Descriptive overview of the 2011 epidemic of arboviral disease in horses in <scp>A</scp>ustralia

Roche, SE; Wicks, R. M.; Garner, M. G.; East, I.J.; Paskin, Roger; Moloney, Barbara; Carr, M; Kirkland, PD

doi:10.1111/avj.12018

Cited by 57 publications

(62 citation statements)

References 20 publications

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“…Although an antigenically similar strain of WNV, WNV KUN , is found endemically in Australia, infections with WNV KUN are usually asymptomatic (Hall et al, 2002). But in 2011, an unprecedented outbreak of equine encephalitis occurred in southeastern Australia following heavy rainfall and severe flooding (Frost et al, 2012), leading to a total of 982 equine cases with a case fatality rate of .9 % (Roche et al, 2013). The virus, named WNV NSW2011 , resulted in an unusually high number of equine cases and fatalities atypical of WNV KUN infections, and produced clinical presentation in horses similar to that of WNV NY99 .…”

Section: Introductionmentioning

confidence: 99%

“…WNV NSW2011 was shown to be significantly more virulent than the prototype WNV KUN strain but less virulent than the WNV NY99 strain in mice (Frost et al, 2012), indicating that virulence of WNV strains in a mouse model of infection correlates well with their virulence in humans. Although the different ecological and epidemiological features of the WNV NSW2011 outbreak, such as a low mosquito population, have been suggested as reasons for the lack of human infections, co-circulation of Murray Valley encephalitis virus was reported in both humans and horses around the time of the WNV NSW2011 outbreak (Frost et al, 2012;Roche et al, 2013), indicating that vector coverage was unlikely to be a factor. Therefore, differences in the viral genome between WNV NSW2011 and WNV NY99 strains are most likely to be responsible for their apparent difference in virulence for humans.…”

Section: Introductionmentioning

confidence: 99%

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Systematic analysis of viral genes responsible for differential virulence between American and Australian West Nile virus strains

Setoh

Prow

Rawle

et al. 2015

Journal of General Virology

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A variant Australian West Nile virus (WNV) strain, WNV NSW2011 , emerged in 2011 causing an unprecedented outbreak of encephalitis in horses in south-eastern Australia. However, no human cases associated with this strain have yet been reported. Studies using mouse models for WNV pathogenesis showed that WNV NSW2011 was less virulent than the human-pathogenic American strain of WNV, New York 99 (WNV NY99 ). To identify viral genes and mutations responsible for the difference in virulence between WNV NSW2011 and WNV NY99 strains, we constructed chimeric viruses with substitution of large genomic regions coding for the structural genes, non-structural genes and untranslated regions, as well as seven individual non-structural gene chimeras, using a modified circular polymerase extension cloning method. Our results showed that the complete non-structural region of WNV NSW2011 , when substituted with that of WNV NY99 , significantly enhanced viral replication and the ability to suppress type I IFN response in cells, resulting in higher virulence in mice. Analysis of the individual non-structural gene chimeras showed a predominant contribution of WNV NY99 NS3 to increased virus replication and evasion of IFN response in cells, and to virulence in mice. Other WNV NY99 non-structural proteins (NS2A, NS4B and NS5) were shown to contribute to the modulation of IFN response. Thus a combination of non-structural proteins, likely NS2A, NS3, NS4B and NS5, is primarily responsible for the difference in virulence between WNV NSW2011 and WNV NY99 strains, and accumulative mutations within these proteins would likely be required for the Australian WNV NSW2011 strain to become significantly more virulent.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Systematic analysis of viral genes responsible for differential virulence between American and Australian West Nile virus strains

Setoh

Prow

Rawle

et al. 2015

Journal of General Virology

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“…This would allow screening for other viruses of public health importance to Australia, such as Barmah Forest virus, Ross River virus and Chikungunya virus to be included in the one assay. Recent outbreaks of arboviral disease in horses in Australia has also highlighted the usefulness of this assay for veterinary diagnostics (Roche, 2013). Recent progress in mosquitobased arbovirus surveillance may also prove compatible with the suspension microarray, with the utilisation of the assay to detect virus in sugar-baited nucleic preservation acid cards rather than mosquito pools (Lothrop et al, 2012, van den Hurk et al, 2012.…”

