West nile virus pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathogenesis

Transmission

The West Nile Virus is transmitted by the bite of a mosquito. Its life-cycle is based on a "bird-mosquito-bird transmission". Although the virus may have 65 species of mosquitos as natural hosts, only a few of those are capable of transmitting the virus among birds and humans. Those responsible for the viral transmission belong to different families, depending of the region of the US:[1]

  • Northern half of the United States - Culex pipiens
  • Southern states - Culex quinquefasciatus
  • Western states and overlapping areas of distribution of Culex pipiens and Culex quinquefasciatus - Culex tarsal is

Some birds behave as amplifier hosts. Particularly those of the order Passeriformes, develop high viral loads, that infect mosquitos that feed upod their blood.[2] Humans, on the other hand, behave as dead-end hosts since they do not develop high-level serum viremias to infect mosquitoes.[3][4]

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.[5]

In mammals the virus does not multiply as readily, and it is believed that mosquitoes biting infected mammals do not further transmit the virus,[6] 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,[7] or conjunctival exposure to infected blood.[8] The US outbreak revealed novel transmission methods, through blood transfusion,[9] organ transplant,[10] intrauterine exposure,[11] and breast feeding.[12] Since 2003 blood banks in the US routinely screen for the virus amongst their donors.[13] 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

  1. Petersen LR, Brault AC, Nasci RS (2013). "West Nile virus: review of the literature". JAMA. 310 (3): 308–15. doi:10.1001/jama.2013.8042. PMID 23860989.
  2. "Emerging Infectious Diseases".
  3. Zou S, Foster GA, Dodd RY, Petersen LR, Stramer SL (2010). "West Nile fever characteristics among viremic persons identified through blood donor screening". J Infect Dis. 202 (9): 1354–61. doi:10.1086/656602. PMID 20874087.
  4. Pealer LN, Marfin AA, Petersen LR, Lanciotti RS, Page PL, Stramer SL; et al. (2003). "Transmission of West Nile virus through blood transfusion in the United States in 2002". N Engl J Med. 349 (13): 1236–45. doi:10.1056/NEJMoa030969. PMID 14500806.
  5. 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
  6. 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
  7. CDC. "Laboratory-acquired West Nile virus infections - United States,2002." MMWR 2002c; 51: 1133-1135.
  8. 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.
  9. CDC. "Investigation of blood transfusion recipients with West Nile virus infections." MMWR 2002b; 51: 823.
  10. CDC. "West Nile virus infection in organ donor and transplant recipients - Georgia and Florida, 2002." MMWR 2002e; 51: 790.
  11. CDC. "Intrauterine West Nile virus infection - New York, 2002." MMWR 2002a; 51: 1135-1136.
  12. CDC. "Possible West Nile virus transmission to an infant through breast-feeding - Michigan, 2002." MMWR 2002d; 51: 877-878.
  13. CDC. "Detection of West Nile virus in blood donations - United States, 2003." MMWR 2003; 52: 769-772


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