Protective versus Pathogenic Type I Interferon Responses during Virus Infections.
Protective versus Pathogenic Type I Interferon Responses during Virus Infections.
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DOI：
10.3390/v15091916
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发表时间：
2023-09-13
期刊：
影响因子：
--
通讯作者：
Hahm B
中科院分区：
文献类型：
--
作者：
Jung KI;McKenna S;Vijayamahantesh V;He Y;Hahm B
在病毒感染后，合成I型干扰素以诱导抗病毒分子的表达并干扰病毒复制。在COVID-19期间以及微生物组研究中，早期抗病毒I型IFN应答对病毒入侵的重要性得到了强调。此外，I型IFN可直接作用于各种免疫细胞以增强对病毒感染的保护性宿主免疫应答。然而，越来越多的数据表明，干扰素反应可能是有害的主机通过煽动炎症反应或诱导T细胞抑制病毒感染期间。此外，抑制淋巴细胞和树突状细胞的发展可以引起的I型干扰素，这是独立于传统的信号转导和转录激活因子1信号。此外，干扰素被证明会损害气道上皮细胞增殖，这可能会影响后期肺组织从感染中恢复。因此，I型IFN-病毒相互作用的研究是多种多样的，包括细胞中的宿主抗病毒先天免疫机制、IFN逃避的病毒策略、保护性免疫、过度炎症、免疫抑制和组织修复的调节。在这份报告中，这些IFN活动进行了总结，重点放在最近观察到的急性或慢性病毒感染过程中的I型IFN的功能。
Following virus infections, type I interferons are synthesized to induce the expression of antiviral molecules and interfere with virus replication. The importance of early antiviral type I IFN response against virus invasion has been emphasized during COVID-19 as well as in studies on the microbiome. Further, type I IFNs can directly act on various immune cells to enhance protective host immune responses to viral infections. However, accumulating data indicate that IFN responses can be harmful to the host by instigating inflammatory responses or inducing T cell suppression during virus infections. Also, inhibition of lymphocyte and dendritic cell development can be caused by type I IFN, which is independent of the traditional signal transducer and activator of transcription 1 signaling. Additionally, IFNs were shown to impair airway epithelial cell proliferation, which may affect late-stage lung tissue recovery from the infection. As such, type I IFN–virus interaction research is diverse, including host antiviral innate immune mechanisms in cells, viral strategies of IFN evasion, protective immunity, excessive inflammation, immune suppression, and regulation of tissue repair. In this report, these IFN activities are summarized with an emphasis placed on the functions of type I IFNs recently observed during acute or chronic virus infections.
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