A Japanese encephalitis virus biological clone with an gene point mutation exhibits and attenuation of neurovirulence.

The Japanese encephalitis virus (JEV), a leading cause of viral encephalitis, exists as similar but non-identical biological clones whose genomic variations/mutations may determine neurovirulence. Two biological clones purified from a brain-derived, clinical isolate were tested for neurovirulence using human neuronal cells (SK-N-MC) and mouse neuronal cells (NIE-115) and on a footpad-inoculation mouse model. One clone (JEV-M) demonstrated significantly reduced infectivity in both neuronal cells and the mouse model compared to another clone (JEV-V).

Neuronal transcriptomic responses to Japanese encephalitis virus infection with a special focus on chemokine CXCL11 and pattern recognition receptors RIG-1 and MDA5.

Japanese encephalitis virus (JEV) causes central nervous system neuronal injury and inflammation. A clear understanding of neuronal responses to JEV infection remains elusive. Using the Affymetrix array to investigate the transcriptome of infected SK-N-MC cells, 1316 and 2737 dysregulated genes (≥ 2/-2 fold change, P < 0.

[Effects of typical organic pollutants on marine dioxide carbon system in simulated experiments].

The effects of typical organic pollutants (ethanol, acetone, ON, OP) on pH and marine carbon dioxide system were investigated in laboratory simulated experiments. The results indicated that the growth of biological carbon fixed system was promoted by ethanol and acetone of low concentration (< 0.5 mmol x L(-1)) (t = 7 d).