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The Role of Interferon in Persistent Viral Infection: Insights from Murine Norovirus

机译:干扰素在持续性病毒感染中的作用:鼠诺维病毒的见解

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Persistent viral infections result from evasion or avoidance of sterilizing immunity, extend the timeframe of virus transmission, and can trigger disease. Prior studies in mouse models of persistent infection have suggested that ineffective adaptive immune responses are necessary for persistent viral infection. However, recent work in the murine norovirus (MNV) model of persistent infection demonstrates that innate immunity can control both early and persistent viral replication independently of adaptive immune effector functions. Interferons (IFNs) are central to the innate control of persistent MNV, apart from a role in modulating adaptive immunity. Furthermore, subtypes of IFN play distinct tissue-specific roles in innate control of persistent MNV infection. Type I IFN (IFN-alpha/beta) controls systemic replication, and type III IFN (IFN-lambda) controls MNV persistence in the intestinal epithelium. In this article, we review recent findings in the MNV model, highlighting the role of IFNs and innate immunity in clearing persistent viral infection, and discussing the broader implications of these findings for control of persistent human infections.
机译:持续性病毒感染因逃避或避免灭菌免疫而导致,延长病毒传播的时间表,并且可以引发疾病。在持续感染的小鼠模型中的前提研究表明,持续性病毒感染是必需的。然而,近期在持续感染的鼠诺维病毒(MNV)模型中的工作表明,先天免疫可以独立于适应性免疫效应功能控制早期和持续的病毒复制。干扰素(IFNS)是持久性MNV的先天控制的核心,除了调节适应性免疫中的作用。此外,IFN的亚型在持续的MNV感染先天控制中发挥着不同的组织特异性作用。 I型IFN(IFN-alpha / beta)控制全身复制,III型IFN(IFN-Lambda)控制肠上皮中的MNV持久性。在本文中,我们在MNV模型中审查了最近的发现,突出了IFNS和先天免疫在清除持续性病毒感染方面的作用,并讨论了这些发现对控制持续人类感染的更广泛影响。

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