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Editing West nile virus historical perspective


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.

Overview

WNV was first isolated in 1937 in Uganda from a hospitalized patient who presented with isolated fever. Between 1950 and 1960, small villages in the Mediterranean basin had repeated outbreaks, especially in Israel and Egypt. These outbreaks allowed researchers to study the molecular and clinical features of the disease and further understand its mode of transmission and natural history. Several WNV outbreaks were recorded in the second half of the 20th century in Europe, Middle East, Far East, and Africa. It was not until 1999 when the first WNV outbreak was documented in USA, making WNV a worldwide infection. Perhaps the most severe outbreak documented was in 2002 in USA, recording the highest number of meningoencephalitis from a single WNV outbreak. The first description of a person-to-person transmission was reported in 2002 among patients with blood transfusions and tissue transplantation.

Discovery

WNV was first discovered following its isolation in 1937 from a hospitalized patient presenting with isolated fever in the West Nile district of Northern Uganda.[1] Initial reports described a virus whose physical and pathological characteristics resemble that of St. Louis encephalitis virus and Japanese B encephalitis virus. Early studies noted the frequent involvement of the CNS among infected patients, suggesting neurotropism of the virus. It was not until the 1950-1960 Mediterranean basin outbreaks in small towns that clinical and pathological features of West Nile virus were really revealed.

Famous outbreaks

The first epidemic was documented in 1951 in Isreal, when Bernkopf and colleagues isolated WNV among 123 cases.[2][3] Further understanding of the viral pattern, mode of transmission, and pathogenesis was conducted by studies in 1951-1954 following outbreaks in Cairo, Egypt.[2][4][5] The first report of neurological sequelae following WNV infection was documented in 1957 during an outbreak in Israel.[1] Other outbreaks in other regions, such as Europe, India, South Africa, were later described in the 1970s and 1980s.[1] In 1996, an outbreak of WNV in Romania in Europe spiraled a series of outbreaks in the Middle East, North Africa, and Europe region.[6][7] Unlike early reports that mostly included children, these outbreaks unveiled adult preponderance and an increased rate of CNS complications associated with the disease.[6][7]

In 1999, the first outbreak in USA initially described 8 cases, most of which had neurological symptoms, in Queens, New York City.[8] The 1999 outbreak in USA finally marked the global spread of the virus. The outbreak eventually infected a total of 62 individuals, whose symptoms were mostly severe and necessitated hospitalization. Although initially believed to be caused by an endemic arbovirus, WNV was eventually demonstrated to be the agent responsible for the outbreak after the discovery of a coinciding outbreak among infected birds within the same geographical region and during the same time frame[9][10][11][12][13] Only 3 years after its documented presence in USA, the clinically most severe WNV outbreak occurred in North America in 2002, where the largest number of meningoencephalitis from a single outbreak was recorded. In the same year, the first human-to-human transmission was discovered; it was attributed to transmission via blood transfusion and tissue transplantation.[14]

Development of diagnostic and treatment strategies

  • The first WNV MAC-ELISA-based commercial diagnostic test for arboviruses was also developed and later commercialized to assays that may be used in the field.[15]
  • Following the 1999 outbreak in USA, the first animal vaccine was developed and later approved by the U.S. department of agriculture (USDA). The WNV-DNA virus is considered the only USDA-approved vaccine.[15][16]

Impact on cultural history

  • The 1999 outbreak in New York in USA drove the Center of Disease Control (CDC) to fund its own Zoo Surveillance Program at Cornell University School of Veterinary Medicine. During the outbreak, CDC assigned other channels to test infected bird species that might help in identifying the virus. The delay in diagnosis was presumed to be a significant element for the outbreak's detrimental outcomes.[17]
  • Following the 1999 outbreak, WNV was considered a nationally reportable disease in USA. Annual meetings were held in USA to provide public health information about WNV, and guidelines for surveillance, prevention, and control of WNV were developed and frequently updated.[15]
  • ArboNET, a real-time disease reporting network developed by CDC, was first launched in 2000 after the 1999 outbreak to follow WNV disease in humans and animals.[15]
  • Funding to the CDC - Enhanced Laboratory Capacity (ELC) cooperative agreement program reached $2.7 million dollars in 2000. In a few years, the program's funding was higher than $20 million dollars. Grants were utilized to train arbovirologists and to fund research programs, lab diagnosis, and surveillance programs.[15]

