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抗氧化纳米酶通过调节细胞内氧化还原电势来抵抗 HIV-1。

Antioxidant nanozyme counteracts HIV-1 by modulating intracellular redox potential.

机构信息

Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.

Centre for Infectious Disease Research (CIDR), Indian Institute of Science, Bangalore, India.

出版信息

EMBO Mol Med. 2021 May 7;13(5):e13314. doi: 10.15252/emmm.202013314. Epub 2021 Apr 1.

DOI:10.15252/emmm.202013314
PMID:33793064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8103102/
Abstract

Reactive oxygen species (ROS) regulates the replication of human immunodeficiency virus (HIV-1) during infection. However, the application of this knowledge to develop therapeutic strategies remained unsuccessful due to the harmful consequences of manipulating cellular antioxidant systems. Here, we show that vanadium pentoxide (V O ) nanosheets functionally mimic natural glutathione peroxidase activity to mitigate ROS associated with HIV-1 infection without adversely affecting cellular physiology. Using genetic reporters of glutathione redox potential and hydrogen peroxide, we showed that V O nanosheets catalyze ROS neutralization in HIV-1-infected cells and uniformly block viral reactivation and replication. Mechanistically, V O nanosheets suppressed HIV-1 by affecting the expression of pathways coordinating redox balance, virus transactivation (e.g., NF-κB), inflammation, and apoptosis. Importantly, a combination of V O nanosheets with a pharmacological inhibitor of NF-κB (BAY11-7082) abrogated reactivation of HIV-1. Lastly, V O nanosheets inhibit viral reactivation upon prostratin stimulation of latently infected CD4 T cells from HIV-infected patients receiving suppressive antiretroviral therapy. Our data successfully revealed the usefulness of V O nanosheets against HIV and suggested nanozymes as future platforms to develop interventions against infectious diseases.

摘要

活性氧（ROS）在感染过程中调节人类免疫缺陷病毒（HIV-1）的复制。然而，由于操纵细胞抗氧化系统会带来有害后果，将这一知识应用于开发治疗策略的尝试并未成功。在这里，我们表明五氧化二钒（V O ）纳米片通过模拟天然谷胱甘肽过氧化物酶的功能来减轻与 HIV-1 感染相关的 ROS，而不会对细胞生理学产生不利影响。使用谷胱甘肽氧化还原电位和过氧化氢的遗传报告器，我们表明 V O 纳米片在 HIV-1 感染的细胞中催化 ROS 中和，并均匀地阻断病毒的重新激活和复制。从机制上讲，V O 纳米片通过影响协调氧化还原平衡、病毒转激活（例如 NF-κB）、炎症和细胞凋亡的途径的表达来抑制 HIV-1。重要的是，V O 纳米片与 NF-κB 的药理学抑制剂（BAY11-7082）的组合消除了 HIV-1 的重新激活。最后，V O 纳米片抑制了潜伏感染的 CD4 T 细胞在接受抑制性抗逆转录病毒治疗的 HIV 感染者中经普瑞巴林刺激后的病毒重新激活。我们的数据成功地揭示了 V O 纳米片在抗 HIV 方面的有用性，并表明纳米酶是开发针对传染病干预措施的未来平台。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/540663f9015c/EMMM-13-e13314-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/72f98a30ae8f/EMMM-13-e13314-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/9b4a48881008/EMMM-13-e13314-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/540663f9015c/EMMM-13-e13314-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/72f98a30ae8f/EMMM-13-e13314-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/0240c5b4a85c/EMMM-13-e13314-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/f61505ec276e/EMMM-13-e13314-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/c4ca617c79b1/EMMM-13-e13314-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/3b1d976e6cbf/EMMM-13-e13314-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/3ca5676dada0/EMMM-13-e13314-g014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/789852b8289d/EMMM-13-e13314-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/cfd6830f8389/EMMM-13-e13314-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbdc/8103102/540663f9015c/EMMM-13-e13314-g011.jpg

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