an over 50% increase in the number of DENV genomes from Brazil available in public databases. Using both phylogenetic and epidemiological models we retrospectively reconstructed the recent transmission history of DENV1-2. Phylogenetic analysis revealed complex patterns of transmission, with both lineage co-circulation and replacement. We identified two lineages within the DENV2 BR-4 clade, for which we estimated the effective reproduction number and pattern of seasonality. Overall, the surveillance outputs and training initiative described here serve as a proof-of-concept for the utility of real-time portable sequencing for research and local capacity building in the genomic surveillance of emerging viruses