References

  1. ↑ 1.0 1.1 1.2 Sejvar JJ (2003). dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21765761 "West nile virus: an historical overview" Check |url= value (help). Ochsner J. 5 (3): 6–10. PMC 3111838. PMID 21765761.
  2. ↑ 2.0 2.1 Murgue B, Murri S, Triki H, Deubel V, Zeller HG (2001). "West Nile in the Mediterranean basin: 1950-2000". Ann N Y Acad Sci. 951: 117–26. PMID 11797769.
  3. ↑ Bernkopf H, Levine S, Nerson R (1953). "Isolation of West Nile virus in Israel". J Infect Dis. 7: 128–132.
  4. ↑ HURLBUT HS, RIZK F, TAYLOR RM, WORK TH (1956). "A study of the ecology of West Nile virus in Egypt". Am J Trop Med Hyg. 5 (4): 579–620. PMID 13354882.
  5. ↑ Philip CB, Samdel JE (1943). "Transmission of West Nile virus by infected Aedes albopictus". Proc Soc Exp Biol Med. 53: 49–50.
  6. ↑ 6.0 6.1 Tsai TF, Popovici F, Cernescu C, Campbell GL, Nedelcu NI (1998). "West Nile encephalitis epidemic in southeastern Romania". Lancet. 352 (9130): 767–71. PMID 9737281.
  7. ↑ 7.0 7.1 Campbell GL, Ceianu CS, Savage HM (2001). "Epidemic West Nile encephalitis in Romania: waiting for history to repeat itself". Ann N Y Acad Sci. 951: 94–101. PMID 11797808.
  8. ↑ Nash D, Mostashari F, Fine A, Miller J, O'Leary D, Murray K; et al. (2001). "The outbreak of West Nile virus infection in the New York City area in 1999". N Engl J Med. 344 (24): 1807–14. doi:10.1056/NEJM200106143442401. PMID 11407341.
  9. ↑ Giladi M, Metzkor-Cotter E, Martin DA, Siegman-Igra Y, Korczyn AD, Rosso R; et al. (2001). "West Nile encephalitis in Israel, 1999: the New York connection". Emerg Infect Dis. 7 (4): 659–61. doi:10.3201/eid0704.010410. PMC 2631756. PMID 11585528.
  10. ↑ Briese T, Jia XY, Huang C, Grady LJ, Lipkin WI (1999). "Identification of a Kunjin/West Nile-like flavivirus in brains of patients with New York encephalitis". Lancet. 354 (9186): 1261–2. PMID 10520637.
  11. ↑ Jia XY, Briese T, Jordan I, Rambaut A, Chi HC, Mackenzie JS; et al. (1999). "Genetic analysis of West Nile New York 1999 encephalitis virus". Lancet. 354 (9194): 1971–2. PMID 10622305.
  12. ↑ Lanciotti RS, Roehrig JT, Deubel V, Smith J, Parker M, Steele K; 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.
  13. ↑ Weiss D, Carr D, Kellachan J, Tan C, Phillips M, Bresnitz E; et al. (2001). "Clinical findings of West Nile virus infection in hospitalized patients, New York and New Jersey, 2000". Emerg Infect Dis. 7 (4): 654–8. doi:10.3201/eid0704.010409. PMC 2631758. PMID 11589170.
  14. ↑ Charatan F (2002). "Organ transplants and blood transfusions may transmit West Nile virus". BMJ. 325 (7364): 566. PMC 1169473. PMID 12228130.
  15. ↑ 15.0 15.1 15.2 15.3 15.4 Roehrig JT (2013). "West nile virus in the United States - a historical perspective". Viruses. 5 (12): 3088–108. doi:10.3390/v5123088. PMC 3967162. PMID 24335779.
  16. ↑ Davis BS, Chang GJ, Cropp B, Roehrig JT, Martin DA, Mitchell CJ; et al. (2001). "West Nile virus recombinant DNA vaccine protects mouse and horse from virus challenge and expresses in vitro a noninfectious recombinant antigen that can be used in enzyme-linked immunosorbent assays". J Virol. 75 (9): 4040–7. doi:10.1128/JVI.75.9.4040-4047.2001. PMC 114149. PMID 11287553.
  17. ↑ Knight J (2002). "US zoos keep watch for cross-species killer". Nature. 417 (6888): 477. doi:10.1038/417477a. PMID 12037534.


