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cGAS–STING-mediated sensing pathways in DNA and RNA virus infections: crosstalk with other sensing pathways
Archives of Virology ( IF 2.7 ) Pub Date : 2021-10-07 , DOI: 10.1007/s00705-021-05211-x
Saleem Anwar 1 , Khursheed Ul Islam 1 , Md Iqbal Azmi 1 , Jawed Iqbal 1
Affiliation  

Viruses cause a variety of diseases in humans and other organisms. The most important defense mechanism against viral infections is initiated when the viral genome is sensed by host proteins, and this results in interferon production and pro-inflammatory cytokine responses. The sensing of the viral genome or its replication intermediates within host cells is mediated by cytosolic proteins. For example, cGAS and IFI16 recognize non-self DNA, and RIG-I and MDA5 recognize non-self RNA. Once these sensors are activated, they trigger a cascade of reactions activating downstream molecules, which eventually results in the transcriptional activation of type I and III interferons, which play a critical role in suppressing viral propagation, either by directly limiting their replication or by inducing host cells to inhibit viral protein synthesis. The immune response against viruses relies solely upon sensing of viral genomes and their downstream signaling molecules. Although DNA and RNA viruses are sensed by distinct classes of receptor proteins, there is a possibility of overlap between the viral DNA and viral RNA sensing mechanisms. In this review, we focus on various host sensing molecules and discuss the associated signaling pathways that are activated in response to different viral infections. We further highlight the possibility of crosstalk between the cGAS-STING and the RIG-I-MAVS pathways to limit viral infections. This comprehensive review delineates the mechanisms by which different viruses evade host cellular responses to sustain within the host cells.



中文翻译:

cGAS-STING 介导的 DNA 和 RNA 病毒感染中的传感通路:与其他传感通路的串扰

病毒在人类和其他生物体中引起多种疾病。当病毒基因组被宿主蛋白感知时,最重要的针对病毒感染的防御机制就会启动,这会导致干扰素的产生和促炎细胞因子反应。病毒基因组或其在宿主细胞内的复制中间体的感知是由胞质蛋白介导的。例如,cGAS 和 IFI16 识别非自身 DNA,RIG-I 和 MDA5 识别非自身 RNA。一旦这些传感器被激活,它们就会触发一系列激活下游分子的反应,最终导致 I 型和 III 型干扰素的转录激活,这些干扰素通过直接限制其复制或诱导宿主在抑制病毒传播中发挥关键作用细胞抑制病毒蛋白合成。针对病毒的免疫反应仅依赖于对病毒基因组及其下游信号分子的感知。尽管 DNA 和 RNA 病毒被不同类别的受体蛋白感知,但病毒 DNA 和病毒 RNA 感知机制之间可能存在重叠。在这篇综述中,我们关注各种宿主传感分子,并讨论响应不同病毒感染而激活的相关信号通路。我们进一步强调了 cGAS-STING 和 RIG-I-MAVS 途径之间的串扰以限制病毒感染的可能性。这篇全面的综述描述了不同病毒逃避宿主细胞反应以维持在宿主细胞内的机制。尽管 DNA 和 RNA 病毒被不同类别的受体蛋白感知,但病毒 DNA 和病毒 RNA 感知机制之间可能存在重叠。在这篇综述中,我们关注各种宿主传感分子,并讨论响应不同病毒感染而激活的相关信号通路。我们进一步强调了 cGAS-STING 和 RIG-I-MAVS 途径之间的串扰以限制病毒感染的可能性。这篇全面的综述描述了不同病毒逃避宿主细胞反应以维持在宿主细胞内的机制。尽管 DNA 和 RNA 病毒被不同类别的受体蛋白感知,但病毒 DNA 和病毒 RNA 感知机制之间可能存在重叠。在这篇综述中,我们关注各种宿主传感分子,并讨论响应不同病毒感染而激活的相关信号通路。我们进一步强调了 cGAS-STING 和 RIG-I-MAVS 途径之间的串扰以限制病毒感染的可能性。这篇全面的综述描述了不同病毒逃避宿主细胞反应以维持在宿主细胞内的机制。我们专注于各种宿主传感分子,并讨论响应不同病毒感染而激活的相关信号通路。我们进一步强调了 cGAS-STING 和 RIG-I-MAVS 途径之间的串扰以限制病毒感染的可能性。这篇全面的综述描述了不同病毒逃避宿主细胞反应以维持在宿主细胞内的机制。我们专注于各种宿主传感分子,并讨论响应不同病毒感染而激活的相关信号通路。我们进一步强调了 cGAS-STING 和 RIG-I-MAVS 途径之间的串扰以限制病毒感染的可能性。这篇全面的综述描述了不同病毒逃避宿主细胞反应以维持在宿主细胞内的机制。

更新日期:2021-11-26
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