Article ID: JJID.2016.236
Encephalitis has been reported worldwide as a severe complication in patients infected by dengue virus. Reactive oxygen species (ROS) production is a key mechanism involved in the neuronal damage caused by viral encephalitis. Here the capability of the dengue virus serotypes 2 and 4 (DV2 and DV4) to induce ROS production was investigated in a rat microglia cell line, HAPI cells. The cells were infected with DV2 and DV4 at a MOI of 0.1 for a 2-h adsorption period. Japanese encephalitis virus (JEV) was used as the reference. DV2- and DV4-induced microglia activation and significantly increased ROS production corresponded to decreased cell viability. The activity of DV4 was significantly higher than the activities of DV2 and JEV at 48 and 72 h post infection. DV4 partly induced ROS production via an iron-induced Fenton reaction, as demonstrated by the treatment of an iron chelator, deferiprone. Despite the induction of increased iNOS expression and NO production by JEV, DV2 and DV4 did not induce NO production, suggesting the activation of different pathways in response to infections by different viruses. In conclusion, DV2 and DV4 have the capability to induce ROS production and activate microglia, which have been reported as the key components for neuronal damage.
