West Nile virus: Difference between revisions

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{{Taxobox | color=violet
| name = ''West Nile virus
| virus_group = IV
| familia = ''[[Flaviviridae]]''
| genus = ''[[Flavivirus]]''
| sero_complex = Japanese encephalitis
| subdivision_ranks = Species
| subdivision =
* '''''West Nile virus, lineage 1'''''
* '''''West Nile virus, lineage 2'''''
}}
'''West Nile virus''' (WNV), may cause severe, persistent or fatal disease, although about 80% of infections are asymptomatic.  It is found throughout much of Asia, Europe, Africa, Australia 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.<ref>{{cite web |url=http://www.cdc.gov/ncidod/dvbid/westnile/ |title=CDC West Nile Virus Homepage |accessdate=2007-10-09 |format= |work=}}</ref><ref name="pmid12160365">{{cite journal |author=Petersen LR, Marfin AA |title=West Nile virus: a primer for the clinician |journal=Ann. Intern. Med. |volume=137 |issue=3 |pages=173–9 |year=2002 |pmid=12160365 |doi=|url=http://www.annals.org/cgi/content/full/137/3/173}}</ref>
==Signs and symptoms==
WNV is a neurotropic disease that attacks the central nervous system.  The virus has an incubation time ranging from 3 to 15 days. Though the virus has shown to cause mortality among varied species of birds, it appears that it may only cause mild to moderate flu-like symptoms in humans that become infected. However, this excludes the elderly or those with weak immune systems, such as HIV or cancer, allowing the virus to more easily penetrate the blood-brain barrier and they therefore more often present with severe cases of the neurological disease.1 Typical symptoms of classic WN fever include:
*fever
*headaches
*body aches <ref name="pmid15353427">{{cite journal |author=Watson JT, Pertel PE, Jones RC, ''et al'' |title=Clinical characteristics and functional outcomes of West Nile Fever |journal=Ann. Intern. Med. |volume=141 |issue=5 |pages=360–5 |year=2004 |pmid=15353427 |doi=}}</ref>
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.<ref name="pmid12876094">{{cite journal |author=Sejvar JJ, Haddad MB, Tierney BC, ''et al'' |title=Neurologic manifestations and outcome of West Nile virus infection |journal=JAMA |volume=290 |issue=4 |pages=511–5 |year=2003 |pmid=12876094 |doi=10.1001/jama.290.4.511}}</ref> Neurological effects may be permanent. In the more serious cases, [[encephalitis]] and [[meningitis]] may occur.
== Transmission and Spread of West Nile virus ==
== 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);the first time that the virus has appeared in the Western hemisphere.  In NYC, 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.</ref> 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.<ref name=Lanciotti> Lanciotti, R. S., Roehrig, J. T.,  Deubel, V., Smith, J., et al.  “Origin of the West Nile Virus Responsible for an Outbreak of Encephalitis in the Northeastern United States”.  ''Science''.  Dec, 1999.  Vol 286. p. 2333.</ref>  
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);the first time that the virus has appeared in the Western hemisphere.  In NYC, 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.</ref> 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.<ref name=Lanciotti> Lanciotti, R. S., Roehrig, J. T.,  Deubel, V., Smith, J., et al.  “Origin of the West Nile Virus Responsible for an Outbreak of Encephalitis in the Northeastern United States”.  ''Science''.  Dec, 1999.  Vol 286. p. 2333.</ref>  
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Clinical symptoms track closely with the particular strain of the West Nile fever infection <ref name="pmid12036314">{{cite journal |author=Beasley DW, Li L, Suderman MT, Barrett AD |title=Mouse neuroinvasive phenotype of West Nile virus strains varies depending upon virus genotype |journal=Virology |volume=296 |issue=1 |pages=17–23 |year=2002 |pmid=12036314 |doi=10.1006/viro.2002.1372}}</ref><ref name="pmid9780042">{{cite journal |author=Chambers TJ, Halevy M, Nestorowicz A, Rice CM, Lustig S |title=West Nile virus envelope proteins: nucleotide sequence analysis of strains differing in mouse neuroinvasiveness |journal=J. Gen. Virol. |volume=79 ( Pt 10) |issue= |pages=2375–80 |year=1998 |pmid=9780042 |doi=}}</ref> 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.<ref name="pmid10622305">{{cite journal |author=Jia XY, Briese T, Jordan I, ''et al'' |title=Genetic analysis of West Nile New York 1999 encephalitis virus |journal=Lancet |volume=354 |issue=9194 |pages=1971–2 |year=1999 |pmid=10622305 |doi=}}</ref><ref name="pmid10600742">{{cite journal |author=Lanciotti RS, Roehrig JT, Deubel V, ''et al'' |title=Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States |journal=Science |volume=286 |issue=5448 |pages=2333–7 |year=1999 |pmid=10600742 |doi=}}</ref> Virus strains found in North America are particularly neuroinvasive.  At present, no vaccines for humans or antiviral agents exist for WNV and its spread can, therefore, not be stopped, but only slowed. However, there are vaccines available for horses and birds. For now, recovery from the virus is dependant on the body’s own immune response and production of IgM antibodies.<ref> Nash,  Denis. “The Outbreak of West Nile Virus Infection in the New York City Area in 1999”. ''New England Journal of Medicine''.  June, 2001.  Vol. 344, No. 24. p. 1807-1814. </ref>
Clinical symptoms track closely with the particular strain of the West Nile fever infection <ref name="pmid12036314">{{cite journal |author=Beasley DW, Li L, Suderman MT, Barrett AD |title=Mouse neuroinvasive phenotype of West Nile virus strains varies depending upon virus genotype |journal=Virology |volume=296 |issue=1 |pages=17–23 |year=2002 |pmid=12036314 |doi=10.1006/viro.2002.1372}}</ref><ref name="pmid9780042">{{cite journal |author=Chambers TJ, Halevy M, Nestorowicz A, Rice CM, Lustig S |title=West Nile virus envelope proteins: nucleotide sequence analysis of strains differing in mouse neuroinvasiveness |journal=J. Gen. Virol. |volume=79 ( Pt 10) |issue= |pages=2375–80 |year=1998 |pmid=9780042 |doi=}}</ref> 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.<ref name="pmid10622305">{{cite journal |author=Jia XY, Briese T, Jordan I, ''et al'' |title=Genetic analysis of West Nile New York 1999 encephalitis virus |journal=Lancet |volume=354 |issue=9194 |pages=1971–2 |year=1999 |pmid=10622305 |doi=}}</ref><ref name="pmid10600742">{{cite journal |author=Lanciotti RS, Roehrig JT, Deubel V, ''et al'' |title=Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States |journal=Science |volume=286 |issue=5448 |pages=2333–7 |year=1999 |pmid=10600742 |doi=}}</ref> Virus strains found in North America are particularly neuroinvasive.  At present, no vaccines for humans or antiviral agents exist for WNV and its spread can, therefore, not be stopped, but only slowed. However, there are vaccines available for horses and birds. For now, recovery from the virus is dependant on the body’s own immune response and production of IgM antibodies.<ref> Nash,  Denis. “The Outbreak of West Nile Virus Infection in the New York City Area in 1999”. ''New England Journal of Medicine''.  June, 2001.  Vol. 344, No. 24. p. 1807-1814. </ref>
== 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, with a genome of 11,029 neucleotide bases.  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. 
Within the virus genome there is a 5’ noncoding region of 96 nucleotide bases, followed by an ATG initiation codon, and then a single open reading frame of 10,302 nucleotides. Within this reading frame, 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 other seven encoded proteins are nonstructural.  The genome is then completed by a 3’ noncoding region of 631 nucleotide bases. 3
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.<ref name="pmid16381598">{{cite journal |author=Korves CT, Goldie SJ, Murray MB |title=Cost-effectiveness of alternative blood-screening strategies for West Nile Virus in the United States |journal=PLoS Med. |volume=3 |issue=2 |pages=e21 |year=2006 |pmid=16381598 |doi=10.1371/journal.pmed.0030021}}</ref>  Controlling mosquito populations may be the best preventative measure for controlling the spread of West Nile virus.
== References ==
<references/>
==External links==
[http://www.cdc.gov/ncidod/dvbid/westnile/ CDC summary]==Signs and symptoms==

