期刊
JOURNAL OF VIROLOGY
卷 81, 期 13, 页码 6984-6992出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00467-07
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资金
- NIAID NIH HHS [T32 AI007537, T32AI07537, K08 AI076518] Funding Source: Medline
- NINDS NIH HHS [R01 NS051403-03, 5R01NS050138, R01 NS050138-04, R01 NS050138, R01 NS051403, 1R01NS051403] Funding Source: Medline
Viral encephalitis is a major cause of morbidity and mortality worldwide, yet there is no proven efficacious therapy for most viral infections of the central nervous system (CNS). Many of the viruses that cause encephalitis induce apoptosis and activate c-Jun N-terminal kinase (JNK) following infection. We have previously shown that reovirus infection of epithelial cell lines activates JNK-dependent apoptosis. We now show that reovirus infection resulted in activation of JNK and caspase-3 in the CNS. Treatment of reovinis-infected mice with a cell-permeating peptide that competitively inhibits JNK activity resulted in significantly prolonged survival of intracerebrally infected mice following an otherwise lethal challenge with T3D (100 X 501% lethal dose). Protection correlated with reduced CNS injury, reduced neuronal apoptosis, and reduced c-Jun activation without altering the viral titer or viral antigen distribution. Given the efficacy of the inhibitor in protecting mice from viral encephalitis, JNK inhibition represents a promising and novel treatment strategy for viral encephalitis.
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