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Herpes simplex virus types 1 and 2 modulate autophagy in SIRC corneal cells |
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| Authors: | Goran Petrovski Kata Pásztor László Orosz Réka Albert Edina Mencel Morten C Moe Kai Kaarniranta Andrea Facskó Klára Megyeri |
| Institution: | 1. Department of Ophthalmology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary 2. Stem Cells and Eye Research Laboratory and Apoptosis and Genomics Research Group of Hungarian Academy of Sciences, Department of Biochemistry and Molecular Biology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary 3. Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary 4. Department of Ophthalmology, Center of Eye Research, Oslo University Hospital, University of Oslo, Oslo, Norway 5. Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland 6. Department of Ophthalmology, Kuopio University Hospital, Kuopio, Finland 7. Department of Ophthalmology, University of Szeged, Szeged, Hungary |
| Abstract: | Autophagy and apoptosis function as important early cellular defense mechanisms in infections and other diseases. The outcome of an infection is determined by a complex interplay between the pathogenic microorganism and these intracellular pathways. To better understand the cytopathogenicity of Herpes simplex virus types 1 and 2 (HSV-1 and -2), we studied the effect of these viruses on the autophagic and apoptotic processes in the SIRC corneal cell line. Infection with the KOS strain of HSV-1 and a wild-type strain of HSV-2 enhanced autophagosome formation, triggered cytoplasmic acidification, increased LC3B lipidation and elevated the ratio of apoptotic cells. The autophagy inhibitor bafilomycin A1 triggered a significant increase in the apoptotic responses of HSV-1- and HSV-2-infected cells. Thus, both HSV types affect autophagy and apoptosis in a coordinated fashion, and autophagy plays cytoprotective role in HSV-infected cells via antagonizing apoptosis. Together these data implicate autophagy in the pathogenic mechanism of herpetic keratitis. |
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