Revision as of 19:13, 7 May 2009

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);the first time that the virus has appeared in the Western hemisphere. In NYC, 62 people were infected and six died from the disease. [1] 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.[2]

It is not yet known how the virus was introduced to the US, though it has been hypothesized that the cases found in the US can be attributed to the strain of the WNV that had been spreading in the Mediterranean region since 1998.[2] Since the initial outbreak in 1999, there have been 23,975 reported human cases by the CDC of the virus and 962 deaths around the world through 2006.[3]

The virus is primarily transmitted to humans by the Culex pipiens and Culex. quinquefasciatus species of mosquitoes . Birds serve as a natural reservoir, with humans, horses and other mammals acting as incidental, dead-end hosts. Although primarily transmitted to humans by mosquitoes, the virus can be transmitted from human to human by blood transfusion, organ tranplantation, and by 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. After research was conducted on the species of mosquitoes that carry the virus, scientists claimed that the rapid spread may be due to the hybridization of the Culex pipiens species of mosquitoes. It is believed by some researchers that the mosquitoes in Europe feast on either humans or animals, but not both, thereby limiting the spread of the virus. They hypothesis that the hybridization of US mosquitoes has led to their feasting of both humans and animals, and allows for the spread of the virus from species to species.[4]

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 for humans or antiviral agents exist for WNV and its spread can, therefore, not be stopped, but only slowed. However, there are vaccines available for horses and birds. For now, recovery from the virus is dependant on the body’s own immune response and production of IgM antibodies.[9]

  1. ↑ 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.
  2. ↑ 2.0 2.1 Lanciotti, R. S., Roehrig, J. T., Deubel, V., Smith, J., et al. “Origin of the West Nile Virus Responsible for an Outbreak of Encephalitis in the Northeastern United States”. Science. Dec, 1999. Vol 286. p. 2333.
  3. ↑ Grinev, Andriyan. “Genetic Variability of West Nile Virus in US Blood Donors, 2002–2005”. Emerging Infectious Diseases- www.cdc.gov/eid. March 2008. Vol. 14, No. 3. p. 436-444.
  4. ↑ Couzin, Jennifer. “Hybrid Mosquitoes Suspected in West Nile Virus Spread”. Science. Mar, 2004. Vol 303. p. 1451.
  5. ↑ 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.
  6. ↑ 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]
  7. ↑ 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]
  8. ↑ 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]
  9. ↑ Nash, Denis. “The Outbreak of West Nile Virus Infection in the New York City Area in 1999”. New England Journal of Medicine. June, 2001. Vol. 344, No. 24. p. 1807-1814.
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