薄荷醇对柯萨奇 B 型病毒的抗病毒作用。,Viruses

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薄荷醇对柯萨奇 B 型病毒的抗病毒作用。
Viruses ( IF 3.8 ) Pub Date : 2020-03-28 , DOI: 10.3390/v12040373
David J R Taylor ₁ , Syed M Hamid ₁ , Allen M Andres ₁ , Hannaneh Saadaeijahromi ₁ , Honit Piplani ₁ , Juliana F Germano ₁ , Yang Song ₁ , Savannah Sawaged ₁ , Ralph Feuer ₂ , Stephen J Pandol ₃ , Jon Sin ₁

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柯萨奇病毒 B (CVB) 是一种常见的人类肠道病毒，可引起全身感染，但会在胰腺中特异性复制到高滴度。据报道，某些病毒会诱导线粒体裂变来支持感染。我们记录了 CVB 触发线粒体裂变并阻止线粒体裂变限制感染。瞬时受体电位通道与调节线粒体动力学有关。即，热和辣椒素受体瞬时受体电位阳离子通道亚家族 V 成员 1 (TRPV1) 有助于线粒体去极化和裂变。当我们在 CVB 暴露之前将 HeLa 细胞短暂加热至 39°C 时，感染会加剧，而将细胞冷却至 25°C 则会减少感染。通过用薄荷醇刺激瞬时受体电位阳离子通道亚家族 M 成员 8 (TRPM8) 来诱导“寒冷”，可减少感染，并降低感染期间线粒体裂变的水平。此外，薄荷醇可稳定线粒体抗病毒信号（MAVS）的水平，已知该信号与线粒体动力学有关。总而言之，这突出了一条新途径，其中 CVB 依赖 TRPV1 启动原病毒线粒体裂变，这可能导致抗病毒免疫的破坏。TRPM8 已被证明可以拮抗 TRPV1，因此我们假设刺激 TRPM8 可以阻断 CVB 暴露后 TRPV1 介导的线粒体断裂并减弱感染。

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Antiviral Effects of Menthol on Coxsackievirus B.

Coxsackievirus B (CVB) is a common human enterovirus that causes systemic infection but specifically replicates to high titers in the pancreas. It was reported that certain viruses induce mitochondrial fission to support infection. We documented that CVB triggers mitochondrial fission and blocking mitochondrial fission limits infection. The transient receptor potential channels have been implicated in regulating mitochondrial dynamics; namely, the heat and capsaicin receptor transient receptor potential cation channel subfamily V member 1 (TRPV1) contributes to mitochondrial depolarization and fission. When we transiently warmed HeLa cells to 39 °C prior to CVB exposure, infection was heightened, whereas cooling cells to 25 °C reduced infection. Inducing "cold" by stimulating transient receptor potential cation channel subfamily M member 8 (TRPM8) with menthol led to reduced infection and also resulted in lower levels of mitochondrial fission during infection. Additionally, menthol stabilized levels of mitochondrial antiviral signaling (MAVS) which is known to be tied to mitochondrial dynamics. Taken together, this highlights a novel pathway wherein CVB relies on TRPV1 to initiate proviral mitochondrial fission, which may contribute to the disruption of antiviral immunity. TRPM8 has been shown to antagonize TRPV1, and thus we hypothesize that stimulating TRPM8 blocks TRPV1-mediated mitochondrial fragmentation following CVB exposure and attenuates infection.

更新日期：2020-04-20

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