scholarly journals Physiological biomarkers of Hendra virus infection in Australian Flying-foxes (Pteropus spp.)

2017 ◽  
Author(s):  
Lee Anne McMichael
PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28816 ◽  
Author(s):  
Andrew C. Breed ◽  
Martin F. Breed ◽  
Joanne Meers ◽  
Hume E. Field

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0144055 ◽  
Author(s):  
Hume Field ◽  
David Jordan ◽  
Daniel Edson ◽  
Stephen Morris ◽  
Debra Melville ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0128835 ◽  
Author(s):  
Lauren K. Goldspink ◽  
Daniel W. Edson ◽  
Miranda E. Vidgen ◽  
John Bingham ◽  
Hume E. Field ◽  
...  

2008 ◽  
Vol 275 (1636) ◽  
pp. 861-869 ◽  
Author(s):  
Raina K Plowright ◽  
Hume E Field ◽  
Craig Smith ◽  
Anja Divljan ◽  
Carol Palmer ◽  
...  

2007 ◽  
Vol 85 (7) ◽  
pp. 268-270 ◽  
Author(s):  
HE Field ◽  
AC Breed ◽  
J Shield ◽  
RM Hedlefs ◽  
K Pittard ◽  
...  

2017 ◽  
Vol 53 (1) ◽  
pp. 111 ◽  
Author(s):  
Lee McMichael ◽  
Daniel Edson ◽  
David Mayer ◽  
Alice Broos ◽  
Steven Kopp ◽  
...  

2019 ◽  
Author(s):  
Jaewoon Jeong ◽  
Alison J. Peel ◽  
Raina K. Plowright ◽  
Olivier Restif ◽  
Hamish Mccallum

AbstractIncreasing outbreaks of emerging infectious diseases, originating from wildlife, has intensified interest in understanding the dynamics of these diseases in their wildlife reservoir hosts. Until recently, the effect of seasonal birth pulses and subsequent waning of maternally derived antibodies on epidemics in a wild mammal population has received little attention and has remained obscure. In this study, we explore how population structure, influenced by seasonal breeding and maternally derived immunity, affects viral invasion and persistence, using a hypothetical system loosely based on Hendra virus infection in black flying foxes (Pteropus alecto). We used deterministic epidemic models to simulate transient epidemics, following viral introduction into an infection-free population, with a variety of timings within a year and different levels of pre-existing herd immunity. Moreover, we applied different levels of birth synchrony and different modelling methods of waning maternal immunity to examine the effect of birth pulses and maternally derived immunity, both individually and in combination. The presence of waning maternal immunity dispersed the supply time of susceptible individuals in seasonally breeding populations, hence diminishing the effect of birth pulse. Dampened epidemics, caused by waning maternal immunity, made viral invasion and persistence easier. This study enhanced our understanding of viral invasion, persistence, and timing of epidemics in wildlife populations.


PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64360 ◽  
Author(s):  
Jana L. McCaskill ◽  
Glenn A. Marsh ◽  
Paul Monaghan ◽  
Lin-Fa Wang ◽  
Timothy Doran ◽  
...  

2009 ◽  
Vol 83 (22) ◽  
pp. 11979-11982 ◽  
Author(s):  
Jackie Pallister ◽  
Deborah Middleton ◽  
Gary Crameri ◽  
Manabu Yamada ◽  
Reuben Klein ◽  
...  

ABSTRACT Hendra virus and Nipah virus, two zoonotic paramyxoviruses in the genus Henipavirus, have recently emerged and continue to cause sporadic disease outbreaks in humans and animals. Mortality rates of up to 75% have been reported in humans, but there are presently no clinically licensed therapeutics for treating henipavirus-induced disease. A recent report indicated that chloroquine, used in malaria therapy for over 70 years, prevented infection with Nipah virus in vitro. Chloroquine was assessed using a ferret model of lethal Nipah virus infection and found to be ineffective against Nipah virus infection in vivo.


2021 ◽  
Author(s):  
Jianning Wang ◽  
Danielle E Anderson ◽  
Kim Halpin ◽  
Xiao Hong ◽  
Honglei Chen ◽  
...  

Abstract Background Hendra virus (HeV) has caused lethal disease outbreaks in humans and horses in Australia. Pteropid bats (flying foxes) are the wildlife reservoir from which the virus was first isolated in 1996. Following a heat stress mortality event in Australian flying foxes in 2013, a novel HeV variant was discovered. This study describes the subsequent surveillance of Australian flying foxes for this novel virus over a nine year period using qRT-PCR testing of bat tissues submitted primarily for Australian bat lyssavirus (ABLV) diagnosis. Genome sequencing and characterisation of the novel HeV variant was also undertaken. Methods Spleen and kidney samples harvested from flying fox carcasses were initially screened with two real-time qRT-PCR assays specific for the prototype HeV. Two additional qRT-PCR assays were developed specific for the HeV variant first detected in samples from a flying fox in 2013. Next-generation sequencing and virus isolation was attempted from selected samples to further characterise the new virus. Results Since 2013, 98 flying foxes were tested and 11 were positive for the new HeV variant. No samples were positive for the original HeV. Ten of the positive samples were from grey-headed flying foxes (GHFF, Pteropus poliocephalus), however this species was over-represented in the opportunistic sampling (83% of bats tested were GHFF). The positive GHFF samples were collected from Victoria and South Australia and one positive Little red flying fox (LRFF, Pteropus scapulatus) was collected from Western Australia. Immunohistochemistry (IHC) confirmed the presence of henipavirus antigen, associated with an inflammatory lesion in cardiac blood vessels of one GHFF. Positive samples were sequenced and the complete genome was obtained from three samples. When compared to published HeV genomes, there was 84% sequence identity at the nucleotide level. Based on phylogenetic analyses, the newly detected HeV belongs to the HeV species but occupies a distinct lineage. We have therefore designated this virus HeV genotype 2 (HeV-G2). Attempts to isolate virus from PCR positive samples have not been successful. Conclusions A novel HeV genotype (HeV-G2) has been identified in two flying fox species submitted from three states in Australia, indicating that the level of genetic diversity for HeV is broader than first recognised. Given its high genetic relatedness to HeV, HeV-G2 should be considered a zoonotic pathogen.


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