Abstract
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) |
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Pages (from-to) | 457-462 |
Number of pages | 6 |
Journal | Viral Immunology |
Volume | 22 |
Issue number | 6 |
DOIs | |
State | Published - Dec 1 2009 |
ASJC Scopus subject areas
- Immunology
- Molecular Medicine
- Virology