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细胞质中病毒的感应。

Cytosolic sensing of viruses.

机构信息

Immunobiology Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.

出版信息

Immunity. 2013 May 23;38(5):855-69. doi: 10.1016/j.immuni.2013.05.007.

Abstract

Cells are equipped with mechanisms that allow them to rapidly detect and respond to viruses. These defense mechanisms rely partly on receptors that monitor the cytosol for the presence of atypical nucleic acids associated with virus infection. RIG-I-like receptors detect RNA molecules that are absent from the uninfected host. DNA receptors alert the cell to the abnormal presence of that nucleic acid in the cytosol. Signaling by RNA and DNA receptors results in the induction of restriction factors that prevent virus replication and establish cell-intrinsic antiviral immunity. In light of these formidable obstacles, viruses have evolved mechanisms of evasion, masking nucleic acid structures recognized by the host, sequestering themselves away from the cytosol or targeting host sensors, and signaling adaptors for deactivation or degradation. Here, we detail recent advances in the molecular understanding of cytosolic nucleic acid detection and its evasion by viruses.

摘要

细胞配备了允许它们快速检测和响应病毒的机制。这些防御机制部分依赖于受体,这些受体监测细胞质中是否存在与病毒感染相关的非典型核酸。RIG-I 样受体检测未感染宿主中不存在的 RNA 分子。DNA 受体提醒细胞注意细胞质中异常存在的这种核酸。RNA 和 DNA 受体的信号转导导致限制因子的诱导,从而阻止病毒复制并建立细胞内在的抗病毒免疫。鉴于这些艰巨的障碍,病毒已经进化出逃避机制,掩盖宿主识别的核酸结构,将自身隔离在细胞质之外,或针对宿主传感器,并对失活或降解的信号转导适配器进行靶向。在这里,我们详细介绍了细胞质核酸检测及其逃避病毒的分子理解方面的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/248a/7111113/4083cafed541/gr1_lrg.jpg

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