Role of Oxidative and Nitrosative Stress in Dengue Pathogenesis: A Mini-ReviewRaimundo Castro-Orozco1* and Nelson Rafael Alvis-Guzmán2
- *Corresponding Author:
- Raimundo Castro-Orozco
University of San Buenaventura
University of Cartagena
E-mail: [email protected]
Received Date: August 26, 2016; Accepted Date: October 15, 2016; Published Date: October 18, 2016
Citation: Castro-Orozco R, Alvis-Guzmán NR (2016) Role of Oxidative and Nitrosative Stress in Dengue Pathogenesis: A Mini-Review. J Mol Genet Med 10:229 doi: 10.4172/1747-0862.1000229
Copyright: © 2016 Castro-Orozco R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Dengue is a mosquito–borne acute viral disease with ubiquitous distribution in tropical and subtropical areas of the world. Dengue virus (DENV) infection is transmitted by the bite of a female Aedes aegypti mosquito (the most important vector) infected with DENV. Clinical presentation of this typical arboviral disease varies along a wide spectrum of clinical symptoms. During the course of DENV infection, some individuals develop severe manifestations relates to plasma leakage into tissues caused by increased vascular permeability. The severity of dengue disease may vary considerably according to age, ethnicity, genetic factors, immune status and underlying disease. It may also depend on the co-circulation of DENV serotypes and sequential (secondary) infections with different DENV serotypes. While the exact mechanism of pathogenesis of dengue remains elusive, several lines of evidence demonstrating that DENV infection-derived oxidative stress may trigger the release of proinflammatory cytokines, including TNF-alpha, participating in collective action in dengue disease pathogenesis. In conclusion, we review these findings and discuss about the recent advances that propose a major role of oxidative-nitrosative stress on dengue pathogenesis.