West nile virus pathophysiology: Difference between revisions

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{{West nile virus}}
{{CMG}}
==Overview==
==Pathogenesis==
==Pathogenesis==
Following inoculation, replication of WNV takes place in Langerhans epidermal dendritic cells, which are antigen-presenting immune cells.<ref name="pmid11564180">{{cite journal| author=Byrne SN, Halliday GM, Johnston LJ, King NJ| title=Interleukin-1beta but not tumor necrosis factor is involved in West Nile virus-induced Langerhans cell migration from the skin in C57BL/6 mice. | journal=J Invest Dermatol | year= 2001 | volume= 117 | issue= 3 | pages= 702-9 | pmid=11564180 | doi=10.1046/j.0022-202x.2001.01454.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11564180 }} </ref> These cells then migrate to lymph nodes, resulting in lymph node drainage, followed by viremia and dissemination of the virus into other organs, namely the spleen and the kidneys. Within one week, the virus is successfully cleared from serum and tissue compartments among immunocompetent individuals. Interferons (IFN) have a crucial role in upregulating genes that carry antiviral functions and in stimulating the maturation of dendritic cells that eventually combine both the innate and the adaptive immune responses.<ref name="pmid15795237">{{cite journal| author=Asselin-Paturel C, Brizard G, Chemin K, Boonstra A, O'Garra A, Vicari A et al.| title=Type I interferon dependence of plasmacytoid dendritic cell activation and migration. | journal=J Exp Med | year= 2005 | volume= 201 | issue= 7 | pages= 1157-67 | pmid=15795237 | doi=10.1084/jem.20041930 | pmc=PMC2213121 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15795237  }} </ref> Viral sensors, such as Toll-like receptor 3, help in activation of transcription factors and IFN-stimulated genes.<ref name="pmid12719735">{{cite journal| author=Barton GM, Medzhitov R| title=Linking Toll-like receptors to IFN-alpha/beta expression. | journal=Nat Immunol | year= 2003 | volume= 4 | issue= 5 | pages= 432-3 | pmid=12719735 | doi=10.1038/ni0503-432 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12719735 }} </ref><ref name="pmid16973548">{{cite journal| author=Keller BC, Fredericksen BL, Samuel MA, Mock RE, Mason PW, Diamond MS et al.| title=Resistance to alpha/beta interferon is a determinant of West Nile virus replication fitness and virulence. | journal=J Virol | year= 2006 | volume= 80 | issue= 19 | pages= 9424-34 | pmid=16973548 | doi=10.1128/JVI.00768-06 | pmc=PMC1617238 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16973548 }} </ref> Similarly, complement activation through classical, lectin, and alternative pathways offers significant immunity against WNV by opsonization, cytolysis, and chemotaxis. Finally, innate immune cells, such as macrophages, along with humoral, primary, and memory adaptive immune cells are also activated during viral infection. These cells also contribute to the clearance of the virus and the prevention of its dissemination to the CNS.<ref name="pmid16973541">{{cite journal| author=Samuel MA, Diamond MS| title=Pathogenesis of West Nile Virus infection: a balance between virulence, innate and adaptive immunity, and viral evasion. | journal=J Virol | year= 2006 | volume= 80 | issue= 19 | pages= 9349-60 | pmid=16973541 | doi=10.1128/JVI.01122-06 | pmc=PMC1617273 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16973541  }} </ref>
===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:<ref name="pmid23860989">{{cite journal| author=Petersen LR, Brault AC, Nasci RS| title=West Nile virus: review of the literature. | journal=JAMA | year= 2013 | volume= 310 | issue= 3 | pages= 308-15 | pmid=23860989 | doi=10.1001/jama.2013.8042 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23860989 }} </ref>
* 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.<ref name=CDC>{{cite web | title = Emerging Infectious Diseases | url = http://wwwnc.cdc.gov/eid/article/9/3/02-0628_article }}</ref> Humans, on the other hand, behave as '''dead-end hosts''' since they do not develop high-level serum [[viremia]]s to infect mosquitoes.<ref name="pmid20874087">{{cite journal| author=Zou S, Foster GA, Dodd RY, Petersen LR, Stramer SL| title=West Nile fever characteristics among viremic persons identified through blood donor screening. | journal=J Infect Dis | year= 2010 | volume= 202 | issue= 9 | pages= 1354-61 | pmid=20874087 | doi=10.1086/656602 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20874087 }} </ref><ref name="pmid14500806">{{cite journal| author=Pealer LN, Marfin AA, Petersen LR, Lanciotti RS, Page PL, Stramer SL et al.| title=Transmission of West Nile virus through blood transfusion in the United States in 2002. | journal=N Engl J Med | year= 2003 | volume= 349 | issue= 13 | pages= 1236-45 | pmid=14500806 | doi=10.1056/NEJMoa030969 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14500806 }} </ref>
 
