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Viral evasion mechanisms of early antiviral responses involving regulation of ubiquitin pathways

机译:涉及抗泛素途径调控的早期抗病毒应答的病毒逃逸机制

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摘要

Early innate and cell-intrinsic responses are essential to protect host cells against pathogens. In turn, viruses have developed sophisticated mechanisms to establish productive infections, counteracting the host innate immune responses. Increasing evidence indicates that these antiviral factors may have a dual role by directly inhibiting viral replication, as well as by sensing and transmitting signals to induce antiviral cytokines. Recent studies have pointed at new, unappreciated mechanisms of viral evasion of host innate protective responses including manipulating the host ubiquitin system. Viral inhibition of antiviral factors by ubiquitin-dependent degradation is emerging as critical evasion mechanism of the antiviral response. In addition, recent studies have uncovered new mechanisms by which viral encoded proteins inhibit ubiquitin and ubiquitin-like modification of host proteins involved innate immune signaling pathways. Here we discuss recent findings and novel strategies that viruses have developed to counteract these early innate antiviral defenses.
机译:早期的先天和细胞内源性反应对于保护宿主细胞免受病原体的侵害至关重要。反过来,病毒已经开发出复杂的机制来建立生产性感染,从而抵消宿主的先天免疫反应。越来越多的证据表明,这些抗病毒因子可能通过直接抑制病毒复制以及通过感测和传递信号来诱导抗病毒细胞因子发挥双重作用。最近的研究指出了新的,未知的病毒逃逸宿主先天性保护性反应的机制,包括操纵宿主泛素系统。泛素依赖性降解对抗病毒因子的病毒抑制作用正在成为抗病毒反应的关键逃避机制。此外,最近的研究发现了病毒编码蛋白抑制遍在蛋白和宿主蛋白的遍在蛋白修饰的新机制,所述修饰涉及先天免疫信号传导途径。在这里,我们讨论病毒已经发展起来以抵消这些早期先天性抗病毒防御的最新发现和新策略。

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