Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch, Galveston, Texas 77555-0609, USA.
Viral Immunol. 2009 Dec;22(6):457-62. doi: 10.1089/vim.2009.0034.
Lassa virus pathogenesis is believed to involve dysregulation of cytokines. We have previously shown nuclear factor-kappaB (NF-kappaB) inhibition using a BSL-2 model for Lassa fever. Here we further define the potential mechanism for NF-kappaB inhibition as involving increased levels of repressive p50/p50 homodimers, and suggest a novel therapeutic strategy that acts via modulation of host signaling.
拉沙病毒发病机制被认为涉及细胞因子失调。我们之前已经在拉沙热的 BSL-2 模型中展示了使用核因子-κB(NF-κB)抑制剂。在这里,我们进一步定义了 NF-κB 抑制的潜在机制,涉及增加抑制性 p50/p50 同源二聚体的水平,并提出了一种通过调节宿主信号转导发挥作用的新型治疗策略。