Yakoub Abraam M, Shukla Deepak
Department of Microbiology and Immunology, University of Illinois, Chicago, IL United States of America, 60612; Department of Ophthalmology and Visual Sciences, University of Illinois Medical Center, Chicago, IL United States of America, 60612.
PLoS One. 2015 Apr 20;10(4):e0124646. doi: 10.1371/journal.pone.0124646. eCollection 2015.
Herpes simplex virus-1 (HSV-1) infection causes severe conditions, with serious complications, including corneal blindness from uncontrolled ocular infections. An important cellular defense mechanism against HSV-1 infection is autophagy. The autophagic response of the host cell was suggested to be regulated by HSV-1. In this study, we performed a detailed analysis of autophagy in multiple HSV-1-targeted cell types, and under various infection conditions that recapitulate a productive infection model. We found that autophagy was slightly inhibited in one cell type, while in other cell types autophagy maintained its basal levels mostly unchanged during productive infection. This study refines the concept of HSV-1-mediated autophagy regulation to imply either inhibition, or prevention of activation, of the innate immune pathway.
单纯疱疹病毒1型（HSV-1）感染会引发严重病症，并伴有包括因眼部感染失控导致角膜失明在内的严重并发症。针对HSV-1感染的一种重要细胞防御机制是自噬。据推测，宿主细胞的自噬反应受HSV-1调控。在本研究中，我们对多种HSV-1靶向细胞类型中的自噬进行了详细分析，并在各种模拟有效感染模型的感染条件下进行了研究。我们发现，在一种细胞类型中自噬受到轻微抑制，而在其他细胞类型中，自噬在有效感染期间大多维持其基础水平不变。本研究完善了HSV-1介导的自噬调控概念，意味着对先天免疫途径的抑制或激活的预防。
