Nuss Jonathan E, Kehn-Hall Kylene, Benedict Ashwini, Costantino Julie, Ward Michael, Peyser Brian D, Retterer Cary J, Tressler Lyal E, Wanner Laura M, McGovern Hugh F, Zaidi Anum, Anthony Scott M, Kota Krishna P, Bavari Sina, Hakami Ramin M
US Army Medical Research Institute of Infectious Diseases, Frederick, Maryland, United States of America.
School of Systems Biology, and National Center for Biodefense & Infectious Diseases, George Mason University, Manassas, Virginia, United States of America.
PLoS One. 2014 May 8;9(5):e93483. doi: 10.1371/journal.pone.0093483. eCollection 2014.
Rift Valley fever is a potentially fatal disease of humans and domestic animals caused by Rift Valley fever virus (RVFV). Infection with RVFV in ruminants can cause near 100% abortion rates and recent outbreaks in naïve human populations have suggested case fatality rates of greater than thirty percent. To elucidate the roles that host proteins play during RVFV infection, proteomic analysis of RVFV virions was conducted using complementary analytical approaches, followed by functional validation studies of select identified host factors. Coupling the more traditional Gel LC/MS/MS approach (SDS PAGE followed by liquid chromatography tandem mass spectrometry) with an alternative technique that preserves protein complexes allowed the protein complement of these viral particles to be thoroughly examined. In addition to viral proteins present within the virions and virion-associated host proteins, multiple macromolecular complexes were identified. Bioinformatic analysis showed that host chaperones were among over-represented protein families associated with virions, and functional experiments using siRNA gene silencing and small molecule inhibitors identified several of these heat shock proteins, including heat shock protein 90 (HSP90), as important viral host factors. Further analysis indicated that HSP inhibition effects occur during the replication/transcription phase of the virus life cycle, leading to significant lowering of viral titers without compromising the functional capacity of released virions. Overall, these studies provide much needed further insight into interactions between RVFV and host cells, increasing our understanding of the infection process and suggesting novel strategies for anti-viral development. In particular, considering that several HSP90 inhibitors have been advancing through clinical trials for cancer treatment, these results also highlight the exciting potential of repurposing HSP90 inhibitors to treat RVF.
裂谷热是一种由裂谷热病毒(RVFV)引起的、对人类和家畜具有潜在致命性的疾病。反刍动物感染RVFV可导致近100%的流产率,并且最近在未接触过该病毒的人群中爆发的疫情显示病死率超过30%。为了阐明宿主蛋白在RVFV感染过程中所起的作用,采用互补分析方法对RVFV病毒粒子进行了蛋白质组学分析,随后对选定的已鉴定宿主因子进行了功能验证研究。将更传统的凝胶液相色谱串联质谱法(SDS-PAGE后接液相色谱串联质谱)与一种能够保留蛋白质复合物的替代技术相结合,使得能够对这些病毒颗粒的蛋白质组成进行全面检查。除了病毒粒子中存在的病毒蛋白和与病毒粒子相关的宿主蛋白外,还鉴定出了多个大分子复合物。生物信息学分析表明,宿主伴侣蛋白属于与病毒粒子相关的过度表达的蛋白质家族,并且使用siRNA基因沉默和小分子抑制剂进行的功能实验确定了其中几种热休克蛋白,包括热休克蛋白90(HSP90),是重要的病毒宿主因子。进一步分析表明,HSP抑制作用发生在病毒生命周期的复制/转录阶段,导致病毒滴度显著降低,而不会损害释放的病毒粒子的功能能力。总体而言,这些研究为深入了解RVFV与宿主细胞之间的相互作用提供了急需的进一步见解,增进了我们对感染过程的理解,并为抗病毒药物开发提出了新策略。特别是,鉴于几种HSP90抑制剂已在癌症治疗的临床试验中取得进展,这些结果还凸显了重新利用HSP90抑制剂治疗裂谷热的令人兴奋的潜力。