期刊
VIROLOGY
卷 400, 期 2, 页码 224-232出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2010.02.001
关键词
Mixed Lineage Kinase 3; Influenza virus; Viability; JNK; T cell
类别
资金
- NIH [T32 A1007362]
- [RO1 HL75432]
- [HL088325]
- [RO1 HL083761]
- [NS054578]
- [MH64570]
- [HHSN266200700008C]
Influenza virus leads to acute respiratory disease resulting in seasonal epidemics and periodic pandemics. Little is known about the signaling events that regulate host defense to influenza. One particular pathway, the c-Jun amino-terminal kinase (JNK) cascade is activated following influenza infection and blocking JNK leads to enhanced viral replication. We hypothesize that Mixed Lineage Kinase 3 (MLK3), an upstream regulator of JNK, is involved in the host response to influenza. To test this, wild-type and MLK3-/- mice were infected with pathogenic strain of influenza A virus, A/PR/8/34 (PR8). Although, cellular and humoral immune responses were similar between wild-type and MIX3-/- hosts, the viral load in the lungs was comparatively higher in MLK3-/- mice at day 8 post-infection. Consistent with this, MLK3-/- murine lung fibroblast and epithelial cells had prolonged survival and increased virion production following infection compared to wild-type. These findings support a role for MLK3 in viral production during influenza infection. (C) 2010 Elsevier Inc. All rights reserved.
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