West nile virus pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | |||
WNV is a member of the family Flaviviridae (genus Flavivirus). Serologically, it is a member of the Japanese encephalitis virus antigenic complex, which includes St. Louis, Japanese, Kunjin, and Murray Valley encephalitis viruses. WNV was first isolated in the WN province of Uganda in 1937. Human and equine outbreaks have been recorded in portions of Africa, southern | |||
Europe, North America, and Asia. Although it is still not known when or how WNV was introduced into North America, international travel of infected persons to New York, importation of infected birds or mosquitoes, or migration of infected birds are all possibilities. | |||
[http://www.cdc.gov/ncidod/dvbid/westnile/resources/wnv-guidelines-aug-2003.pdf] | |||
The virus is transmitted through mosquito vectors, which bite and infect birds. The birds are amplifying hosts, developing sufficient viral levels to transmit the infection to other biting mosquitoes which go on to infect other birds (in the [[Western hemisphere]] the [[American robin]] and the [[American crow]] are the most common carriers) and also humans. The infected mosquito species vary according to geographical area; in the US ''Culex pipiens'' (Eastern US), ''Culex tarsalis'' (Midwest and West), and ''Culex quinquefasciatus'' (Southeast) are the main sources.<ref>Hayes E B, Komar N, Nasci R S, Montgomery S P, Oleary D R, Campbell G L. "Epidemiology and transmission dynamics of West Nile virus disease." ''Emerging Infectious Diseases Journal'' 2005a; 11: 1167-1173</ref> | |||
In mammals the virus does not multiply as readily, and it is believed that mosquitoes biting infected mammals do not further transmit the virus,<ref>Taylor R M, Hurlbut H S, Dressler H R, Spangler E W, Thrasher D. "Isolation of West Nile virus from ''Culex'' mosquitoes." ''Journal of the Egyptian Medical Association'' 1953; 36: 199-208</ref> making mammals so-called dead-end infections. | |||
A 2004 paper in ''Science'' found that ''Culex pipiens'' mosquitoes existed in two populations in [[Europe]], one which bites birds and one which bites humans. In North America 40% of ''Culex pipiens'' were found to be hybrids of the two types which bite both birds and humans, providing a vector for West Nile virus. This is thought to provide an explanation of why the West Nile disease has spread more quickly in North America than Europe. | |||
It was initially believed that direct human-to-human transmission was only caused by occupational exposure,<ref>CDC. "Laboratory-acquired West Nile virus infections - United States,2002." ''MMWR'' 2002c; 51: 1133-1135.</ref> or conjunctival exposure to infected blood.<ref>Fonseca K, Prince G D, Bratvold J, Fox J D, Pybus M, Preksaitis J K, Tilley P. "West Nile virus infection and conjunctival exposure." ''Emerging Infectious Diseases Journal'' 3005; 11: 1648-1649.</ref> The US outbreak revealed novel transmission methods, through blood transfusion,<ref>CDC. "Investigation of blood transfusion recipients with West Nile virus infections." ''MMWR'' 2002b; 51: 823.</ref> organ transplant,<ref>CDC. "West Nile virus infection in organ donor and transplant recipients - Georgia and Florida, 2002." ''MMWR'' 2002e; 51: 790.</ref> intrauterine exposure,<ref>CDC. "Intrauterine West Nile virus infection - New York, 2002." ''MMWR'' 2002a; 51: 1135-1136.</ref> and breast feeding.<ref>CDC. "Possible West Nile virus transmission to an infant through breast-feeding - Michigan, 2002." ''MMWR'' 2002d; 51: 877-878.</ref> Since 2003 blood banks in the US routinely screen for the virus amongst their donors.<ref>CDC. "Detection of West Nile virus in blood donations - United States, 2003." ''MMWR'' 2003; 52: 769-772</ref> As a precautionary measure, the UK's [[National Blood Service]] runs a test for this disease in donors who donate within 28 days of a visit to the United States or [[Canada]]. | |||
==References== | ==References== | ||
Revision as of 19:25, 2 February 2012
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
WNV is a member of the family Flaviviridae (genus Flavivirus). Serologically, it is a member of the Japanese encephalitis virus antigenic complex, which includes St. Louis, Japanese, Kunjin, and Murray Valley encephalitis viruses. WNV was first isolated in the WN province of Uganda in 1937. Human and equine outbreaks have been recorded in portions of Africa, southern Europe, North America, and Asia. Although it is still not known when or how WNV was introduced into North America, international travel of infected persons to New York, importation of infected birds or mosquitoes, or migration of infected birds are all possibilities. [2] The virus is transmitted through mosquito vectors, which bite and infect birds. The birds are amplifying hosts, developing sufficient viral levels to transmit the infection to other biting mosquitoes which go on to infect other birds (in the Western hemisphere the American robin and the American crow are the most common carriers) and also humans. The infected mosquito species vary according to geographical area; in the US Culex pipiens (Eastern US), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main sources.[1]
In mammals the virus does not multiply as readily, and it is believed that mosquitoes biting infected mammals do not further transmit the virus,[2] making mammals so-called dead-end infections.
A 2004 paper in Science found that Culex pipiens mosquitoes existed in two populations in Europe, one which bites birds and one which bites humans. In North America 40% of Culex pipiens were found to be hybrids of the two types which bite both birds and humans, providing a vector for West Nile virus. This is thought to provide an explanation of why the West Nile disease has spread more quickly in North America than Europe.
It was initially believed that direct human-to-human transmission was only caused by occupational exposure,[3] or conjunctival exposure to infected blood.[4] The US outbreak revealed novel transmission methods, through blood transfusion,[5] organ transplant,[6] intrauterine exposure,[7] and breast feeding.[8] Since 2003 blood banks in the US routinely screen for the virus amongst their donors.[9] As a precautionary measure, the UK's National Blood Service runs a test for this disease in donors who donate within 28 days of a visit to the United States or Canada.
References
- ↑ Hayes E B, Komar N, Nasci R S, Montgomery S P, Oleary D R, Campbell G L. "Epidemiology and transmission dynamics of West Nile virus disease." Emerging Infectious Diseases Journal 2005a; 11: 1167-1173
- ↑ Taylor R M, Hurlbut H S, Dressler H R, Spangler E W, Thrasher D. "Isolation of West Nile virus from Culex mosquitoes." Journal of the Egyptian Medical Association 1953; 36: 199-208
- ↑ CDC. "Laboratory-acquired West Nile virus infections - United States,2002." MMWR 2002c; 51: 1133-1135.
- ↑ Fonseca K, Prince G D, Bratvold J, Fox J D, Pybus M, Preksaitis J K, Tilley P. "West Nile virus infection and conjunctival exposure." Emerging Infectious Diseases Journal 3005; 11: 1648-1649.
- ↑ CDC. "Investigation of blood transfusion recipients with West Nile virus infections." MMWR 2002b; 51: 823.
- ↑ CDC. "West Nile virus infection in organ donor and transplant recipients - Georgia and Florida, 2002." MMWR 2002e; 51: 790.
- ↑ CDC. "Intrauterine West Nile virus infection - New York, 2002." MMWR 2002a; 51: 1135-1136.
- ↑ CDC. "Possible West Nile virus transmission to an infant through breast-feeding - Michigan, 2002." MMWR 2002d; 51: 877-878.
- ↑ CDC. "Detection of West Nile virus in blood donations - United States, 2003." MMWR 2003; 52: 769-772