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References


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West nile virus pathophysiology


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.

Overview

The natural reservoir of West Nile virus (WNV) is birds, particularly species with high-level viremia. In contrast, viremia is relatively rare among infected humans, who are considered dead-end hosts of the virus. WNV is transmitted by bites of various species of mosquitoes. Following inoculation, replication of the virus occurs in the Langerhans epidermal dendritic cell. Among immunocompetent hosts, the replication process is immediately followed by activation of the immune system, including complement pathways, and humoral and adaptive immune responses that act simultaneously to clear the infection. On the other hand, immunocompromised patients may suffer CNS dissemination and fatal outcomes due to the failure to activate proper immunological pathways. Finally, the role of genetics in WNV susceptibility is not fully understood; but mice models and a few human experiments have described genetic mutations that may predispose individuals to worse clinical disease of WNV infections.

West Nile virus life cycle

The West Nile virus has an enzootic life cycle, being primarily transmitted between some species of birds and different species of mosquito vectors.[1]

West Nile virus life cycle- Center for Disease Control and Prevention(CDC)[2]

Transmission

Birds are the main reservoir of West Nile virus (WNV). Transmission of the virus is by a mosquito bite of an infected bird with high-level viremia, such as birds of the family Passeriformes.[2] Thus, transmission is frequently denoted as "bird-mosquito-bird" transmission. Other forms of transmission have been speculated, such as direct bird-to-bird transmission, but further validation is still required.[3] Other species may also be infected, such as horses, cats, and dogs. Humans are considered dead-end hosts because the disease rarely progresses to viremia in humans, making transmission of the virus from a human unlikely except in some reported cases of transmission by blood transfusion, breastfeeding, or organ transplantation.[4][5][6]

Mosquitoes responsible for viral transmission belong to different families, varying based on geographical location:[7]

  • Culex pipiens: Northern half and West of USA
  • Culex quinquefasciatus: Southeast and West of USA
  • Culex tarsalis: West of USA
Approximate geographic distribution of the primary WNV vectors, Cx. pipiens, Cx. quinquefasciatus and Cx. tarsalis- Center for Disease Control and Prevention(CDC)[2]

Other transmission routes, not involving vectors, have also been described:[1]

Pathogenesis

Following inoculation, replication of WNV takes place in the Langerhans epidermal dendritic cells, which are antigen-presenting immune cells.[10] 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 the 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.[11] Viral sensors, such as Toll-like receptor 3, help in activation of transcription factors and IFN-stimulated genes.[12][13] Additionally, complement activation through classical, lectin, and alternative pathways offers significant immunity against WNV by opsonization, cytolysis, and chemotaxis. 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.[14]

Mice models have demonstrated that persistent infection, including CNS infiltration, is possible, especially in immunosuppressed states. TNF-alpha has been hypothesized to allow viral migration across the blood-brain barrier (BBB) by promoting the permeability of endothelial cell.[15][16][17] 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 following a retrograde transport mechanism from peripheral neurons.[18][19][20]

Tropism

WNV may be disseminated to include all organ systems. Animal models demonstrated that WNV infection typically first appears in the lymphatic tissue and the spleen before it migrates to other organs, namely the kidneys, lungs, liver, the cardiovascular system, and the nervous system.[21] In animals, tropism of WNV has been described in the following organs:

