A new model for Hendra virus encephalitis in the mouse.

Hendra virus (HeV) infection in humans is characterized by an influenza like illness, which may progress to pneumonia or encephalitis and lead to death. The pathogenesis of HeV infection is poorly understood, and the lack of a mouse model has limited the opportunities for pathogenetic research. In t...

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Main Authors: Johanna Dups, Deborah Middleton, Manabu Yamada, Paul Monaghan, Fenella Long, Rachel Robinson, Glenn A Marsh, Lin-Fa Wang
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3393746?pdf=render
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spelling doaj-56fae4c89f0547919c7257077fda1d6c2020-11-24T21:42:19ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0177e4030810.1371/journal.pone.0040308A new model for Hendra virus encephalitis in the mouse.Johanna DupsDeborah MiddletonManabu YamadaPaul MonaghanFenella LongRachel RobinsonGlenn A MarshLin-Fa WangHendra virus (HeV) infection in humans is characterized by an influenza like illness, which may progress to pneumonia or encephalitis and lead to death. The pathogenesis of HeV infection is poorly understood, and the lack of a mouse model has limited the opportunities for pathogenetic research. In this project we reassessed the role of mice as an animal model for HeV infection and found that mice are susceptible to HeV infection after intranasal exposure, with aged mice reliably developing encephalitic disease. We propose an anterograde route of neuroinvasion to the brain, possibly along olfactory nerves. This is supported by evidence for the development of encephalitis in the absence of viremia and the sequential distribution of viral antigen along pathways of olfaction in the brain of intranasally challenged animals. In our studies mice developed transient lower respiratory tract infection without progressing to viremia and systemic vasculitis that is common to other animal models. These studies report a new animal model of HeV encephalitis that will allow more detailed studies of the neuropathogenesis of HeV infection, particularly the mode of viral spread and possible sequestration within the central nervous system; investigation of mechanisms that moderate the development of viremia and systemic disease; and inform the development of improved treatment options for human patients.http://europepmc.org/articles/PMC3393746?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Johanna Dups
Deborah Middleton
Manabu Yamada
Paul Monaghan
Fenella Long
Rachel Robinson
Glenn A Marsh
Lin-Fa Wang
spellingShingle Johanna Dups
Deborah Middleton
Manabu Yamada
Paul Monaghan
Fenella Long
Rachel Robinson
Glenn A Marsh
Lin-Fa Wang
A new model for Hendra virus encephalitis in the mouse.
PLoS ONE
author_facet Johanna Dups
Deborah Middleton
Manabu Yamada
Paul Monaghan
Fenella Long
Rachel Robinson
Glenn A Marsh
Lin-Fa Wang
author_sort Johanna Dups
title A new model for Hendra virus encephalitis in the mouse.
title_short A new model for Hendra virus encephalitis in the mouse.
title_full A new model for Hendra virus encephalitis in the mouse.
title_fullStr A new model for Hendra virus encephalitis in the mouse.
title_full_unstemmed A new model for Hendra virus encephalitis in the mouse.
title_sort new model for hendra virus encephalitis in the mouse.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description Hendra virus (HeV) infection in humans is characterized by an influenza like illness, which may progress to pneumonia or encephalitis and lead to death. The pathogenesis of HeV infection is poorly understood, and the lack of a mouse model has limited the opportunities for pathogenetic research. In this project we reassessed the role of mice as an animal model for HeV infection and found that mice are susceptible to HeV infection after intranasal exposure, with aged mice reliably developing encephalitic disease. We propose an anterograde route of neuroinvasion to the brain, possibly along olfactory nerves. This is supported by evidence for the development of encephalitis in the absence of viremia and the sequential distribution of viral antigen along pathways of olfaction in the brain of intranasally challenged animals. In our studies mice developed transient lower respiratory tract infection without progressing to viremia and systemic vasculitis that is common to other animal models. These studies report a new animal model of HeV encephalitis that will allow more detailed studies of the neuropathogenesis of HeV infection, particularly the mode of viral spread and possible sequestration within the central nervous system; investigation of mechanisms that moderate the development of viremia and systemic disease; and inform the development of improved treatment options for human patients.
url http://europepmc.org/articles/PMC3393746?pdf=render
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