Reynard Stéphanie, Russier Marion, Fizet Alexandra, Carnec Xavier, Baize Sylvain
Unité de Biologie des Infections Virales Emergentes, Institut Pasteur, Lyon, France; Centre International de Recherche en Infectiologie (CIRI), Université de Lyon, INSERM U1111, Ecole Normale Supérieure de Lyon, Université Lyon 1, CNRS UMR5308, Lyon, France.
Unité de Biologie des Infections Virales Emergentes, Institut Pasteur, Lyon, France; Centre International de Recherche en Infectiologie (CIRI), Université de Lyon, INSERM U1111, Ecole Normale Supérieure de Lyon, Université Lyon 1, CNRS UMR5308, Lyon, France
J Virol. 2014 Dec;88(23):13923-7. doi: 10.1128/JVI.01923-14. Epub 2014 Sep 24.
Lassa virus (LASV), which causes a viral hemorrhagic fever, inhibits the innate immune response. The exonuclease (ExoN) domain of its nucleoprotein (NP) is implicated in the suppression of retinoic acid-inducible gene I (RIG-I) signaling. We show here that a LASV in which ExoN function has been abolished strongly activates innate immunity and that this effect is dependent on RIG-I signaling. These results highlight the key role of NP ExoN function in the immune evasion that occurs during LASV infection.
引起病毒性出血热的拉沙病毒(LASV)会抑制先天性免疫反应。其核蛋白(NP)的核酸外切酶(ExoN)结构域与维甲酸诱导基因I(RIG-I)信号传导的抑制有关。我们在此表明,ExoN功能已被消除的LASV会强烈激活先天性免疫,且这种效应依赖于RIG-I信号传导。这些结果突出了NP ExoN功能在LASV感染期间发生的免疫逃避中的关键作用。