The role of oxidative stress in the pathogenesis of dengue infection is not completely known. A recent study reveals the involvement of oxidative stress responsive molecules in the generation of host immune responses to dengue virus in vitro. Objective of the present study was to analyse the changes in the expression of oxidant-antioxidant genes Nox-2 (NADPH oxidase) and Nrf2 (nuclear factor-erythroid 2-related factor 2) in patients with dengue during the early phase of infection compared to other febrile illness (OFI) cases and healthy controls using Real-time qPCR assay. The study enrolled 88 dengue patients, 31 OFI cases, and 63 healthy individuals as controls. Out of 88 dengue cases, 32 were classified as severe dengue cases (SD) and remaining 56 patients as non-severe dengue (NSD). Blood samples were collected firstly at the time of admission and a second sampling was done from the available individuals (38 dengue and 13 OFI cases) at the time of defervescence. Total RNA was extracted from the Peripheral blood mononuclear cells and the transcripts level of Nox-2 and Nrf2 were analysed by qPCR. On DOA, both Nox-2 and Nrf2 expression was found to be down regulated in dengue and OFI cases (P \ 0.05) compared to healthy controls. Interestingly at defervescence, the transcript levels were found to be significantly increased in dengue cases unlike OFI, where no such increment was evidenced. From DOA to DOD, the study observed a signficant increase in the levels of Nox-2 transcripts (P \ 0.05) both in SD and NSD cases. But a significant Nrf2 activation was not observed in SD cases as we found in NSD cases. Thus a steady and significant increase in Nox-2 transcript level in severe, non-severe and secondary dengue infected groups observed in the current study supports the earlier reports on the involvement of anti-oxidant response in dengue severity. However further studies on its protein levels and mechanistic action would decipher the exact role of these potential molecules in the disease virulence.

Dengue is an arthropod-borne threat among tropical countries. Currently no effective means to treat the virus or to predict which patient will develop the severe form of the disease. Recently the relationship between oxidative/antioxidative response and dengue pathogenesis was suggested. Based on this the present study has analysed the expression of endogenous antioxidant genes: Catalase (CAT), Superoxide dismutase (MnSOD) and Glutathione peroxidase in patients with dengue compared to other febrile illness (OFI) and healthy controls. The study enrolled 88 dengue confirmed patients comprising 56 were patients with non-severe dengue, and 32 were severe dengue cases, 31 were patients with OFI, and 63 healthy controls were also involved. Peripheral blood mononuclear cells isolated from patients and controls during the day of admission and from the available cases on the day of defervescence were used to estimate the transcript levels by quantitative PCR. The expression levels of all the three genes were found to be down-regulated throughout the course of dengue infection ( < 0.05) and OFI cases compared to healthy controls. Within dengue group, no significant difference was observed in any of the parameters between severe and non-severe cases. Interestingly, a significant down-regulation of MnSOD expression was recorded in secondary dengue infection compared to primary during admission ( < 0.05). It was found that all the down-regulated study genes have positively correlated in all dengue cases during the day of admission ( < 0.01). But during defervescence, the same was found only between CAT and MnSOD. Down-regulated endogenous antioxidant enzymes during dengue infection could be the possible rationale of oxidative stress reported in dengue disease earlier. The present study markers could not distinguish dengue from OFI cases and severe from non-severe dengue cases. Mechanism of down-regulation has to be explored further which will pave the way for the therapeutic target in dengue disease.