Lindemann Björn F, Klug Christian, Schwienhorst Andreas
Department of Biochemical Kinetics, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.
J Virol. 2002 Jun;76(11):5784-92. doi: 10.1128/jvi.76.11.5784-5792.2002.
The emergence of viral escape mutants is usually a highly undesirable phenomenon. This phenomenon is frequently observed in antiviral drug applications for the treatment of viral infections and can undermine long-term therapeutic success. Here, we propose a strategy for evaluating a given antiviral approach in terms of its potential to provoke the appearance of resistant virus mutants. By use of Q beta RNA phage as a model system, the effect of an antiviral gene therapy, i.e., a virus-specific repressor protein expressed by a recombinant Escherichia coli host, was studied over the course of more than 100 generations. In 13 experiments carried out in parallel, 12 phage populations became resistant and 1 became extinct. Sequence analysis revealed that only two distinct phage mutants emerged in the 12 surviving phage populations. For both escape mutants, sequence variations located in the repressor binding site of the viral genomic RNA, which decrease affinity for the repressor protein, conferred resistance to translational repression. The results clearly suggest the feasibility of the proposed strategy for the evaluation of antiviral approaches in terms of their potential to allow resistant mutants to appear. In addition, the strategy proved to be a valuable tool for observing virus-specific molecular targets under the impact of antiviral drugs.
病毒逃逸突变体的出现通常是一种极不受欢迎的现象。这种现象在用于治疗病毒感染的抗病毒药物应用中经常观察到,并且可能破坏长期治疗效果。在此,我们提出一种策略,用于根据给定抗病毒方法引发抗性病毒突变体出现的可能性来评估该方法。通过使用Qβ RNA噬菌体作为模型系统,在超过100代的过程中研究了抗病毒基因疗法的效果,即由重组大肠杆菌宿主表达的病毒特异性阻遏蛋白的效果。在并行进行的13个实验中,12个噬菌体群体产生了抗性,1个群体灭绝。序列分析表明,在12个存活的噬菌体群体中仅出现了两种不同的噬菌体突变体。对于这两种逃逸突变体,位于病毒基因组RNA阻遏蛋白结合位点的序列变异降低了对阻遏蛋白的亲和力,从而赋予了对翻译抑制的抗性。结果清楚地表明了所提出的策略在根据抗病毒方法允许抗性突变体出现的可能性来评估抗病毒方法方面的可行性。此外,该策略被证明是观察抗病毒药物影响下病毒特异性分子靶点的有价值工具。