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      The Changing Epidemiology of Kunjin Virus in Australia

      review-article
      1 , 2
      International Journal of Environmental Research and Public Health
      MDPI
      West Nile virus, Kunjin virus, epidemiology, Australia

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          Abstract

          West Nile virus (WNV) is a mosquito-borne virus responsible for outbreaks of viral encephalitis in humans and horses, with particularly virulent strains causing recent outbreaks of disease in Eastern Europe, the Middle East and North America. A strain of WNV, Kunjin (WNV KUN), is endemic in northern Australia and infection with this virus is generally asymptomatic. However in early 2011, an unprecedented outbreak of encephalitis in horses occurred in south-eastern Australia, resulting in mortality in approximately 10%–15% of infected horses. A WNV-like virus (WNV NSW2011) was isolated and found to be most closely related to the indigenous WNV KUN, rather than other exotic WNV strains. Furthermore, at least two amino acid changes associated with increased virulence of the North American New York 99 strain (WNV NY99) compared to the prototype WNV KUN were present in the WNV NSW2011 sequence. This review summarizes our current understanding of WNV KUN and how the epidemiology and ecology of this virus has changed. Analysis of virulence determinants of contemporary WNV KUN isolates will provide clues on where virulent strains have emerged in Australia. A better understanding of the changing ecology and epidemiology associated with the emergence of virulent strains is essential to prepare for future outbreaks of WNV disease in Australia.

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          Most cited references76

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          Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States.

          In late summer 1999, an outbreak of human encephalitis occurred in the northeastern United States that was concurrent with extensive mortality in crows (Corvus species) as well as the deaths of several exotic birds at a zoological park in the same area. Complete genome sequencing of a flavivirus isolated from the brain of a dead Chilean flamingo (Phoenicopterus chilensis), together with partial sequence analysis of envelope glycoprotein (E-glycoprotein) genes amplified from several other species including mosquitoes and two fatal human cases, revealed that West Nile (WN) virus circulated in natural transmission cycles and was responsible for the human disease. Antigenic mapping with E-glycoprotein-specific monoclonal antibodies and E-glycoprotein phylogenetic analysis confirmed these viruses as WN. This North American WN virus was most closely related to a WN virus isolated from a dead goose in Israel in 1998.
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            Transmission of West Nile virus through blood transfusion in the United States in 2002.

            During the 2002 West Nile virus epidemic in the United States, patients were identified whose West Nile virus illness was temporally associated with the receipt of transfused blood and blood components. Patients with laboratory evidence of recent West Nile virus infection within four weeks after receipt of a blood component from a donor with viremia were considered to have a confirmed transfusion-related infection. We interviewed the donors of these components, asking them whether they had had symptoms compatible with the presence of a viral illness before or after their donation; blood specimens retained from the time of donation and collected at follow-up were tested for West Nile virus. Twenty-three patients were confirmed to have acquired West Nile virus through transfused leukoreduced and nonleukoreduced red cells, platelets, or fresh-frozen plasma. Of the 23 recipients, 10 (43 percent) were immunocompromised owing to transplantation or cancer and 8 (35 percent) were at least 70 years of age. Immunocompromised recipients tended to have longer incubation periods than nonimmunocompromised recipients and infected persons in mosquito-borne community outbreaks. Sixteen donors with evidence of viremia at donation were linked to the 23 infected recipients; of these donors, 9 reported viral symptoms before or after donation, 5 were asymptomatic, and 2 were lost to follow-up. Fever, new rash, and painful eyes were independently associated with being an implicated donor with viremia rather than a donor without viremia. All 16 donors were negative for West Nile virus-specific IgM antibody at donation. Transfused red cells, platelets, and fresh-frozen plasma can transmit West Nile virus. Screening of potential donors with the use of nucleic acid-based assays for West Nile virus may reduce this risk. Copyright 2003 Massachusetts Medical Society
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              A newly emergent genotype of West Nile virus is transmitted earlier and more efficiently by Culex mosquitoes.

              Studies examining the evolution of West Nile virus since its introduction into North America have identified the emergence of a new dominant genotype (WN02) that has displaced the introduced genotype (NY99). The mechanistic basis for this displacement, however, remains obscure. Although we found no detectable difference in vitro between the genotypes in either replication or fitness, there were significant differences in vivo in Culex mosquitoes. After peroral infection, the extrinsic incubation period (EIP) of the WN02 genotype was up to 4 days shorter than the EIP of the NY99 genotype; however, after intrathoracic inoculation, there was no difference in EIP between the genotypes, suggesting that differences in genotype interaction with the mosquito midgut are likely to play a role in this phenotype. These results suggest a model for the displacement of the NY99 genotype, where earlier transmission of WN02 viruses leads to higher WN02 infection rates in avian reservoir hosts.
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                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                25 November 2013
                December 2013
                : 10
                : 12
                : 6255-6272
                Affiliations
                [1 ]Australian Infectious Diseases Research Centre, University of Queensland, St Lucia, QLD, 4072, Australia; E-Mail: n.prow@ 123456uq.edu.au ; Tel.: +61-7-3365-4648; Fax: +61-7-3365-4620
                [2 ]School of Chemistry and Molecular Biosciences, University of Queensland, St Lucia, QLD, 4072, Australia
                Article
                ijerph-10-06255
                10.3390/ijerph10126255
                3881112
                24287851
                aed53c5a-1f17-4f27-a5e4-95614fd889cd
                © 2013 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                : 24 September 2013
                : 04 November 2013
                : 07 November 2013
                Categories
                Review

                Public health
                west nile virus,kunjin virus,epidemiology,australia
                Public health
                west nile virus, kunjin virus, epidemiology, australia

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