Division of Molecular Virology and Infectious Diseases, Centre of Excellence in Molecular Biology (CEMB), University of the Punjab, Lahore, Pakistan.
Molecular Diagnostic Lab, Centre for Applied Molecular Biology (CAMB), University of the Punjab, Lahore, Pakistan.
Viral Immunol. 2019 Dec;32(10):424-429. doi: 10.1089/vim.2019.0097. Epub 2019 Oct 10.
Herpes simplex virus type 1 (HSV-1) infection activates a rapid stimulation of host innate immune responses and a delicate interplay between virus and host immune elements regulates the whole events. Although host immune elements play well in limiting the HSV-1 infection by interfering viral replication, they are still unable to remove the virus completely, because HSV-1 proteins are efficient enough to bypass the host antiviral immune responses and virus succeed to reactivate again from latency at opportune time. Type 1 interferon signaling pathway is the central point of innate immunity along with some of the activated neutrophils, monocytes, macrophages, and dendritic cells, and some natural killer cells play role, while the CD8 T cells are crucial in adaptive immunity. In this review, the current knowledge of host and HSV-1 interaction has been described that how the host antiviral immune responses occur and what are the mechanisms of viral evasion adapted by virus to counteract with both arms of immunity.
单纯疱疹病毒 1 型(HSV-1)感染会激活宿主固有免疫反应的快速刺激,病毒和宿主免疫成分之间的微妙相互作用调节着整个事件。尽管宿主免疫成分通过干扰病毒复制在限制 HSV-1 感染方面发挥了很好的作用,但它们仍然无法完全清除病毒,因为 HSV-1 蛋白非常有效地绕过宿主抗病毒免疫反应,并且病毒会在适当的时候从潜伏状态重新激活。I 型干扰素信号通路是固有免疫的中心点,同时还有一些活化的中性粒细胞、单核细胞、巨噬细胞和树突状细胞以及一些自然杀伤细胞发挥作用,而 CD8 T 细胞在适应性免疫中至关重要。在这篇综述中,描述了宿主和 HSV-1 相互作用的最新知识,即宿主抗病毒免疫反应是如何发生的,以及病毒为了对抗免疫的两个分支而适应的逃避机制。