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The significance of autophagy as antiviral defense mechanism is recognized and some viruses hijack and modulate this process to their advantage in certain cell types. Here, we present data demonstrating that the human neurotropic herpesvirus varicella zoster virus (VZV) induces autophagy in human SH\u2010SY5Y neuronal cells, in which the pathway exerts antiviral activity. Productively VZV\u2010infected SH\u2010SY5Y cells showed increased LC3\u2010I\u2010LC3\u2010II conversion as well as co\u2010localization of the viral glycoprotein E and the autophagy receptor p62. The activation of autophagy was dependent on a functional viral genome. Interestingly, inducers of autophagy reduced viral transcription, whereas inhibition of autophagy increased viral transcript expression. Finally, the genotype of patients with severe ocular and brain VZV infection were analyzed to identify potential autophagy\u2010associated inborn errors of immunity. Two patients expressing genetic variants in the autophagy genes\n                    <jats:italic>ULK1<\/jats:italic>\n                    and\n                    <jats:italic>MAP1LC3B2, respectively<\/jats:italic>\n                    , were identified. Notably, cells of both patients showed reduced autophagy, alongside enhanced viral replication and death of VZV\u2010infected cells. In conclusion, these results demonstrate a neuro\u2010protective role for autophagy in the context of VZV infection and suggest that failure to mount an autophagy response is a potential predisposing factor for development of severe VZV disease.\n                  <\/jats:p>","DOI":"10.1002\/jmv.29690","type":"journal-article","created":{"date-parts":[[2024,5,28]],"date-time":"2024-05-28T05:34:05Z","timestamp":1716874445000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Varicella zoster virus\u2010induced autophagy in human neuronal and hematopoietic cells exerts antiviral activity"],"prefix":"10.1002","volume":"96","author":[{"given":"Johanna L.","family":"Heinz","sequence":"first","affiliation":[{"name":"Department of Biomedicine Aarhus University Aarhus Denmark"},{"name":"Department of Infectious Diseases Aarhus University Hospital Aarhus Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dani\u00ebla M.","family":"Hinke","sequence":"additional","affiliation":[{"name":"Department of Biomedicine Aarhus University Aarhus Denmark"},{"name":"Department of Infectious Diseases Aarhus University Hospital Aarhus Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muyesier","family":"Maimaitili","sequence":"additional","affiliation":[{"name":"Department of Biomedicine Aarhus University Aarhus Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiayi","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Virology Hannover Medical School Hannover Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ira K. 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