Host Innate Immune Response and Viral Immune Evasion During Alphaherpesvirus Infection

被引:11
|
作者
Lum, Krystal K. [1 ]
Cristea, Ileana M. [1 ]
机构
[1] Princeton Univ, Dept Mol Biol, Lewis Thomas Lab, Washington Rd, Princeton, NJ 08544 USA
关键词
HERPES-SIMPLEX-VIRUS; VARICELLA-ZOSTER-VIRUS; PROTEASOME-DEPENDENT DEGRADATION; TOLL-LIKE RECEPTORS; KAPPA-B ACTIVATION; CYCLIC GMP-AMP; I-INTERFERON; TEGUMENT PROTEIN; RIG-I; DNA SENSOR;
D O I
10.21775/cimb.042.635
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Both the development of the mammalian innate immune system and the antagonistic strategies acquired by alphaherpesviruses to dismantle it have been shaped by co-evolving virus-host interactions over millions of years. Here, we review mechanisms employed by mammalian cells to detect pathogen molecules, such as viral glycoproteins and nucleic acids, and induce innate immune signaling upon infection with alphaherpesviruses. We further explore strategies acquired by these viruses to bypass immune detection and activation, thereby supporting virus replication and spread. Finally, we discuss the contributions of advanced "omics" and microscopy methods to these discoveries in immune signaling and highlight emerging technologies that can help to further our understanding of the dynamic interplay between host innate immune responses and virus immune evasion.
引用
收藏
页码:635 / 686
页数:52
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