West Nile virus
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West Nile virus (WNV), may cause severe, persistent or fatal disease, although about 80% of infections are asymptomatic. It is found throughout much of Europe, Africa, and North America. In 2006 in the United States, 174 deaths, 1455 cases of West Nile encephalitis/meningitis, and 2612 cases of West Nile Fever were reported to the Center for Disease Control.[1][2]
Signs and symptoms
Typical symptoms of classic WN fever include fever, headaches and body aches.[3] Other symptoms include nausea and vomiting, and may include swollen lymph glands and rashes around the torso.
Neurological symptoms may also include tremor (80% or more of patients), muscle weakness, neck stiffness, stupor, coma, vision loss, numbness and flacid paralysis.[4] Neurological effects may be permanent. In the more serious cases, encephalitis and meningitis may occurr.
Transmission and Spread of West Nile virus
West Nile virus was first isolated in Uganda in 1937. Since then, there have been numerous epidemics of the virus in Israel (1950s),France (1962), South Africa (1974), and Romania (1996). Most recently, there were two epidemic outbreaks in 1999: One in Russia, and the second in the New York City area (NY99), where 62 people were infected and six died from the disease. <ref/Lanciotti, Robert S., Kerst, Amy J., Nasci, Roger S., et al. “Rapid Detection of West Nile Virus from Human Clinical Specimens, Field-Collected Mosquitoes, and Avian Samples by a TaqMan Reverse Transcriptase-PCR Assay”. Journal of Clinical Microbiology. Nov. 2000. Vol. 38, No. 11. p. 4066–4071.> The lineage of the NY99 strain of the WNV is though to be related to the strains found recently in North Africa, Romania, Kenya, Italy, and the Middle East.3 It first appeared in the Western hemisphere in 1999 in New York. The virus is primarily transmitted to humans by mosquitos. Birds serve as a natural reservoir, with humans, horses and other mammals acting as incidental, dead-end hosts. Although primarily transmitted by mosquitoes, the virus can be transmitted by blood transfusion and organ tranplantation, and pregnant women may pass the infection to their child via intrauterine delivery. West Nile virus infects at least 300 bird species, 60 mosquito species, and 30 animal species. Clinical symptoms track closely with the particular strain of the West Nile fever infection [5][6] and two major lineages have been described. Lineage II strains are found primarily in Africa and Madagascar while lineage I strains are widely distributed across North America, Europe and Africa.[7][8] Virus strains found in North America are particularly neuroinvasive. At present, no vaccines or antiviral agents exist for WNV and its spread can, therefore, not be stopped, but only slowed.
Virology and Molecular Biology West Nile virus
West Nile virus, a flavivirus (family Flaviviridae, genus Flavivirus), is a small, enveloped, single-stranded, positive-sense RNA virus. West Nile virus belongs to the Japanese encephalitis serocomplex (antigenic complex) of flaviviruses and is closely related to Japanese encephatitis virus, Kunjin virus, St. Louis encephalitis virus, Murray valley encephalitis virus, Usutus virus, Cacipacore virus, Koutango virus and Yaounde virus. The West Nile virus RNA encodes for the production of a polyprotein, which is then cleaved into ten proteins. Of these, three are structural proteins, the capsid protein, the membrane protein, and the envelope protein, which together encapsulate and protect the viral RNA by forming a viral particle about 50 nm in diameter. The viral particles multiply in tissue and lymphodes near the site of infection, and travel to the blood via lymphacytes. Viremia is detected early in the infection.
Prevention
As West Nile virus can be spread in blood products, screening donors may be effective.[9] Controlling mosquito populations may be the best preventative measure for controlling the spread of West Nile virus.
References
- ↑ CDC West Nile Virus Homepage. Retrieved on 2007-10-09.
- ↑ Petersen LR, Marfin AA (2002). "West Nile virus: a primer for the clinician". Ann. Intern. Med. 137 (3): 173–9. PMID 12160365. [e]
- ↑ Watson JT, Pertel PE, Jones RC, et al (2004). "Clinical characteristics and functional outcomes of West Nile Fever". Ann. Intern. Med. 141 (5): 360–5. PMID 15353427. [e]
- ↑ Sejvar JJ, Haddad MB, Tierney BC, et al (2003). "Neurologic manifestations and outcome of West Nile virus infection". JAMA 290 (4): 511–5. DOI:10.1001/jama.290.4.511. PMID 12876094. Research Blogging.
- ↑ Beasley DW, Li L, Suderman MT, Barrett AD (2002). "Mouse neuroinvasive phenotype of West Nile virus strains varies depending upon virus genotype". Virology 296 (1): 17–23. DOI:10.1006/viro.2002.1372. PMID 12036314. Research Blogging.
- ↑ Chambers TJ, Halevy M, Nestorowicz A, Rice CM, Lustig S (1998). "West Nile virus envelope proteins: nucleotide sequence analysis of strains differing in mouse neuroinvasiveness". J. Gen. Virol. 79 ( Pt 10): 2375–80. PMID 9780042. [e]
- ↑ Jia XY, Briese T, Jordan I, et al (1999). "Genetic analysis of West Nile New York 1999 encephalitis virus". Lancet 354 (9194): 1971–2. PMID 10622305. [e]
- ↑ Lanciotti RS, Roehrig JT, Deubel V, et al (1999). "Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States". Science 286 (5448): 2333–7. PMID 10600742. [e]
- ↑ Korves CT, Goldie SJ, Murray MB (2006). "Cost-effectiveness of alternative blood-screening strategies for West Nile Virus in the United States". PLoS Med. 3 (2): e21. DOI:10.1371/journal.pmed.0030021. PMID 16381598. Research Blogging.