Moderator of 1 Session
Presenter of 1 Presentation
MOLECULAR MECHANISM OF INNATE IMMUNE RESPONSE DURING JAPANESE ENCEPHALITIS VIRUS INFECTION
Abstract
Background
Japanese encephalitis (JE) is an arboviral disease which accounts for significant pediatric mortality annually in Asia and Australia, including India. Encephalitis is merely the result of viral invasion in CNS and pathological consequences. Neuronal loss is the outcome of both JEV infection of neurons and bystander damage caused by activated microglia. Recent studies have shown that micro RNAs (miRs) holds a major platform during JEV infection and modulate cellular pathways to determine the pathological condition.
Aims
Therefore, the present study was planned to characterize the NS3 gene of JEV GP05 and investigate the role of miRs in controlling the IL-10 expression (Th2 response) during JEV infection in macrophages.
Methods
See Methods in following Figure 1
Results
We report that miR-98, miR-27a and miR-106b might have a possible role in posttranscriptional regulation of IL-10 gene expression during JEV infection. Our analysis predicted the novel miRs having potential to bind with the 3’UTR region of IL-10 mRNA. From the predicted miRs, miR-98 and miR-27a were selected on the basis of published article showing their role in regulation of IL-10 expression. Novel microRNA miR-106b was selected on the basis of free energy and prediction from the software. Gel PCR, real time PCR (RT-PCR) and western blotting was performed to validate the data. Our results exhibited the correlation between the expression of IL-10 and three miRNAs mainly miR-98, miR-27a miR-106b during JEV infection.
Conclusions
Collectively our data suggested that miR-98, miR-27a and miR-106b might have potential role in posttranscriptional regulation of Interleukin-10 expression during Japanese encephalitis virus infection.