Abstract
Cytosolic DNA sensors are the most recently described class of pattern recognition receptors (PRRs), which induce the production of type I interferons (IFN-I) and trigger the induction of a rapid and efficient innate immune response. Herpes simplex virus type I (HSV-1), a typical DNA virus, has displayed the ability to manipulate and evade host antiviral innate immune responses. Therefore, with an aim to highlight IFN-I-mediated innate immune response in a battle against viral infection, we have summarized the current understandings of DNA-sensing signal pathways and the most recent findings on the molecular mechanisms utilized by HSV-1 to counteract antiviral immune responses. A comprehensive understanding of the interplay between HSV-1 and host early antiviral immune responses will contribute to the development of novel therapies and vaccines in the future.
Highlights
Herpes simplex virus type I (HSV-1), a member of the alphaherpesvirus subfamily, has already co-evolved with human beings for thousands of years and is well known for its high prevalence in the population worldwide (Davison, 2010; Sharma et al, 2016; Ibanez et al, 2018)
At the downstream of the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)/stimulator of interferon genes (STING) signaling pathway, studies from our lab demonstrated that VP24, a serine protease of HSV-1, could block double-stranded DNA (dsDNA)-triggered IFN production by abrogating the interaction between TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3) and inhibiting the activation of IRF3 (Zhang et al, 2016), while HSV-1 VP16 could prevent IRF3 from recruiting the CREB-binding protein (CBP) coactivator, blocking IRF3-mediated transcription (Xing et al, 2013)
Our study has showed that HSV-1 UL36 ubiquitin-specific protease (UL36USP) deubiquitinates IκBα and prevents its degradation, which inhibits p50/p65 transportation and abrogates nuclear factor κB (NF-κB) activation (Ye et al, 2017)
Summary
Specialty section: This article was submitted to Virology, a section of the journal Frontiers in Microbiology. Cytosolic DNA sensors are the most recently described class of pattern recognition receptors (PRRs), which induce the production of type I interferons (IFN-I) and trigger the induction of a rapid and efficient innate immune response. Herpes simplex virus type I (HSV-1), a typical DNA virus, has displayed the ability to manipulate and evade host antiviral innate immune responses. With an aim to highlight IFN-I-mediated innate immune response in a battle against viral infection, we have summarized the current understandings of DNA-sensing signal pathways and the most recent findings on the molecular mechanisms utilized by HSV-1 to counteract antiviral immune responses. A comprehensive understanding of the interplay between HSV-1 and host early antiviral immune responses will contribute to the development of novel therapies and vaccines in the future
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