期刊
CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY
卷 51, 期 6, 页码 452-481出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/10409238.2016.1226250
关键词
Viral immune evasion; virus-host interactions; intrinsic immunity; innate immunity; proteasomal degradation; post-translational modification; apoptosis; viral mimicry
资金
- National Institute of Allergy and Infectious Diseases National Institute of General Medical Sciences [10.13039/100000060, AI102187, AI114240-01A1, 10.13039/100000057, GM114141]
In mammalian cells, early defenses against infection by pathogens are mounted through a complex network of signaling pathways shepherded by immune-modulatory pattern-recognition receptors. As obligate parasites, the survival of viruses is dependent on the evolutionary acquisition of mechanisms that tactfully dismantle and subvert the cellular intrinsic and innate immune responses. Here, we review the diverse mechanisms by which viruses that accommodate DNA genomes are able to circumvent activation of cellular immunity. We start by discussing viral manipulation of host defense protein levels by either transcriptional regulation or protein degradation. We next review viral strategies used to repurpose or inhibit these cellular immune factors by molecular hijacking or by regulating their post-translational modification status. Additionally, we explore the infection-induced temporal modulation of apoptosis to facilitate viral replication and spread. Lastly, the co-evolution of viruses with their hosts is highlighted by the acquisition of elegant mechanisms for suppressing host defenses via viral mimicry of host factors. In closing, we present a perspective on how characterizing these viral evasion tactics both broadens the understanding of virus-host interactions and reveals essential functions of the immune system at the molecular level. This knowledge is critical in understanding the sources of viral pathogenesis, as well as for the design of antiviral therapeutics and autoimmunity treatments.
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