  • Eyes
  • Peripheral and central nervous system
  • Heart
  • Blood vessels
  • Spleen and other lymphoid organs
  • Liver
  • Kidneys
  • Lungs
  • GI tract
  • Endocrine system, including gonads
  • Skeletal muscles
  • Skin
  • Bone marrow

Genetics

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 more likely to be symptomatic with worse WNV clinical disease. Nonetheless, the true role of genetics in the susceptibility and resistance to WNV is yet to be elucidated.[22][23]

References

  1. ↑ 1.0 1.1 Campbell, Grant L; Marfin, Anthony A; Lanciotti, Robert S; Gubler, Duane J (2002). "West Nile virus". The Lancet Infectious Diseases. 2 (9): 519–529. doi:10.1016/S1473-3099(02)00368-7. ISSN 1473-3099.
  2. ↑ 2.0 2.1 2.2 2.3 "Center for Disease Control and Prevention (CDC)".
  3. ↑ Komar N, Langevin S, Hinten S, Nemeth N, Edwards E, Hettler D; et al. (2003). ; "Experimental infection of North American birds with the New York 1999 strain of West Nile virus" Check |url= value (help). Emerg Infect Dis. 9 (3): 311–22. doi:10.3201/eid0903.020628. PMC 2958552. PMID 12643825.
  4. ↑ Iwamoto M, Jernigan DB, Guasch A, Trepka MJ, Blackmore CG, Hellinger WC; et al. (2003). ; "Transmission of West Nile virus from an organ donor to four transplant recipients" Check |url= value (help). N Engl J Med. 348 (22): 2196–203. doi:10.1056/NEJMoa022987. PMID 12773646.
  5. ↑ 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" Check |url= value (help). N Engl J Med. 349 (13): 1236–45. doi:10.1056/NEJMoa030969. PMID 14500806.
  6. ↑ Centers for Disease Control and Prevention (CDC) (2002). ; "Possible West Nile virus transmission to an infant through breast-feeding--Michigan, 2002" Check |url= value (help). MMWR Morb Mortal Wkly Rep. 51 (39): 877–8. PMID 12375687.
  7. ↑ Petersen LR, Brault AC, Nasci RS (2013). ; "West Nile virus: review of the literature" Check |url= value (help). JAMA. 310 (3): 308–15. doi:10.1001/jama.2013.8042. PMID 23860989.
  8. ↑ 8.0 8.1 8.2 "Investigations of West Nile Virus Infections in Recipients of Organ Transplantation and Blood Transfusion".
  9. ↑ Iwamoto, Martha; Jernigan, Daniel B.; Guasch, Antonio; Trepka, Mary Jo; Blackmore, Carina G.; Hellinger, Walter C.; Pham, Si M.; Zaki, Sherif; Lanciotti, Robert S.; Lance-Parker, Susan E.; DiazGranados, Carlos A.; Winquist, Andrea G.; Perlino, Carl A.; Wiersma, Steven; Hillyer, Krista L.; Goodman, Jesse L.; Marfin, Anthony A.; Chamberland, Mary E.; Petersen, Lyle R. (2003). "Transmission of West Nile Virus from an Organ Donor to Four Transplant Recipients". New England Journal of Medicine. 348 (22): 2196–2203. doi:10.1056/NEJMoa022987. ISSN 0028-4793.
  10. ↑ Byrne SN, Halliday GM, Johnston LJ, King NJ (2001). ; "Interleukin-1beta but not tumor necrosis factor is involved in West Nile virus-induced Langerhans cell migration from the skin in C57BL/6 mice" Check |url= value (help). J Invest Dermatol. 117 (3): 702–9. doi:10.1046/j.0022-202x.2001.01454.x. PMID 11564180.
  11. ↑ Asselin-Paturel C, Brizard G, Chemin K, Boonstra A, O'Garra A, Vicari A; et al. (2005). "Type I interferon dependence of plasmacytoid dendritic cell activation and migration". J Exp Med. 201 (7): 1157–67. doi:10.1084/jem.20041930. PMC 2213121. PMID 15795237.
