108 research outputs found

    Full-length genome sequence of Ntaya virus

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    Presentation of pyrosequencing data and phylogenetic analysis for the full genome of Ntaya virus, type virus of the Ntaya virus group of the Flaviviridae isolated in Cameroon in 1966

    Genetic Characterization of Zika Virus Strains: Geographic Expansion of the Asian Lineage

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    Zika virus (ZIKV) is a mosquito-transmitted flavivirus found in both Africa and Asia. Human infection with the virus may result in a febrile illness similar to dengue fever and many other tropical infections found in these regions. Previously, little was known about the genetic relationships between ZIKV strains collected in Africa and those collected in Asia. In addition, the geographic origins of the strains responsible for the recent outbreak of human disease on Yap Island, Federated States of Micronesia, and a human case of ZIKV infection in Cambodia were unknown. Our results indicate that there are two geographically distinct lineages of ZIKV (African and Asian). The virus has circulated in Southeast Asia for at least the past 50 years, whereupon it was introduced to Yap Island resulting in an epidemic of human disease in 2007, and in 2010 was the cause of a pediatric case of ZIKV infection in Cambodia. This study also highlights the danger of ZIKV introduction into new areas and the potential for future epidemics of human disease

    Neutralising antibodies for West Nile virus in horses from Brazilian Pantanal

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    Despite evidence of West Nile virus (WNV) activity in Colombia, Venezuela and Argentina, this virus has not been reported in most South American countries. In February 2009, we commenced an investigation for WNV in mosquitoes, horses and caimans from the Pantanal, Central-West Brazil. The sera of 168 horses and 30 caimans were initially tested using a flaviviruses-specific epitope-blocking enzyme-linked immunosorbent assay (blocking ELISA) for the detection of flavivirus-reactive antibodies. The seropositive samples were further tested using a plaque-reduction neutralisation test (PRNT90) for WNV and its most closely-related flaviviruses that circulate in Brazil to confirm the detection of specific virus-neutralising antibodies. Of the 93 (55.4%) blocking ELISA-seropositive horse serum samples, five (3%) were seropositive for WNV, nine (5.4%) were seropositive for St. Louis encephalitis virus, 18 (10.7%) were seropositive for Ilheus virus, three (1.8%) were seropositive for Cacipacore virus and none were seropositive for Rocio virus using PRNT90, with a criteria of > four-fold antibody titre difference. All caimans were negative for flaviviruses-specific antibodies using the blocking ELISA. No virus genome was detected from caiman blood or mosquito samples. The present study is the first report of confirmed serological evidence of WNV activity in Brazil

    Investigating the spatial risk distribution of West Nile virus disease in birds and humans in southern Ontario from 2002 to 2005

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    <p>Abstract</p> <p>Background</p> <p>The West Nile virus (WNv) became a veterinary public health concern in southern Ontario in 2001 and has continued to threaten public health. Wild bird mortality has been shown to be an indicator for tracking the geographic distribution of the WNv. The purpose of this study was to investigate the latent risk distribution of WNv disease among dead birds and humans in southern Ontario and to compare the spatial risk patterns for the period 2002–2005. The relationship between the mortality fraction in birds and incidence rate in humans was also investigated.</p> <p>Methods</p> <p>Choropleth maps were created to investigate the spatial variation in bird and human WNv risk for the public health units of southern Ontario. The data were smoothed by empirical Bayesian estimation before being mapped. Isopleth risk maps for both the bird and human data were created to identify high risk areas and to investigate the potential relationship between the WNv mortality fraction in birds and incidence rates in humans. This was carried out by the geostatistical prediction method of kriging. A Poisson regression analysis was used to model regional human WNv case counts as a function of the spatial coordinates in the east and north direction and the regional bird mortality fractions. The presence of disease clustering and the location of disease clusters were investigated by the spatial scan test.</p> <p>Results</p> <p>The isopleth risk maps exhibited high risk areas that were relatively constant from year to year. There was an overlap in the bird and human high risk areas, which occurred in the central-west and south-west areas of southern Ontario. The annual WNv cause-specific mortality fractions in birds for 2002 to 2005 were 31.9, 22.0, 19.2 and 25.2 positive birds per 100 birds tested, respectively. The annual human WNv incidence rates for 2002 to 2005 were 2.21, 0.76, 0.13 and 2.10 human cases per 100,000 population, respectively. The relative risk of human WNv disease was 0.72 times lower for a public health unit that was 100 km north of another public health unit. The relative risk of human WNv disease increased by the factor 1.44 with every 10 positive birds per 100 tested. The scan statistic detected disease cluster in the bird and human data. The human clusters were not significant, when the analysis was conditioned on the bird data.</p> <p>Conclusion</p> <p>The study indicates a significant relationship between the spatial pattern of WNv risk in humans and birds.</p

    Culex pipiens, an Experimental Efficient Vector of West Nile and Rift Valley Fever Viruses in the Maghreb Region

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    West Nile fever (WNF) and Rift Valley fever (RVF) are emerging diseases causing epidemics outside their natural range of distribution. West Nile virus (WNV) circulates widely and harmlessly in the old world among birds as amplifying hosts, and horses and humans as accidental dead-end hosts. Rift Valley fever virus (RVFV) re-emerges periodically in Africa causing massive outbreaks. In the Maghreb, eco-climatic and entomologic conditions are favourable for WNV and RVFV emergence. Both viruses are transmitted by mosquitoes belonging to the Culex pipiens complex. We evaluated the ability of different populations of Cx. pipiens from North Africa to transmit WNV and the avirulent RVFV Clone 13 strain. Mosquitoes collected in Algeria, Morocco, and Tunisia during the summer 2010 were experimentally infected with WNV and RVFV Clone 13 strain at titers of 107.8 and 108.5 plaque forming units/mL, respectively. Disseminated infection and transmission rates were estimated 14–21 days following the exposure to the infectious blood-meal. We show that 14 days after exposure to WNV, all mosquito st developed a high disseminated infection and were able to excrete infectious saliva. However, only 69.2% of mosquito strains developed a disseminated infection with RVFV Clone 13 strain, and among them, 77.8% were able to deliver virus through saliva. Thus, Cx. pipiens from the Maghreb are efficient experimental vectors to transmit WNV and to a lesser extent, RVFV Clone 13 strain. The epidemiologic importance of our findings should be considered in the light of other parameters related to mosquito ecology and biology

    Genetic Variation in OAS1 Is a Risk Factor for Initial Infection with West Nile Virus in Man

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    West Nile virus (WNV) is a re-emerging pathogen that can cause fatal encephalitis. In mice, susceptibility to WNV has been reported to result from a single point mutation in oas1b, which encodes 2′–5′ oligoadenylate synthetase 1b, a member of the type I interferon-regulated OAS gene family involved in viral RNA degradation. In man, the human ortholog of oas1b appears to be OAS1. The ‘A’ allele at SNP rs10774671 of OAS1 has previously been shown to alter splicing of OAS1 and to be associated with reduced OAS activity in PBMCs. Here we show that the frequency of this hypofunctional allele is increased in both symptomatic and asymptomatic WNV seroconverters (Caucasians from five US centers; total n = 501; OR = 1.6 [95% CI 1.2–2.0], P = 0.0002 in a recessive genetic model). We then directly tested the effect of this SNP on viral replication in a novel ex vivo model of WNV infection in primary human lymphoid tissue. Virus accumulation varied markedly among donors, and was highest for individuals homozygous for the ‘A’ allele (P<0.0001). Together, these data identify OAS1 SNP rs10774671 as a host genetic risk factor for initial infection with WNV in humans
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