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Henipavirus Encephalitis: Recent Developments and Advances

Identifieur interne : 001A23 ( Istex/Corpus ); précédent : 001A22; suivant : 001A24

Henipavirus Encephalitis: Recent Developments and Advances

Auteurs : Kien Chai Ong ; Kum Thong Wong

Source :

RBID : ISTEX:DDAE120273802D9A53863EEE25AECA90DA0B017F

Abstract

The genus Henipavirus within the family Paramyxoviridae includes the Hendra virus (HeV) and Nipah virus (NiV) which were discovered in the 1990s in Australia and Malaysia, respectively, after emerging to cause severe and often fatal outbreaks in humans and animals. While HeV is confined to Australia, more recent NiV outbreaks have been reported in Bangladesh, India and the Philippines. The clinical manifestations of both henipaviruses in humans appear similar, with a predominance of an acute encephalitic syndrome. Likewise, the pathological features are similar and characterized by disseminated, multi‐organ vasculopathy comprising endothelial infection/ulceration, vasculitis, vasculitis‐induced thrombosis/occlusion, parenchymal ischemia/microinfarction, and parenchymal cell infection in the central nervous system (CNS), lung, kidney and other major organs. This unique dual pathogenetic mechanism of vasculitis‐induced microinfarction and neuronal infection causes severe tissue damage in the CNS. Both viruses can also cause relapsing encephalitis months and years after the acute infection. Many animal models studied to date have largely confirmed the pathology of henipavirus infection, and provided the means to test new therapeutic agents and vaccines. As the bat is the natural host of henipaviruses and has worldwide distribution, spillover events into human populations are expected to occur in the future.

Url:
DOI: 10.1111/bpa.12278

Links to Exploration step

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<keyword xml:id="bpa12278-kwd-0004">pathological</keyword>
</keywordGroup>
<fundingInfo>
<fundingAgency>University of Malaya/Ministry of Education High Impact Research Grant</fundingAgency>
<fundingNumber>H‐20001‐00‐E000004</fundingNumber>
</fundingInfo>
<abstractGroup>
<abstract type="main">
<title type="main">Abstract</title>
<p>The genus
<fc>
<i>H</i>
</fc>
<i>enipavirus</i>
within the family
<fc>P</fc>
aramyxoviridae includes the Hendra virus (
<fc>HeV</fc>
) and
<fc>N</fc>
ipah virus (
<fc>NiV</fc>
) which were discovered in the 1990s in
<fc>A</fc>
ustralia and
<fc>M</fc>
alaysia, respectively, after emerging to cause severe and often fatal outbreaks in humans and animals. While
<fc>HeV</fc>
is confined to
<fc>A</fc>
ustralia, more recent
<fc>NiV</fc>
outbreaks have been reported in
<fc>B</fc>
angladesh,
<fc>I</fc>
ndia and the
<fc>P</fc>
hilippines. The clinical manifestations of both henipaviruses in humans appear similar, with a predominance of an acute encephalitic syndrome. Likewise, the pathological features are similar and characterized by disseminated, multi‐organ vasculopathy comprising endothelial infection/ulceration, vasculitis, vasculitis‐induced thrombosis/occlusion, parenchymal ischemia/microinfarction, and parenchymal cell infection in the central nervous system (
<fc>CNS</fc>
), lung, kidney and other major organs. This unique dual pathogenetic mechanism of vasculitis‐induced microinfarction and neuronal infection causes severe tissue damage in the
<fc>CNS</fc>
. Both viruses can also cause relapsing encephalitis months and years after the acute infection. Many animal models studied to date have largely confirmed the pathology of henipavirus infection, and provided the means to test new therapeutic agents and vaccines. As the bat is the natural host of henipaviruses and has worldwide distribution, spillover events into human populations are expected to occur in the future.</p>
</abstract>
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<noteGroup>
<note numbered="no" xml:id="bpa12278-note-0001">Conflict of interest: The authors declare no conflict of interest.</note>
</noteGroup>
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<titleInfo lang="en">
<title>Henipavirus Encephalitis: Recent Developments and Advances</title>
</titleInfo>
<titleInfo type="abbreviated" lang="en">
<title>Update on Henipavirus Encephalitis</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en">
<title>Henipavirus Encephalitis: Recent Developments and Advances</title>
</titleInfo>
<name type="personal">
<namePart type="given">Kien Chai</namePart>
<namePart type="family">Ong</namePart>
<affiliation>Department of Biomedical Science, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Kum Thong</namePart>
<namePart type="family">Wong</namePart>
<affiliation>Department ofPathology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia</affiliation>
<affiliation>Kum Thong Wong, MBBS, MPATH, FRCPATH, MD, Department of Pathology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia (E‐mail: )</affiliation>
<affiliation>E-mail: wongkt@ummc.edu.my</affiliation>
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<roleTerm type="text">author</roleTerm>
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</name>
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<publisher>Blackwell Publishing Ltd</publisher>
<dateIssued encoding="w3cdtf">2015-09</dateIssued>
<dateCreated encoding="w3cdtf">2015-07-02</dateCreated>
<dateCaptured encoding="w3cdtf">2015-06-13</dateCaptured>
<dateValid encoding="w3cdtf">2015-06-18</dateValid>
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<abstract>The genus Henipavirus within the family Paramyxoviridae includes the Hendra virus (HeV) and Nipah virus (NiV) which were discovered in the 1990s in Australia and Malaysia, respectively, after emerging to cause severe and often fatal outbreaks in humans and animals. While HeV is confined to Australia, more recent NiV outbreaks have been reported in Bangladesh, India and the Philippines. The clinical manifestations of both henipaviruses in humans appear similar, with a predominance of an acute encephalitic syndrome. Likewise, the pathological features are similar and characterized by disseminated, multi‐organ vasculopathy comprising endothelial infection/ulceration, vasculitis, vasculitis‐induced thrombosis/occlusion, parenchymal ischemia/microinfarction, and parenchymal cell infection in the central nervous system (CNS), lung, kidney and other major organs. This unique dual pathogenetic mechanism of vasculitis‐induced microinfarction and neuronal infection causes severe tissue damage in the CNS. Both viruses can also cause relapsing encephalitis months and years after the acute infection. Many animal models studied to date have largely confirmed the pathology of henipavirus infection, and provided the means to test new therapeutic agents and vaccines. As the bat is the natural host of henipaviruses and has worldwide distribution, spillover events into human populations are expected to occur in the future.</abstract>
<note type="funding">University of Malaya/Ministry of Education High Impact Research Grant - No. H‐20001‐00‐E000004; </note>
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