The Gladstone Institutes, San Francisco, California, USA.
J Virol. 2013 Feb;87(4):2081-93. doi: 10.1128/JVI.02741-12. Epub 2012 Dec 5.
Defective interfering particles (DIPs) are viral deletion mutants lacking essential transacting or packaging elements and must be complemented by wild-type virus to propagate. DIPs transmit through human populations, replicating at the expense of the wild-type virus and acting as molecular parasites of viruses. Consequently, engineered DIPs have been proposed as therapies for a number of diseases, including human immunodeficiency virus (HIV). However, it is not clear if DIP-based therapies would face evolutionary blocks given the high mutation rates and high within-host diversity of lentiviruses. Divergent evolution of HIV and DIPs appears likely since natural DIPs have not been detected for lentiviruses, despite extensive sequencing of HIVs and simian immunodeficiency viruses (SIVs). Here, we tested if the apparent lack of lentiviral DIPs is due to natural selection and analyzed which molecular characteristics a DIP or DIP-based therapy would need to maintain coadaptive stability with HIV-1. Using a well-established mathematical model of HIV-1 in a host extended to include its replication in a single cell and interference from DIP, we calculated evolutionary selection coefficients. The analysis predicts that interference by codimerization between DIPs and HIV-1 genomes is evolutionarily unstable, indicating that recombination between DIPs and HIV-1 would be selected against. In contrast, DIPs that interfere via competition for capsids have the potential to be evolutionarily stable if the capsid-to-genome production ratio of HIV-1 is >1. Thus, HIV-1 variants that attempt to "starve" DIPs to escape interference would be selected against. In summary, the analysis suggests specific experimental measurements that could address the apparent lack of naturally occurring lentiviral DIPs and specifies how therapeutic approaches based on engineered DIPs could be evolutionarily robust and avoid recombination.
缺陷干扰颗粒(DIPs)是缺乏必需的反式作用或包装元件的病毒缺失突变体,必须通过野生型病毒来补充才能繁殖。DIPs 通过人群传播,以牺牲野生型病毒为代价进行复制,并作为病毒的分子寄生虫。因此,工程 DIP 已被提议作为许多疾病的治疗方法,包括人类免疫缺陷病毒(HIV)。然而,鉴于慢病毒的高突变率和宿主内多样性,基于 DIP 的治疗方法是否会面临进化障碍尚不清楚。HIV 和 DIP 的分歧进化似乎是可能的,因为尽管对 HIV 和猴免疫缺陷病毒(SIV)进行了广泛的测序,但尚未检测到慢病毒的天然 DIP。在这里,我们测试了慢病毒 DIP 的明显缺乏是否是由于自然选择,并分析了 DIP 或基于 DIP 的治疗方法需要保持与 HIV-1 共适应稳定性所需的分子特征。我们使用一种已建立的 HIV-1 宿主的数学模型,该模型扩展到包括其在单个细胞中的复制和 DIP 的干扰,计算了进化选择系数。分析预测,DIP 与 HIV-1 基因组之间的二聚化干扰在进化上是不稳定的,这表明 DIP 与 HIV-1 之间的重组将受到选择的抵制。相比之下,如果 HIV-1 的衣壳到基因组产生比大于 1,则通过竞争衣壳干扰的 DIP 具有进化稳定的潜力。因此,试图通过“饥饿”DIP 来逃避干扰的 HIV-1 变体将受到选择的抵制。总之,该分析提出了具体的实验测量方法,可以解决自然发生的慢病毒 DIP 明显缺乏的问题,并指定了基于工程 DIP 的治疗方法如何在进化上具有稳健性并避免重组。