{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:52:14Z","timestamp":1790776334263,"version":"4.1.0"},"reference-count":112,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2019,3,1]],"date-time":"2019-03-01T00:00:00Z","timestamp":1551398400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,3,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Nipah virus (NiV) and Hendra virus are highly pathogenic zoonotic viruses of the genus Henipavirus, family Paramyxoviridae. These viruses were first identified as the causative agents of severe respiratory and encephalitic disease in the 1990s across Australia and Southern Asia with mortality rates reaching up to 75%. While outbreaks of Nipah and Hendra virus infections remain rare and sporadic, there is concern that NiV has pandemic potential. Despite increased attention, little is understood about the neuropathogenesis of henipavirus infection. Neuropathogenesis appears to arise from dual mechanisms of vascular disease and direct parenchymal brain infection, but the relative contributions remain unknown while respiratory disease arises from vasculitis and respiratory epithelial cell infection. This review will address NiV basic clinical disease, pathology and pathogenesis with a particular focus on central nervous system (CNS) infection and address the necessity of a model of relapsed CNS infection. Additionally, the innate immune responses to NiV infection in vitro and in the CNS are reviewed as it is likely linked to any persistent CNS infection.<\/jats:p>","DOI":"10.1093\/femspd\/ftz023","type":"journal-article","created":{"date-parts":[[2019,4,14]],"date-time":"2019-04-14T11:07:16Z","timestamp":1555240036000},"source":"Crossref","is-referenced-by-count":33,"title":["Henipavirus infection of the central nervous system"],"prefix":"10.1093","volume":"77","author":[{"given":"Brian E","family":"Dawes","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas, 77555, USA"},{"name":"Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas, 77555, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander N","family":"Freiberg","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas, 77555, USA"},{"name":"Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas, 77555, USA"},{"name":"Institute for Human Infections and Immunity, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas, 77555, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,4,15]]},"reference":[{"key":"2021052203492414500_bib1","first-page":"71","article-title":"Late-onset Nipah virus encephalitis 11 years after the initial outbreak: a case report","volume":"17","author":"Abdullah","year":"2012","journal-title":"Neurol Asia"},{"key":"2021052203492414500_bib2","first-page":"663","article-title":"Henipavirus Encephalitis","volume-title":"Handb Clin 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