RT Journal Article
SR Electronic
T1 Dengue virus infection induces inflammation and oxidative stress on the heart
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 388
OP 396
DO 10.1136/heartjnl-2020-318912
VO 108
IS 5
A1 Lucas Miranda Kangussu
A1 Vivian Vasconcelos Costa
A1 Vania Claudia Olivon
A1 Celso Martins Queiroz-Junior
A1 Antônio Nei Santana Gondim
A1 Marcos Barrouin Melo
A1 Daniela Reis
A1 Natália Nóbrega
A1 Natália Araújo
A1 Milene Alvarenga Rachid
A1 Renan Pedra de Souza
A1 Carlos Renato Tirapelli
A1 Robson Augusto Souza dos Santos
A1 Jader dos Santos Cruz
A1 Mauro Martins Teixeira
A1 Danielle da Glória de Souza
A1 Daniella Bonaventura
YR 2022
UL http://heart.bmj.com/content/108/5/388.abstract
AB Objective Dengue fever is one of the most important arboviral diseases in the world, and its severe forms are characterised by a broad spectrum of systemic and cardiovascular hallmarks. However, much remains to be elucidated regarding the pathogenesis triggered by Dengue virus (DENV) in the heart. Herein, we evaluated the cardiac outcomes unleashed by DENV infection and the possible mechanisms associated with these effects.Methods A model of an adapted DENV-3 strain was used to infect male BALB/c mice to assess haemodynamic measurements and the functional, electrophysiological, inflammatory and oxidative parameters in the heart.Results DENV-3 infection resulted in increased systemic inflammation and vascular permeability with consequent reduction of systolic blood pressure and increase in heart rate. These changes were accompanied by a decrease in the cardiac output and stroke volume, with a reduction trend in the left ventricular end-systolic and end-diastolic diameters and volumes. Also, there was a reduction trend in the calcium current density in the ventricular cardiomyocytes of DENV-3 infected mice. Indeed, DENV-3 infection led to leucocyte infiltration and production of inflammatory mediators in the heart, causing pericarditis and myocarditis. Moreover, increased reactive oxygen species generation and lipoperoxidation were also verified in the cardiac tissue of DENV-3 infected mice.Conclusions DENV-3 infection induced a marked cardiac dysfunction, which may be associated with inflammation, oxidative stress and electrophysiological changes in the heart. These findings provide new cardiac insights into the mechanisms involved in the pathogenesis triggered by DENV, contributing to the research of new therapeutic targets for clinical practice.All data relevant to the study are included in the article or uploaded as supplementary information.