Atg6/BECN1(自噬相关6)介导的自噬激活抑制了Sindbis病毒在黄热病蚊子埃及伊蚊中的传播。

Sujit Pujhari, Chan C Heu, Marco Brustolin, Rebecca M Johnson, Donghun Kim, Jason L Rasgon
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引用次数: 0

摘要

巨噬/自噬是脊椎动物和无脊椎动物病原体入侵反应的重要调节因子。然而,它是如何影响严重影响公共卫生的蚊媒病毒病原体的,这方面的研究仍相对不足。为了解决这一空白,我们使用遗传方法激活了表达自噬激活因子的重组Sindbis病毒(SINV)感染的黄热病蚊子(埃及伊蚊)的自噬。我们首先展示了一个17个氨基酸的肽(“AaBec-1”),它来源于Ae。埃及伊蚊Atg6/BECN1 (autophagy -related 6)基因足以诱导C6/36蚊子细胞自噬,表现为Atg8脂化和斑点形成。接下来,我们设计了一种表达AaBec-1肽的重组SINV,并利用它感染并诱导成蚊自噬。我们发现利用重组SINV对自噬的调节负向调节感染性病毒的产生。本研究的结果提高了我们对自噬在无脊椎动物宿主中调节虫媒病毒感染的作用的理解,并强调了利用自噬途径控制虫媒病毒的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sindbis virus is suppressed in the yellow fever mosquito aedes aegypti by Atg6/BECN1 (autophagy-related 6)-mediated activation of autophagy.

Macroautophagy/autophagy is a critical modulator of pathogen invasion response in vertebrates and invertebrates. However, how it affects mosquito-borne viral pathogens that significantly burden public health remains relatively underexplored. To address this gap, we use a genetic approach to activate autophagy in the yellow fever mosquito (Aedes aegypti) infected with a recombinant Sindbis virus (SINV) expressing an autophagy activator. We first demonstrate a 17-amino acid peptide ("AaBec-1") derived from the Ae. aegypti Atg6/BECN1 (Autophagy-related 6) gene is sufficient to induce autophagy in C6/36 mosquito cells, as marked by lipidation of Atg8 and puncta formation. Next, we engineered a recombinant SINV expressing the AaBec-1 peptide and used it to infect and induce autophagy in adult mosquitoes. We find that modulation of autophagy using this recombinant SINV negatively regulates production of infectious virus. The results from this study improve our understanding of the role of autophagy in regulating arbovirus infection in invertebrate hosts and highlight the potential for the autophagy pathway to be exploited for arbovirus control.

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