Abstract
BackgroundJapanese encephalitis (JE) is one of the leading causes of acute encephalopathy with the highest mortality rate of 30-50%. The purpose of this study was to understand complex biological processes of host response during the progression of the disease. Virus was subcutaneously administered in mice and brain was used for whole genome expression profiling by cDNA microarray.ResultsThe comparison between viral replication efficiency and disease progression confirms the active role of host response in immunopathology and disease severity. The histopathological analysis confirms the severe damage in the brain in a time dependent manner. Interestingly, the transcription profile reveals significant and differential expression of various pattern recognition receptors, chemotactic genes and the activation of inflammasome. The increased leukocyte infiltration and aggravated CNS inflammation may be the cause of disease severity.ConclusionThis is the first report that provides a detailed picture of the host transcriptional response in a natural route of exposure and opens up new avenues for potential therapeutic and prophylactic strategies against Japanese encephalitis virus.
Highlights
Japanese encephalitis (JE) is one of the leading causes of acute encephalopathy with the highest mortality rate of 30-50%
The viral load remained constant until death at 6 day post-infection (DPI)
The major set of genes/pathways with increased expression observed in present study with JEV are similar to those reported for other neuroinvasive viruses like West Nile virus (WNV). These results suggest that some pathways are commonly activated during neurotropic viral infection of the CNS, and the gene products like Ifn-g, Cxcl10/IP-10 etc. involved in protective roles at early phase of infection may contribute to the pathogenesis of the disease at later stage [2,12]
Summary
Japanese encephalitis (JE) is one of the leading causes of acute encephalopathy with the highest mortality rate of 30-50%. Infection of host with a viral pathogen marks the onset of changes in the host cell’s microenvironment. Such changes in host gene expression could be a cellular antivirus response, a virus induced response that facilitate its own replication and spread or a non-specific response that neither promotes nor prevents virus infection. This alteration of expression of many cellular genes can be identified using cDNA microarray [1]. Viruses from several families can infect neurons in the CNS (Central Nervous System) and the study of gene expression changes in the CNS during virus infection can lead to identification of new genes
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