Attenuated and lethal variants of pichindé virus induce differential patterns of NF-κB activation suggesting a potential target for novel therapeutics

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.