AI Article Synopsis

  • Dengue virus is prevalent in Malaysia and G6PD deficiency may lead to more severe cases, prompting a study on the oxidative responses of infected monocytes in these individuals.
  • Monocytes from G6PD-deficient individuals showed higher infection rates and increased oxidative stress when compared to normal controls, along with lower levels of nitric oxide and superoxide anions.
  • These findings suggest that the altered redox state in G6PD-deficient individuals enhances viral replication, potentially leading to higher viral loads and increased transmission risk.

Article Abstract

Background: Dengue 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.

Methodology: Monocytes 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 Findings: Monocytes 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/significance: Altered 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953068PMC
http://dx.doi.org/10.1371/journal.pntd.0002711DOI Listing

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