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dc.contributor.authorYakoub, AM
dc.contributor.authorShukla, D.
dc.date.accessioned2016-01-27T16:41:30Z
dc.date.available2016-01-27T16:41:30Z
dc.date.issued2015-08-07
dc.identifier.bibliographicCitationYakoub, A. M. and Shukla, D. Basal Autophagy Is Required for Herpes simplex Virus-2 Infection. Scientific Reports. 2015. 5. DOI: 10.1038/srep12985.en_US
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/10027/20049
dc.descriptionThis is the copy of an article published in Scientific Reports © 2015 Nature Publishing Group Publications. © The Author(s).en_US
dc.description.abstractAutophagy is a conserved catabolic process of the cell, which plays an important role in regulating plethora of infections. The role of autophagy in Herpes simplex virus-2 (HSV-2) infection is unknown. Here, we found that HSV-2 does not allow induction of an autophagic response to infection, but maintains basal autophagy levels mostly unchanged during productive infection. Thus, we investigated the importance of basal autophagy for HSV-2 infection, using pharmacological autophagy suppression or cells genetically deficient in an autophagy-essential gene (ATG5). Interference with basal autophagy flux in cells significantly reduced viral replication and diminished the infection. These results indicate that basal autophagy plays an indispensable role required for a productive infection. Importantly, this study draws a sharp distinction between induced and basal autophagy, where the former acts as a viral clearance mechanism abrogating infection, while the latter supports infection.en_US
dc.description.sponsorshipThis study was supported by a NIH grant (EY023058) to D.S. and a core grant (EY01792). The authors claim no conflicts of interest.en_US
dc.publisherNature Publishing Groupen_US
dc.titleBasal Autophagy Is Required for Herpes simplex Virus-2 Infection.en_US
dc.typeArticleen_US


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