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埃及伊蚊中基孔肯雅病毒感染受 L-半胱氨酸、牛磺酸、次牛磺酸和谷胱甘肽代谢调节。

Chikungunya virus infection in Aedes aegypti is modulated by L-cysteine, taurine, hypotaurine and glutathione metabolism.

机构信息

Vector Borne Diseases Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.

出版信息

PLoS Negl Trop Dis. 2023 May 2;17(5):e0011280. doi: 10.1371/journal.pntd.0011280. eCollection 2023 May.

DOI:10.1371/journal.pntd.0011280
PMID:37130109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10153688/
Abstract

BACKGROUND

Blood meal and infections cause redox imbalance and oxidative damage in mosquitoes which triggers the mosquito's system to produce antioxidants in response to increased oxidative stress. Important pathways activated owing to redox imbalance include taurine, hypotaurine and glutathione metabolism. The present study was undertaken to evaluate the role of these pathways during chikungunya virus (CHIKV) infection in Aedes aegypti mosquitoes.

METHODOLOGY

Using a dietary L-cysteine supplement system, we upregulated these pathways and evaluated oxidative damage and oxidative stress response upon CHIKV infection using protein carbonylation and GST assays. Further, using a dsRNA based approach, we silenced some of the genes involved in synthesis and transport of taurine and hypotaurine and then evaluated the impact of these genes on CHIKV infection and redox biology in the mosquitoes.

CONCLUSIONS

We report that CHIKV infection exerts oxidative stress in the A. aegypti, leading to oxidative damage and as a response, an elevated GST activity was observed. It was also observed that dietary L-cysteine treatment restricted CHIKV infection in A. aegypti mosquitoes. This L-cysteine mediated CHIKV inhibition was coincided by enhanced GST activity that further resulted in reduced oxidative damage during the infection. We also report that silencing of genes involved in synthesis of taurine and hypotaurine modulates CHIKV infection and redox biology of Aedes mosquitoes during the infection.

摘要

背景

血粉和感染会导致蚊子的氧化还原失衡和氧化损伤,从而触发蚊子系统产生抗氧化剂,以应对增加的氧化应激。由于氧化还原失衡而激活的重要途径包括牛磺酸、次牛磺酸和谷胱甘肽代谢。本研究旨在评估这些途径在基孔肯雅病毒(CHIKV)感染埃及伊蚊中的作用。

方法

使用膳食 L-半胱氨酸补充系统,我们上调了这些途径,并通过蛋白质羰基化和 GST 测定法评估了 CHIKV 感染后的氧化损伤和氧化应激反应。此外,我们使用基于 dsRNA 的方法沉默了一些参与牛磺酸和次牛磺酸合成和运输的基因,然后评估了这些基因对蚊子中 CHIKV 感染和氧化还原生物学的影响。

结论

我们报告称,CHIKV 感染会对埃及伊蚊施加氧化应激,导致氧化损伤,作为反应,观察到 GST 活性升高。还观察到膳食 L-半胱氨酸处理限制了埃及伊蚊中 CHIKV 的感染。这种 L-半胱氨酸介导的 CHIKV 抑制与 GST 活性增强同时发生,这进一步导致感染过程中的氧化损伤减少。我们还报告称,沉默参与牛磺酸和次牛磺酸合成的基因会调节感染过程中埃及伊蚊的 CHIKV 感染和氧化还原生物学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/82e3c9f9e08a/pntd.0011280.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/3c5c875d9a4e/pntd.0011280.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/18f0d19a3df0/pntd.0011280.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/28a4b4a08cfa/pntd.0011280.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/5686e937029e/pntd.0011280.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/82e3c9f9e08a/pntd.0011280.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/3c5c875d9a4e/pntd.0011280.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/18f0d19a3df0/pntd.0011280.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/28a4b4a08cfa/pntd.0011280.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/5686e937029e/pntd.0011280.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8e/10153688/82e3c9f9e08a/pntd.0011280.g005.jpg

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