Lassa virus pathogenesis is believed to involve dysregulation of cytokines. We have previously shown nuclear factor-κB (NF-κB) inhibition using a BSL-2 model for Lassa fever. Here we further define the potential mechanism for NF-κB inhibition as involving increased levels of repressive p50/p50 homodimers, and suggest a novel therapeutic strategy that acts via modulation of host signaling.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Dec 1 2009|
ASJC Scopus subject areas
- Molecular Medicine