Zhu Huifang, Zheng Chunfu
Neonatal/Pediatric Intensive Care Unit, Children's Medical Center, First Affiliated Hospital of Gannan Medical University, Ganzhou, China.
Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada.
Microbiol Mol Biol Rev. 2020 Sep 30;84(4). doi: 10.1128/MMBR.00099-20. Print 2020 Nov 18.
Herpes simplex virus 1 (HSV-1) is very successful in establishing acute and latent infections in humans by counteracting host antiviral innate immune responses. HSV-1 has evolved various strategies to evade host antiviral innate immunity and some cellular survival-associated pathways. Since there is still no vaccine available for HSV-1, a continuous update of information regarding the interaction between HSV-1 infection and the host antiviral innate immunity will provide novel insights to develop new therapeutic strategies for HSV-1 infection and its associated diseases. Here, we update recent studies about how HSV-1 evades the host antiviral innate immunity, specifically how HSV-1 proteins directly or indirectly target the adaptors in the antiviral innate immunity signaling pathways to downregulate the signal transduction. Additionally, some classical intracellular stress responses, which also play important roles in defense of viral invasion, will be discussed here. With a comprehensive review of evasion mechanisms of antiviral innate immunity by HSV-1, we will be able to develop potential new targets for therapies and a possible vaccine against HSV-1 infections.
单纯疱疹病毒1型（HSV-1）通过对抗宿主抗病毒固有免疫反应，在人类中成功建立急性和潜伏感染。HSV-1已进化出多种策略来逃避宿主抗病毒固有免疫及一些与细胞存活相关的途径。由于目前仍没有针对HSV-1的疫苗，持续更新有关HSV-1感染与宿主抗病毒固有免疫相互作用的信息，将为开发针对HSV-1感染及其相关疾病的新治疗策略提供新见解。在此，我们更新了关于HSV-1如何逃避宿主抗病毒固有免疫的最新研究，特别是HSV-1蛋白如何直接或间接靶向抗病毒固有免疫信号通路中的衔接蛋白以下调信号转导。此外，这里还将讨论一些在抵御病毒入侵中也起重要作用的经典细胞内应激反应。通过全面综述HSV-1对抗病毒固有免疫的逃逸机制，我们将能够开发出潜在的新治疗靶点以及针对HSV-1感染的可能疫苗。
