Abstract
BackgroundDengue virus is endemic in peninsular Malaysia. The clinical manifestations vary depending on the incubation period of the virus as well as the immunity of the patients. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is prevalent in Malaysia where the incidence is 3.2%. It has been noted that some G6PD-deficient individuals suffer from more severe clinical presentation of dengue infection. In this study, we aim to investigate the oxidative responses of DENV2-infected monocytes from G6PD-deficient individuals.MethodologyMonocytes from G6PD-deficient individuals were infected with DENV2 and infection rate, levels of oxidative species, nitric oxide (NO), superoxide anions (O2 −), and oxidative stress were determined and compared with normal controls.Principal FindingsMonocytes from G6PD-deficient individuals exhibited significantly higher infection rates compared to normal controls. In an effort to explain the reason for this enhanced susceptibility, we investigated the production of NO and O2 − in the monocytes of individuals with G6PD deficiency compared with normal controls. We found that levels of NO and O2 − were significantly lower in the DENV-infected monocytes from G6PD-deficient individuals compared with normal controls. Furthermore, the overall oxidative stress in DENV-infected monocytes from G6PD-deficient individuals was significantly higher when compared to normal controls. Correlation studies between DENV-infected cells and oxidative state of monocytes further confirmed these findings.Conclusions/SignificanceAltered redox state of DENV-infected monocytes from G6PD-deficient individuals appears to augment viral replication in these cells. DENV-infected G6PD-deficient individuals may contain higher viral titers, which may be significant in enhanced virus transmission. Furthermore, granulocyte dysfunction and higher viral loads in G6PD-deificient individuals may result in severe form of dengue infection.
Highlights
Dengue infection is among the leading causes of morbidity and mortality in the tropics and subtropics where as many as 100 million people are infected with 22,000 deaths yearly [1]
In an effort to explain the reason for this enhanced susceptibility, we investigated the production of nitric oxide (NO) and O22 in the monocytes of individuals with Glucose-6-phosphate dehydrogenase (G6PD) deficiency compared with normal controls
We found that levels of NO and O22 were significantly lower in the dengue virus (DENV)-infected monocytes from G6PD-deficient individuals compared with normal controls
Summary
Dengue infection is among the leading causes of morbidity and mortality in the tropics and subtropics where as many as 100 million people are infected with 22,000 deaths yearly [1]. Dengue infection is caused by dengue virus (DENV), an RNA virus of the family Flaviviridae. There are four serotypes of the virus which are referred to as DENV1, DENV2, DENV3 and DENV4. All four serotypes can cause the full spectrum of disease [2]. DENV is primarily transmitted to humans by the bite of infected Aedes mosquitoes, Aedes aegypti. DENV can be transmitted via infected blood products and through organ transplantation [4,5]. Dengue virus is endemic in peninsular Malaysia. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is prevalent in Malaysia where the incidence is 3.2%. It has been noted that some G6PD-deficient individuals suffer from more severe clinical presentation of dengue infection. We aim to investigate the oxidative responses of DENV2infected monocytes from G6PD-deficient individuals
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