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A characteristic feature of PD is the aggregation of mutated \u03b1-synuclein (\u03b1-syn) that damages the dopaminergic neurons. Considering this link between JEV-induced PD-like symptoms and \u03b1-syn pathogenesis, we explored the role of \u03b1-syn in JEV infectivity in neuronal cells. Our investigation revealed a significant increase in endogenous \u03b1-syn expression in JEV-infected cells. In addition, exogenous \u03b1-syn (Exo\u03b1-syn) treatment substantially reduced JEV replication, suggesting its anti-JEV effect. Furthermore, Exo\u03b1-syn treatment led to the upregulation of superoxide dismutase 1 (SOD1) and reduction in reactive oxygen species (ROS). The results were validated by endogenous \u03b1-syn-silencing, which decreased SOD1 and raised ROS levels in neuronal cells. Similarly, the SOD1 inhibition\n                      <jats:italic>via<\/jats:italic>\n                      LCS-1 also intensified ROS and JEV infection. Silencing of SOD1 in \u03b1-syn overexpressing neuro2a cells exhibited increased JEV replication. Overall, our results suggest that \u03b1-syn exerts an anti-JEV effect by regulating protein involved in oxidative stress inside neuronal cells. This study contributes valuable insights into the interplay between \u03b1-syn expression and JEV infectivity, shedding light on avenues further to investigate the potential role of \u03b1-syn in JEV pathogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>Japanese encephalitis virus (JEV) poses a significant threat, particularly to children. Despite extensive research efforts, the development of effective treatments against JEV has been impeded. One of the major setbacks is a lack of comprehensive understanding of neurotropism. The study focuses on alpha-synuclein (\u03b1-syn), a neuronal protein, and aims to determine its role in JEV pathogenesis. The present study reveals that the host cell upregulates \u03b1-syn in response to JEV infection. \u03b1-syn restrains JEV propagation by modulating superoxide dismutase 1 (SOD1) expression which further blocks JEV-induced ROS generation. Endogenous \u03b1-syn silencing led to a decrease in SOD1 expression and increased viral titer. \u03b1-syn plays a crucial role in counteracting oxidative stress through SOD1, which is essential for limiting JEV replication. This study provides broader implications for antiviral strategies and their possible role in neurodegenerative diseases; however, there is still much to explore, particularly regarding \u03b1-syn aggregation kinetics in JEV infection.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.00418-24","type":"journal-article","created":{"date-parts":[[2024,11,7]],"date-time":"2024-11-07T09:00:57Z","timestamp":1730970057000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":11,"title":["Alpha-synuclein expression in neurons modulates Japanese encephalitis virus infection"],"prefix":"10.1128","volume":"98","author":[{"given":"Anjali","family":"Gupta","sequence":"first","affiliation":[{"name":"Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0680-1138","authenticated-orcid":false,"given":"Vijay Singh","family":"Bohara","sequence":"additional","affiliation":[{"name":"Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aditya Singh","family":"Chauhan","sequence":"additional","affiliation":[{"name":"Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anshuman","family":"Mohapatra","sequence":"additional","affiliation":[{"name":"Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harpreet","family":"Kaur","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Communicable Diseases, Indian Council of Medical Research, Ansari Nagar","place":["New Delhi, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ajanta","family":"Sharma","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Gauhati Medical College","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3542-8157","authenticated-orcid":true,"given":"Nitin","family":"Chaudhary","sequence":"additional","affiliation":[{"name":"Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8526-6013","authenticated-orcid":true,"given":"Sachin","family":"Kumar","sequence":"additional","affiliation":[{"name":"Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati","place":["Guwahati, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1212\/wnl.57.12.2313"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.12688\/f1000research.19693.1"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jns.2012.11.007"},{"key":"e_1_3_4_5_2","first-page":"219","article-title":"Temporal changes of Japanese encephalitits virus in different brain regions of rat","volume":"138","author":"Srivastava R","year":"2013","unstructured":"Srivastava R, Kalita J, Khan MY, Gore MM, Bondre VP, Misra UK. 2013. 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