Nat Methods. Epitope analysis of the envelope and non-structural glycoproteins of Murray Valley encephalitis virus. Nat Genet. Synthesis of glycoproteins in cells infected by the flavivirus Kunjin.
Vector Borne Zoonotic Dis. Arbovirus infection in horses—Victoria. Commun Dis Intell. Isolation of arboviruses from mosquitoes Diptera: Culicidae collected from the Gulf Plains region of northwest Queensland, Australia. J Med Entomol. Prow NA. The changing epidemiology of Kunjin virus in Australia. Factors shaping the adaptive landscape for arboviruses: implications for the emergence of disease.
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CDC is not responsible for Section compliance accessibility on other federal or private website. Cancel Continue. However, a high incidence of Ross River virus—specific antibody in these animals implicated that virus rather than WNV KUN as the primary etiologic agent Our results are also supported by another recent study showing virulence of WNV Boort in 18—day-old mice Of note, this virus was isolated in the absence of any reported disease outbreak, as part of a survey for the presence of Japanese encephalitis virus in northern Queensland Furthermore, the circulation of neuroinvasive strains may often appear in the absence of disease outbreaks.
This lack of cases suggests that the persistence of virulent strains in southeastern Australia is not the sole determinant for initiating disease outbreaks and that specific climatic and ecologic conditions, perhaps influencing mosquito populations and viral transmission, are also required. A similar scenario occurred in North America, where an unusually high number of cases in humans 5, , most in Texas, USA, were reported in However, sequence analysis of WNV isolates from revealed that the strains circulating in Texas were virulent and attenuated, and no specific virulence determinants responsible for the increase in cases could be identified Instead, other factors, including temperature and changes in mosquito or bird populations, were speculated to have contributed to the magnitude of the outbreak To identify a phylogenetic association with virulence and to identify potential virulence determinants encoded in the genome of WNV KUN strains, we also performed full-length sequencing of the ORF of several of the viruses studied.
Although recent virulent strains were phylogenetically closely related, no other association between phylogenetic grouping and virulence phenotype was found Figure 4 ; Technical Appendix Figure. Isolates from samples collected after , including the virulent WNV NSW and attenuated strains, invariably contained this deletion.
This finding suggests that the deletion is an evolutionary marker but is not directly associated with virulence. This finding is also consistent with our observation that the neuroinvasive Gulf of Carpentaria isolate, WNV Gu , did not have this deletion but that the co-circulating attenuated isolate, WNV Gu , collected from the same region at the same time, did have this deletion. Although these initial observations suggested the involvement of these motifs in the enhanced neuroinvasive properties of the isolate collected from a horse in , our study revealed that, with the exception of WNV KUN , all strains examined contain both of these markers, regardless of virulence phenotype in mouse models.
Thus, it seems that, although these motifs contribute to virulence in mice, they are not likely to be solely responsible for enhancing the neuroinvasive properties of some WNV KUN strains and, hence, not likely to be markers of evolving virulence in recent isolates of WNV KUN. These motifs may include Val 22 and Ser 72 residues in the premembrane, which enhance mouse neuroinvasiveness when introduced into the prototype WNV KUN 11 , and the Pro residue at position in NS3, which is associated with enhanced virulence in birds The absence of the latter motif in all WNV KUN strains is also consistent with the perceived lack of illness and death among birds in Australia, notably during the outbreak among equids.
Extensive passage through cells is known to occasionally lead to passage-adapted mutations, and care should be taken when interpreting sequencing data from these virus strains. WNV KUN is thought to be endemic to the tropical areas of northern Australia, suggesting that virulent viruses emerging in southeastern Australia probably originate from northern Australia.
This finding suggests a different explanation for the evolution of virulent WNV KUN viruses, which may be associated with the adaption of WNV KUN to different hosts avian and terrestrial or different vector species in temperate regions. In this context, virulence in equids may be just a coincidental outcome of the constraints placed on virus fitness in different geographic locations 35 — Further studies evaluating viral fitness of West Nile virus quasispecies in terms of population-dependent host—virus interactions, are warranted.
She also has a special interest in understanding the neuroinvasive properties of neurotrophic flaviviruses. Table of Contents — Volume 22, Number 8—August Please use the form below to submit correspondence to the authors or contact them at the following address:. Roy A. Hall or Alexander A. Khromykh, The University of Queensland, St. Lucia, , Queensland, Australia; or.
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Facebook Twitter LinkedIn Syndicate. Figure 1 Figure 2 Figure 3 Figure 4. Table 1 Table 2 Table 3 Table 4. Article Metrics. Related Articles. Natalie A. Prow 1 2 , Judith H. Edmonds 2 , David T. Williams, Yin X. Northill, Cheryl A. Kirkland, Stephen Doggett, Christy C.
Andrade 3 , Aaron C. Brault, Alexander A. Khromykh 4 , and Roy A. Hall 4. Author affiliations: The University of Queensland, St. Lucia, Queensland, Australia N.
Prow, J. Edmonds, Y. Setoh, H. Bielefeldt-Ohmann, W. Suen, J. Hobson-Peters, A. Khromykh, R. Figure 3. Groups of 10 mice were infected with each virus. The mice were monitored for 21 days after infection for signs of encephalitis and then euthanized.
The significance of clinical differences between groups was calculated by Kaplan-Meier analysis and analyzed by log-rank test. Section Navigation. Facebook Twitter LinkedIn Syndicate.
Prow 1 2 , Judith H. Edmonds 2 , David T. Williams, Yin X. Northill, Cheryl A. Kirkland, Stephen Doggett, Christy C. Andrade 3 , Aaron C.
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