Though virus isolation is possible, cultures of blood, CSF, and tissues generally test negative in infected individuals due to the peculiar characteristics of WNV infection, i.e. In these cases, IgG detection by an avidity assay can be useful to sort out recent from prior infections with persistent IgM. Therefore, in areas where WNV circulation has occurred for more than a season, the sole detection of IgM could lead to a misdiagnosis of WNV infection as the symptoms could be due to another febrile illness. Moreover, IgM persistence can occur as these antibodies can sometimes be detected for months after infection. This test is also adopted by the European Union (EU) case definition. IgM-positive samples should be systematically confirmed by a plaque reduction neutralization assay that is considered the gold standard diagnostic method for flavivirus serology. However, seropositivity has to be interpreted with care because of the frequent cross-reactivity with infection caused by other flaviviruses, as also reported by a recent external quality assessment (EQA) study on WNV serology. This class of antibodies is detectable one to several days after the onset of symptoms either by enzyme-linked immunosorbent assay or by hemagglutination inhibition methods. Because of short-term viremia and a low level of circulating virus as well as a late appearance of clinical signs when the viremic phase is over, the primary tools used to diagnose WNV infection consist of serological tests for specific IgM in serum or in cerebrospinal fluid (CSF). As these neurological symptoms are not specific only to WNV infections, laboratory tests are essential to confirm or exclude WNV infection. In less than 1% of infected individuals, particularly the elderly or immunocompromised subjects, WNV infects neurons and causes a neuroinvasive disease with meningitis or encephalitis (WNND) and long-term sequelae like altered mental status, lethargy, cranial nerve palsies, acute flaccid paralysis, and movement disorders. The majority of WNV infections in humans are asymptomatic, while approximately 20% of infected individuals develop, after an incubation period of 3-14 days, a febrile self-limiting illness (West Nile fever, WNF) associated with headaches, myalgia, nausea, vomiting, and chills. breast feeding, blood transfusion, and organ transplantation. Human to human transmission of WNV infection has been documented through intrauterine exposure and other transmission routes, i.e. A vertical transmission of the virus, demonstrated by virus isolation from male mosquitoes as they do not take blood meals, followed by horizontal transmission can explain the maintenance of the infection cycle between mosquitoes and birds. Infected mosquitoes also feed on blood of other vertebrate hosts and this leads to frequent infections in humans and horses. Many avian species in Europe are suitable reservoirs/amplifying hosts, producing high viral titers upon WNV infection. Although WNV has been isolated from over 40 species of mosquitoes, the principal mosquitoes involved in WNV transmission belong to the Culex genus, in particular to the Culex pipiens complex of species. ĭuring the enzootic transmission cycle, WNV circulates primarily between mosquitoes and wild birds. Genetic studies demonstrated that all European L1 and L2 isolates derived from a limited number of independent introductions, most likely from Africa, followed by local spread and evolution. An independent L2 strain, firstly detected in 2004 in Southern Russia, has been responsible for outbreaks of West Nile neuroinvasive disease (WNND) in Volvograd Oblast since 2007 and in Romania since 2010. Several virulent L2 isolates were recently identified in other geographic areas such as Eastern Europe, where it has become endemic since its detection in Hungary (in 2004), Austria (in 20), Greece (in 2010), and Italy (in 2011). L2 includes strains mainly present in sub-Saharan Africa and Madagascar and is traditionally associated with asymptomatic infections in humans. L1 is the most widespread and further segregates into different subclasses: WNV-1a (which includes strains from North, Central and South America, Africa and the Middle East), WNV-1b (the Australian Kunjin) and WNV-1c (which includes some Indian strains). However, two major WNV lineages, lineage 1 (L1) and lineage 2 (L2), are responsible for the outbreaks observed in the past years. The intensified surveillance for WNV infections in humans and animals resulted in the detection and isolation of many pathogenic isolates of WNV, classified in at least seven different lineages. West Nile virus (WNV) infection is a vector-borne disease caused by an enveloped ssRNA virus classified within the genus Flavivirus, family Flaviviridae, and phylogenetically and antigenically related to the Japanese encephalitis virus (JEV).
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