Department of Chemistry, New York University, New York, New York 10003, United States.
Department of Microbiology and Immunology, Loyola University Chicago Medical Center, Maywood, Illinois 60130, United States.
ACS Infect Dis. 2023 Aug 11;9(8):1508-1522. doi: 10.1021/acsinfecdis.3c00063. Epub 2023 Aug 2.
The development of durable new antiviral therapies is challenging, as viruses can evolve rapidly to establish resistance and attenuate therapeutic efficacy. New compounds that selectively target conserved viral features are attractive therapeutic candidates, particularly for combating newly emergent viral threats. The innate immune system features a sustained capability to combat pathogens through production of antimicrobial peptides (AMPs); however, these AMPs have shortcomings that can preclude clinical use. The essential functional features of AMPs have been recapitulated by peptidomimetic oligomers, yielding effective antibacterial and antifungal agents. Here, we show that a family of AMP mimetics, called peptoids, exhibit direct antiviral activity against an array of enveloped viruses, including the key human pathogens Zika, Rift Valley fever, and chikungunya viruses. These data suggest that the activities of peptoids include engagement and disruption of viral membrane constituents. To investigate how these peptoids target lipid membranes, we used liposome leakage assays to measure membrane disruption. We found that liposomes containing phosphatidylserine (PS) were markedly sensitive to peptoid treatment; in contrast, liposomes formed exclusively with phosphatidylcholine (PC) showed no sensitivity. In addition, chikungunya virus containing elevated envelope PS was more susceptible to peptoid-mediated inactivation. These results indicate that peptoids mimicking the physicochemical characteristics of AMPs act through a membrane-specific mechanism, most likely through preferential interactions with PS. We provide the first evidence for the engagement of distinct viral envelope lipid constituents, establishing an avenue for specificity that may enable the development of a new family of therapeutics capable of averting the rapid development of resistance.
开发耐用的新型抗病毒疗法具有挑战性,因为病毒可以迅速进化以建立抗性并降低治疗效果。选择性靶向保守病毒特征的新化合物是有吸引力的治疗候选物,特别是用于对抗新出现的病毒威胁。先天免疫系统通过产生抗菌肽(AMPs)具有持续抵抗病原体的能力;然而,这些 AMP 存在一些缺点,可能会排除临床使用。AMPs 的基本功能特征已通过肽模拟低聚物得到重现,从而产生有效的抗菌和抗真菌剂。在这里,我们表明一系列称为肽模拟物的 AMP 模拟物对一系列包膜病毒具有直接抗病毒活性,包括关键的人类病原体寨卡病毒、裂谷热病毒和基孔肯雅病毒。这些数据表明,肽模拟物的活性包括与病毒膜成分的结合和破坏。为了研究这些肽模拟物如何靶向脂质膜,我们使用脂质体渗漏测定来测量膜破坏。我们发现含有磷脂酰丝氨酸(PS)的脂质体对肽模拟物处理非常敏感;相比之下,仅由磷脂酰胆碱(PC)形成的脂质体则没有敏感性。此外,含有高含量包膜 PS 的基孔肯雅病毒对肽模拟物介导的失活更敏感。这些结果表明,模拟 AMP 物理化学特性的肽模拟物通过一种膜特异性机制起作用,最有可能通过与 PS 的优先相互作用起作用。我们提供了与不同病毒包膜脂质成分结合的证据,为特异性开辟了一条途径,这可能使开发一种新的治疗药物家族成为可能,能够避免迅速产生抗性。