先天免疫系统
生物
内部收益率3
病毒复制
干扰素调节因子
干扰素
转录因子
信号转导
RNA干扰
免疫系统
细胞生物学
病毒学
核糖核酸
免疫学
病毒
基因
遗传学
作者
Daniel Sauter,Frank Kirchhoff
出处
期刊:Current Opinion in Hiv and Aids
[Ovid Technologies (Wolters Kluwer)]
日期:2016-03-01
卷期号:11 (2): 173-181
被引量:27
标识
DOI:10.1097/coh.0000000000000233
摘要
Purpose of review The goal of this review is to summarize recent progress in our understanding of innate sensing of HIV. Furthermore, we present the mechanisms that HIV has evolved to attenuate innate immune responses and discuss open questions. Recent findings Toll-like receptors (TLRs) and various cytosolic sensors induce an antiviral interferon response upon detection of genomic HIV RNA or intermediates of reverse transcription. HIV limits activation of these sensing pathways by interfering with TLR signaling and by cloaking viral nucleic acids in the cytoplasm, before proviral dsDNA translocates into the nucleus. Furthermore, the viral accessory protein Vpu mitigates antiviral gene expression by inhibiting canonical nuclear factor kappa B (NF-κB) signaling. These evasion mechanisms, however, are imperfect and HIV infection almost inevitably triggers the activation of IRF3, NF-κB and other key transcription factors of antiviral immunity. Notably, the interplay of these processes plays a critical role in the induction of chronic inflammation that drives progression to AIDS. Summary HIV has evolved sophisticated but imperfect mechanisms to evade and counteract innate sensing. Whether virus-induced immune activation represents merely a suboptimal adaptation of HIV to its human host or even facilitates HIV replication, for example by increasing the number of viral target cells, remains to be clarified.
科研通智能强力驱动
Strongly Powered by AbleSci AI