{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:43:37Z","timestamp":1791333817931,"version":"4.3.1"},"reference-count":52,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T00:00:00Z","timestamp":1398902400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            MicroRNAs (miRNAs) are single-stranded small RNA molecules that regulate various cellular processes. miRNA 155 (miR-155) regulates various aspects of innate and adaptive immune responses and plays a key role in various viral infections and the resulting neuroinflammation. The present study evaluated the involvement of miR-155 in modulating\n            <jats:named-content content-type=\"genus-species\">Japanese encephalitis virus<\/jats:named-content>\n            (JEV)-induced neuroinflammation. We observed that miR-155 expression was upregulated during JEV infection of mouse primary microglia, the BV-2 microglia cell line, and in both mouse and human brains.\n            <jats:italic>In vitro<\/jats:italic>\n            and\n            <jats:italic>in vivo<\/jats:italic>\n            knockdown of miR-155 minimized JEV-induced inflammatory responses. In the present study, we confirmed targeting of the Src homology 2-containing inositol phosphatase 1 (SHIP1) 3\u2032 untranslated region (UTR) by miR-155 in the context of JEV infection. Inhibition of SHIP1 by miR-155 resulted in higher beta interferon (IFN-\u03b2) and proinflammatory cytokine production through activation of TANK-binding kinase 1 (TBK-1). Based on these observations, we conclude that miR-155 modulates the neuroinflammatory response during JEV infection via negative regulation of SHIP1 expression. Thus, modulation of miR-155 could be a novel strategy to regulate JEV-induced neuroinflammation.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            <jats:named-content content-type=\"genus-species\">Japanese encephalitis virus<\/jats:named-content>\n            (JEV), a member of the family\n            <jats:named-content content-type=\"genus-species\">Flaviviridae<\/jats:named-content>\n            that causes Japanese encephalitis (JE), is the most common mosquito-borne encephalitis virus in the Asia-Pacific region. The disease is feared, as currently there are no specific antiviral drugs available. JEV targets the central nervous system, leading to high mortality and neurological and psychiatric sequelae in some of those who survive. The level of inflammation correlates well with the clinical outcome in patients. Recently, microRNA (miRNA), a single-stranded noncoding RNA, has been implicated in various brain disorders. The present study investigates the role of miRNA in JEV-induced neuroinflammation. Our results show that miRNA 155 (miR-155) targets the Src homology 2-containing inositol phosphatase 1 (SHIP1) protein and promotes inflammation by regulating the NF-\u03baB pathway, increasing the expression of various proinflammatory cytokines and the antiviral response. Thus, miR-155 is a potential therapeutic target to develop antivirals in JE and other brain disorders where inflammation plays a significant role in disease progression.\n          <\/jats:p>","DOI":"10.1128\/jvi.02979-13","type":"journal-article","created":{"date-parts":[[2014,2,13]],"date-time":"2014-02-13T05:44:12Z","timestamp":1392270252000},"page":"4798-4810","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":119,"title":["MicroRNA 155 Regulates Japanese Encephalitis Virus-Induced Inflammatory Response by Targeting Src Homology 2-Containing Inositol Phosphatase 1"],"prefix":"10.1128","volume":"88","author":[{"given":"Menaka Chanu","family":"Thounaojam","sequence":"first","affiliation":[{"name":"National Brain Research Centre, Manesar, Haryana, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiran","family":"Kundu","sequence":"additional","affiliation":[{"name":"National Brain Research Centre, Manesar, Haryana, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deepak Kumar","family":"Kaushik","sequence":"additional","affiliation":[{"name":"National Brain Research Centre, Manesar, Haryana, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shalini","family":"Swaroop","sequence":"additional","affiliation":[{"name":"National Brain Research Centre, Manesar, Haryana, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anita","family":"Mahadevan","sequence":"additional","affiliation":[{"name":"Department of Neuropathology, National Institute of Mental Health and Neurosciences, Bangalore, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susarla Krishna","family":"Shankar","sequence":"additional","affiliation":[{"name":"Department of Neuropathology, National Institute of Mental Health and Neurosciences, Bangalore, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anirban","family":"Basu","sequence":"additional","affiliation":[{"name":"National Brain Research Centre, Manesar, Haryana, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pntd.0000437"},{"key":"e_1_3_3_3_2","first-page":"326","article-title":"Japanese encephalitis: pathogenesis, prophylactics and therapeutics","volume":"98","author":"Dutta K","year":"2010","unstructured":"DuttaKRangarajanPNVratiSBasuA. 2010. 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