==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==
{{reflist|2}}


Mice models have demonstrated that persistent infection, including CNS infiltration, is possible, especially in immunosuppressed states with deficient immunity. TNF-alpha has been hypothesized to allow viral crossing of the blood-brain barrier (BBB) by promoting endothelial cell permeability.<ref name="pmid14662909">{{cite journal| author=Diamond MS, Sitati EM, Friend LD, Higgs S, Shrestha B, Engle M| title=A critical role for induced IgM in the protection against West Nile virus infection. | journal=J Exp Med | year= 2003 | volume= 198 | issue= 12 | pages= 1853-62 | pmid=14662909 | doi=10.1084/jem.20031223 | pmc=PMC2194144 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14662909  }} </ref><ref name="pmid16227257">{{cite journal| author=Samuel MA, Diamond MS| title=Alpha/beta interferon protects against lethal West Nile virus infection by restricting cellular tropism and enhancing neuronal survival. | journal=J Virol | year= 2005 | volume= 79 | issue= 21 | pages= 13350-61 | pmid=16227257 | doi=10.1128/JVI.79.21.13350-13361.2005 | pmc=PMC1262587 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16227257  }} </ref><ref name="pmid15558055">{{cite journal| author=Wang T, Town T, Alexopoulou L, Anderson JF, Fikrig E, Flavell RA| title=Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis. | journal=Nat Med | year= 2004 | volume= 10 | issue= 12 | pages= 1366-73 | pmid=15558055 | doi=10.1038/nm1140 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15558055  }} </ref> Other reports showed that the virus may cross the BBB either by using the olfactory bulb in a "Trojan horse" mechanism to cross to the CNS, or utilizing passive transport mechanisms, or follow a retrograde transport mechanism from peripheral neurons.<ref name="pmid15885841">{{cite journal| author=Kramer-Hämmerle S, Rothenaigner I, Wolff H, Bell JE, Brack-Werner R| title=Cells of the central nervous system as targets and reservoirs of the human immunodeficiency virus. | journal=Virus Res | year= 2005 | volume= 111 | issue= 2 | pages= 194-213 | pmid=15885841 | doi=10.1016/j.virusres.2005.04.009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885841  }} </ref><ref name="pmid6300550">{{cite journal| author=Monath TP, Cropp CB, Harrison AK| title=Mode of entry of a neurotropic arbovirus into the central nervous system. Reinvestigation of an old controversy. | journal=Lab Invest | year= 1983 | volume= 48 | issue= 4 | pages= 399-410 | pmid=6300550 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6300550  }} </ref><ref name="pmid16310859">{{cite journal| author=Garcia-Tapia D, Loiacono CM, Kleiboeker SB| title=Replication of West Nile virus in equine peripheral blood mononuclear cells. | journal=Vet Immunol Immunopathol | year= 2006 | volume= 110 | issue= 3-4 | pages= 229-44 | pmid=16310859 | doi=10.1016/j.vetimm.2005.10.003 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16310859  }} </ref>
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===Genetics===
[[Category:Disease]]
Genetic factors may be associated with WNV susceptibility. In mice strains, a truncated isoform mutation of the gene encoding OAS1b may lead to susceptibility of infections by WNV and other flaviviruses. Similarly, human subjects with ''CCR5-Δ32'', a mutant allele of the gene encoding chemokine receptor, were found to be more likely to be symptomatic with worse WNV symptoms. Nonetheless, the true role of genetics in the susceptibility and resistance to WNV is yet to be elucidated.<ref name="pmid16418398">{{cite journal| author=Glass WG, McDermott DH, Lim JK, Lekhong S, Yu SF, Frank WA et al.| title=CCR5 deficiency increases risk of symptomatic West Nile virus infection. | journal=J Exp Med | year= 2006 | volume= 203 | issue= 1 | pages= 35-40 | pmid=16418398 | doi=10.1084/jem.20051970 | pmc=PMC2118086 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16418398  }} </ref><ref name="pmid16235172">{{cite journal| author=Yakub I, Lillibridge KM, Moran A, Gonzalez OY, Belmont J, Gibbs RA et al.| title=Single nucleotide polymorphisms in genes for 2'-5'-oligoadenylate synthetase and RNase L inpatients hospitalized with West Nile virus infection. | journal=J Infect Dis | year= 2005 | volume= 192 | issue= 10 | pages= 1741-8 | pmid=16235172 | doi=10.1086/497340 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16235172  }} </ref>
[[Category:Infectious disease]]
[[Category:Neurology]]

Revision as of 05:55, 11 September 2014


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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