Research ArticleViral Infection

Quantitative phosphoproteomic analysis identifies the critical role of JNK1 in neuroinflammation induced by Japanese encephalitis virus

See allHide authors and affiliations

Science Signaling  04 Oct 2016:
Vol. 9, Issue 448, pp. ra98
DOI: 10.1126/scisignal.aaf5132

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Halting viral encephalitis

Japanese encephalitis virus (JEV) is a member of the mosquito-borne flavivirus family, which includes hepatitis C virus, West Nile virus, yellow fever virus, Zika virus, and dengue virus. Common in Asia and Australia, JEV crosses the blood-brain barrier and produces massive neuroinflammation, which causes neuronal damage and death, such that even people who survive the infection have long-term neurological impairment. Ye et al. took a phosphoproteomic approach and identified several kinase pathways induced by JEV infection of cultured human glial cells. Substrates of the JNK pathway were the most overrepresented in the data set, and treating glial cells in culture with a JNK inhibitor reduced the JEV infection–induced stimulation of inflammatory cytokines. This same inhibitor prevented JEV lethality in mice, which was associated with a decrease in neuroinflammation (reduced astrocytosis and microgliosis), as well as less neuronal injury (reduced apoptotic neurons). These results may prove useful in treating JEV and other neurotropic viruses of this or other viral families.

View Full Text

Stay Connected to Science Signaling