West Nile Virus: Epidemiology and Clinical Features of an Emerging Epidemic in the United States*
Division of Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado 80522, USA. Annual Review of Medicine
(Impact Factor: 12.93).
02/2006; 57(1):181-94. DOI: 10.1146/annurev.med.57.121304.131418
West Nile virus (WNV) was first detected in North America in 1999 during an outbreak of encephalitis in New York City. Since then the virus has spread across North America and into Canada, Latin America, and the Caribbean. The largest epidemics of neuroinvasive WNV disease ever reported occurred in the United States in 2002 and 2003. This paper reviews new information on the epidemiology and clinical aspects of WNV disease derived from greatly expanded surveillance and research on WNV during the past six years.
Available from: Rodolfo Nallar
- "Since its emergence in North America in 1999, WNV has become endemic across southern Canada, particularly in the prairies , where the highest rates of human infection in Canada have occurred (Chen et al. 2013). A mosquito-borne flavivirus, WNV is primarily maintained and amplified in bird populations through transmission by mosquitoes (especially Culex species), with occasional spillover to horses and humans, which are dead end hosts (Hayes and Gubler 2006). Since its introduction into North America, WNV has been reported in .200 "
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ABSTRACT: The Canadian prairies are one of the most important breeding and staging areas for migratory waterfowl in North America. Hundreds of thousands of waterfowl of numerous species from multiple flyways converge in and disperse from this region annually; therefore this region may be a key area for potential intra- and interspecific spread of infectious pathogens among migratory waterfowl in the Americas. Using Blue-winged Teal (Anas discors, BWTE), which have the most extensive migratory range among waterfowl species, we investigated ecologic risk factors for infection and antibody status to avian influenza virus (AIV), West Nile virus (WNV), and avian paramyxovirus-1 (APMV-1) in the three prairie provinces (Alberta, Saskatchewan, and Manitoba) prior to fall migration. We used generalized linear models to examine infection or evidence of exposure in relation to host (age, sex, body condition, exposure to other infections), spatiotemporal (year, province), population-level (local population densities of BWTE, total waterfowl densities), and environmental (local pond densities) factors. The probability of AIV infection in BWTE was associated with host factors (e.g., age and antibody status), population-level factors (e.g., local BWTE population density), and year. An interaction between age and AIV antibody status showed that hatch year birds with antibodies to AIV were more likely to be infected, suggesting an antibody response to an active infection. Infection with AIV was positively associated with local BWTE density, supporting the hypothesis of density-dependent transmission. The presence of antibodies to WNV and APMV-1 was positively associated with age and varied among years. Furthermore, the probability of being WNV antibody positive was positively associated with pond density rather than host population density, likely because ponds provide suitable breeding habitat for mosquitoes, the primary vectors for transmission. Our findings highlight the importance of spatiotemporal, environmental, and host factors at the individual and population levels, all of which may influence dynamics of these and other viruses in wild waterfowl populations.
Journal of wildlife diseases 11/2015; DOI:10.7589/2013-07-191 · 1.36 Impact Factor
Available from: Miguel A. Martín-Acebes
- "WNV is maintained in nature in an enzootic transmission cycle between avian hosts and ornithophilic mosquito vectors, but it can infect multiple vertebrate species, including humans and horses (Martin-Acebes and Saiz, 2012). Although infections in humans are mainly asymptomatic, WNV can also induce a wide range of clinical symptoms that varies from a mild flu-like febrile illness termed WN fever to a neuroinvasive disease characterized by meningitis, encephalitis, or acute flaccid paralysis (Hayes and Gubler, 2006). "
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ABSTRACT: West Nile virus (WNV) is a neurotropic mosquito-borne flavivirus responsible for outbreaks of meningitis and encephalitis. Whereas the activation of autophagy in cells infected with other flaviviruses is well known, the interaction of WNV with the autophagic pathway still remains unclear and there are reports describing opposite findings obtained even analyzing the same viral strain. To clarify this controversy, we first analyzed the induction of autophagic features in cells infected with a panel of WNV strains. WNV was determined to induce autophagy in a strain dependent manner. We observed that all WNV strains or isolates analyzed, except for the WNV NY99 used, upregulated the autophagic pathway in infected cells. Interestingly, a variant derived from this WNV NY99 isolated from a persistently infected mouse increased LC3 modification and aggregation. Genome sequencing of this variant revealed only two non-synonymous nucleotide substitutions when compared to parental NY99 strain. These nucleotide substitutions introduced one amino acid replacement in NS4A and other in NS4B. Using genetically engineered viruses we showed that introduction of only one of these replacements was sufficient to upregulate the autophagic pathway. Thus, in this work we have shown that naturally occurring point mutations in the viral non-structural proteins NS4A and NS4B confer WNV with the ability to induce the hallmarks of autophagy such as LC3 modification and aggregation. Even more, the differences on the induction of an autophagic response observed among WNV variants in infected cells did not correlate with alterations on the activation of the unfolded protein response (UPR), suggesting an uncoupling of UPR and autophagy during flavivirus infection. The findings here reported could help to improve the knowledge of the cellular processes involved on flavivirus-host cell interactions and contribute to the design of effective strategies to combat these pathogens.
Frontiers in Microbiology 01/2015; 5:797. DOI:10.3389/fmicb.2014.00797 · 3.99 Impact Factor
Available from: J David Beckham
- "The intensity of WNV transmission to humans is dictated by seasonal feeding behavior and numbers of mosquitoes , as well as by local ecologic determinants of human exposure (Hayes and Gubler, 2006). WNV epidemics exhibit a seasonal variation in the United States, with most cases observed in the summer and early fall (June through October). "
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ABSTRACT: West Nile virus (WNV) and St. Louis encephalitis virus (SLEV) are arthropod-borne flaviviruses that belong to the Japanese encephalitis virus antigenic complex. SLEV transmission is limited to North and South America, whereas WNV infection occurs on six continents. WNV is now the most common cause of epidemic viral meningoencephalitis in the United States and greater than 30 000 human cases have been reported since its emergence in New York City in 1999. Both viruses are maintained in the natural environment in a cycle between mosquitoes and birds. Human infection is an incidental, non-amplifying, dead-end occurrence in the lifecycle of these enzoonitic viruses and neither WNV nor SLEV is naturally transmitted from person to person. The majority of infections are asymptomatic (80%) and most clinical illness manifests as a self-limited, febrile, flu-like syndrome. However, a small percentage of individuals (<1%) develop neuroinvasive infection (meningitis, encephalitis, and myelitis) that can cause significant illness and death. There is currently no specific therapy of proven benefit or licensed human vaccine for either WNV or SLEV. This chapter reviews the epidemiology, virology, pathogenesis, clinical presentation, diagnosis, treatment, and prognosis of WNV and SLEV, with particular emphasis on WNV, whose recent geographic expansion and global burden warrant in depth review.
Handbook of Clinical Neurology 07/2014; 123C:433-447. DOI:10.1016/B978-0-444-53488-0.00020-1
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