Comparison of a human neuronal model proteome upon Japanese encephalitis or West Nile Virus infection and potential role of mosquito saliva in neuropathogenesis.
Benoit BessonJustine BassetSandrine GatellierHélène ChabrollesThibault ChazeVéronique HourdelMariette MatondoNathalie PardigonValérie ChoumetPublished in: PloS one (2020)
Neurotropic flavivirus Japanese encephalitis virus (JEV) and West Nile virus (WNV) are amongst the leading causes of encephalitis. Using label-free quantitative proteomics, we identified proteins differentially expressed upon JEV (gp-3, RP9) or WNV (IS98) infection of human neuroblastoma cells. Data are available via ProteomeXchange with identifier PXD016805. Both viruses were associated with the up-regulation of immune response (IFIT1/3/5, ISG15, OAS, STAT1, IRF9) and the down-regulation of SSBP2 and PAM, involved in gene expression and in neuropeptide amidation respectively. Proteins associated to membranes, involved in extracellular matrix organization and collagen metabolism represented major clusters down-regulated by JEV and WNV. Moreover, transcription regulation and mRNA processing clusters were also heavily regulated by both viruses. The proteome of neuroblastoma cells infected by JEV or WNV was significantly modulated in the presence of mosquito saliva, but distinct patterns were associated to each virus. Mosquito saliva favored modulation of proteins associated with gene regulation in JEV infected neuroblastoma cells while modulation of proteins associated with protein maturation, signal transduction and ion transporters was found in WNV infected neuroblastoma cells.
Keyphrases
- induced apoptosis
- gene expression
- cell cycle arrest
- immune response
- extracellular matrix
- label free
- endoplasmic reticulum stress
- cell death
- dna methylation
- mass spectrometry
- oxidative stress
- transcription factor
- signaling pathway
- machine learning
- pi k akt
- aedes aegypti
- inflammatory response
- toll like receptor
- high resolution
- induced pluripotent stem cells
- blood brain barrier
- amino acid
- subarachnoid hemorrhage