  12. ↑ Barton GM, Medzhitov R (2003). "Linking Toll-like receptors to IFN-alpha/beta expression". Nat Immunol. 4 (5): 432–3. doi:10.1038/ni0503-432. PMID 12719735.
  13. ↑ Keller BC, Fredericksen BL, Samuel MA, Mock RE, Mason PW, Diamond MS; et al. (2006). "Resistance to alpha/beta interferon is a determinant of West Nile virus replication fitness and virulence". J Virol. 80 (19): 9424–34. doi:10.1128/JVI.00768-06. PMC 1617238. PMID 16973548.
  14. ↑ Samuel MA, Diamond MS (2006). "Pathogenesis of West Nile Virus infection: a balance between virulence, innate and adaptive immunity, and viral evasion". J Virol. 80 (19): 9349–60. doi:10.1128/JVI.01122-06. PMC 1617273. PMID 16973541.
  15. ↑ Diamond MS, Sitati EM, Friend LD, Higgs S, Shrestha B, Engle M (2003). ; "A critical role for induced IgM in the protection against West Nile virus infection" Check |url= value (help). J Exp Med. 198 (12): 1853–62. doi:10.1084/jem.20031223. PMC 2194144. PMID 14662909.
  16. ↑ Samuel MA, Diamond MS (2005). ; "Alpha/beta interferon protects against lethal West Nile virus infection by restricting cellular tropism and enhancing neuronal survival" Check |url= value (help). J Virol. 79 (21): 13350–61. doi:10.1128/JVI.79.21.13350-13361.2005. PMC 1262587. PMID 16227257.
  17. ↑ Wang T, Town T, Alexopoulou L, Anderson JF, Fikrig E, Flavell RA (2004). ; "Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis" Check |url= value (help). Nat Med. 10 (12): 1366–73. doi:10.1038/nm1140. PMID 15558055.
  18. ↑ Kramer-Hämmerle S, Rothenaigner I, Wolff H, Bell JE, Brack-Werner R (2005). ; "Cells of the central nervous system as targets and reservoirs of the human immunodeficiency virus" Check |url= value (help). Virus Res. 111 (2): 194–213. doi:10.1016/j.virusres.2005.04.009. PMID 15885841.
  19. ↑ Monath TP, Cropp CB, Harrison AK (1983). ; "Mode of entry of a neurotropic arbovirus into the central nervous system. Reinvestigation of an old controversy" Check |url= value (help). Lab Invest. 48 (4): 399–410. PMID 6300550.
  20. ↑ Garcia-Tapia D, Loiacono CM, Kleiboeker SB (2006). ; "Replication of West Nile virus in equine peripheral blood mononuclear cells" Check |url= value (help). Vet Immunol Immunopathol. 110 (3–4): 229–44. doi:10.1016/j.vetimm.2005.10.003. PMID 16310859.
  21. ↑ Gamino V, Höfle U (2013). "Pathology and tissue tropism of natural West Nile virus infection in birds: a review". Vet Res. 44: 39. doi:10.1186/1297-9716-44-39. PMC 3686667. PMID 23731695.
  22. ↑ Glass WG, McDermott DH, Lim JK, Lekhong S, Yu SF, Frank WA; et al. (2006). ; "CCR5 deficiency increases risk of symptomatic West Nile virus infection" Check |url= value (help). J Exp Med. 203 (1): 35–40. doi:10.1084/jem.20051970. PMC 2118086. PMID 16418398.
  23. ↑ Yakub I, Lillibridge KM, Moran A, Gonzalez OY, Belmont J, Gibbs RA; et al. (2005). ; "Single nucleotide polymorphisms in genes for 2'-5'-oligoadenylate synthetase and RNase L inpatients hospitalized with West Nile virus infection" Check |url= value (help). J Infect Dis. 192 (10): 1741–8. doi:10.1086/497340. PMID 16235172.


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