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自噬调控登革病毒感染中的固有免疫信号通路。

Regulation of innate immune signaling pathways by autophagy in dengue virus infection.

机构信息

Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan.

出版信息

IUBMB Life. 2022 Feb;74(2):170-179. doi: 10.1002/iub.2554. Epub 2021 Sep 22.

Abstract

Autophagy is not only an intracellular recycling degradation system that maintains cellular homeostasis but is also a component of innate immunity that contributes to host defense against viral infection. The viral components as well as viral particles trapped in autophagosomes can be delivered to lysosomes for degradation. Abundant evidence indicates that dengue virus (DENV) has evolved the potent ability to hijack or subvert autophagy process for escaping host immunity and promoting viral replication. Moreover, autophagy is often required to deliver viral components to pattern recognition receptors signaling for interferon (IFN)-mediated viral elimination. Hence, this review summarizes DENV-induced autophagy, which exhibits dual effects on proviral activity of promoting replication and antiviral activity to eliminating viral particles.

摘要

自噬不仅是一种维持细胞内稳态的细胞内回收降解系统,也是固有免疫的组成部分,有助于宿主防御病毒感染。病毒成分以及被困在自噬体中的病毒颗粒可以递送至溶酶体进行降解。大量证据表明,登革热病毒(DENV)已经进化出强大的劫持或颠覆自噬过程的能力,以逃避宿主免疫并促进病毒复制。此外,自噬通常需要将病毒成分递送至模式识别受体信号,以介导干扰素(IFN)介导的病毒消除。因此,本文综述了 DENV 诱导的自噬,其对促进复制的前病毒活性和消除病毒颗粒的抗病毒活性表现出双重作用。

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