Abstract
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.
Highlights
Herpes simplex virus-1 is a double stranded DNA virus associated with chronic infections in humans [1, 2]
Study of autophagy in Herpes simplex virus-1 (HSV-1) infection may have been hampered by factors as methodological limitations, reliance on single point evaluations, testing a particular cell type, or utilizing specific infection conditions especially those that do not reflect a productive infection situation
In order to eliminate effects or phenomena that might be associated with a particular cell type or infection condition, this study takes a comprehensive approach to address how HSV-1 infection regulates autophagy
Summary
Herpes simplex virus-1 is a double stranded DNA virus associated with chronic infections in humans [1, 2]. HSV-1 infections may result in serious morbid, potentially mortal, conditions. HSV-1 corneal infections may cause herpes stromal keratitis (HSK), a condition that may advance to corneal opacity and blindness [1,2,3]. HSV-1 represents the leading infectious cause of corneal blindness worldwide [3, 4]. HSV-1 utilizes various pathways and strategies for entry into host tissues, including the cornea [3, 4], from which it may disseminate into the nervous system causing a lethal condition, herpes encephalitis [1,2,3,4,5]. HSV-1 may cause severe neonatal infections [1, 5]
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