Section: Resultsmentioning

confidence: 99%

“…The largest epidemic of equine arboviral disease in Australia's history occurred in 2011 (Studdert, 2013, Roche, 2013. Of particular note was that both KUNV and MVEV were co-circulating during the outbreak, causing similar clinical signs and making diagnosis difficult, especially in the early phase of the outbreak.…”

Section: Validationmentioning

confidence: 99%

Development of multiplex suspension microarrays for the detection of alphaviruses and flaviviruses of public health significance

Fischer¹

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“…However, following heavy rainfall and extensive flooding throughout much of eastern Australia, a large-scale arboviral epizootic of equine encephalitis occurred in south-eastern Australia in 2011 [100,216,217].…”

Section: West Nile Virus In the Australian Contextmentioning

confidence: 99%

Investigation of neuropathogenesis and control of an equine-pathogenic Australian West Nile virus isolate in an established CD1 Swiss white mouse and a novel rabbit model

Suen¹

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West Nile virus (WNV) is a globally significant mosquito-borne neurotropic virus. In 2011, a large-scale arboviral encephalitis outbreak occurred in Australia, involving close to 1000 horses. A virulent WNV strain, WNV NSW2011 , was isolated from the brain of an encephalitic horse during this outbreak. Preliminary assessment showed that this strain is intermediate in virulence and belongs in the same lineage as the highly virulent North American strains. However, the pathogenesis of WNV in general, let alone this novel Australian strain, remains largely unclear.The first part of the project aimed to investigate the pathogenesis of lethal WNV NSW2011 infection in the established young adult Swiss white (CD1) mouse model, since previous survival challenge experiments demonstrated high lethality (~70%) of WNV NSW2011 in this animal model. I conducted a pilot time-course experiment, which demonstrated only benign pathological and virological outcomes in sacrificed mice on day 3 and 7 post-infection (pi), despite the relatively high lethality seen in previous survival trials. In a subsequent experiment, I characterised the disease phenotype in moribund/dead and surviving mice after WNV NSW2011 infection. Notably, I detected a high degree of intra-group variability in the neuropathology, neural infection and glial cell activation. Even cases with neuroinvasion are typically not fatal, unless underlying co-morbidities or immunosuppressive disease exist.I chose rabbits as a candidate for a novel animal model, due to the ease of performing intra-vital sampling and monitoring, as well as the possibility for tissue sharing in different assays, given the larger size of rabbits than mice. Rabbits are also hind-gut fermenters, and thus may be a better representation of a horse than a mouse. New Zealand White (NZWRs; Oryctolagus cuniculus) and iii North American cottontail rabbits (CTRs; Sylvilagus sp.) were challenged with WNV strains of different virulence (WNV NSW2011 and WNV TX8667 ), and the prototype Murray Valley encephalitis virus strain (MVE 1-51 ), by the footpad route. The rabbits were consistently resistant to developing severe disease after virulent WNV and MVEV infection, regardless of age, gender and species, despite productive virus replication in the draining popliteal lymph node (PLN). The resultant viraemia for all rabbits was also of low magnitude and transient. Furthermore, establishment of virus infection in the brain was not a feature of the disease, despite mild to moderate neuropathology in a subset of rabbits. This capacity to control flavivirus infection may be explained by the rapid antiviral innate immune response detectable by day 3 pi, as well as a fast anti-WNV neutralising antibody response detectable from day 7 pi.Comparisons of the tissue-specific transcriptional profile of important cytokine and chemokine genes suggested that virus control in rabbits was achieved differently depending on the virus, as well as the rabbit species. However, common transcriptional upregulation of IFNγ in...

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Descriptive overview of the 2011 epidemic of arboviral disease in horses in Australia

Abstract: The epidemic highlights to horse owners and policy makers the potential for future outbreaks of arboviral diseases and the need for vigilance. It also highlights the complex interactions among hosts, vectors and climatic conditions that are required for such an outbreak to occur.

Cited by 57 publications

References 20 publications

Systematic analysis of viral genes responsible for differential virulence between American and Australian West Nile virus strains

Systematic analysis of viral genes responsible for differential virulence between American and Australian West Nile virus strains

Development of multiplex suspension microarrays for the detection of alphaviruses and flaviviruses of public health significance

Investigation of neuropathogenesis and control of an equine-pathogenic Australian West Nile virus isolate in an established CD1 Swiss white mouse and a novel rabbit model

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