West nile virus pathophysiology

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

Overview

West Nile virus pathophysiology

Transmission

Birds are the main reservoir of West Nile virus (WNV), but transmission of the virus is by mosquito bite of an infected bird with high-level viremia, such as birds of the family Passeriformes.[1] Thus, transmission is frequently denoted as "bird-mosquito-bird" transmission. Although direct bird-to-bird transmission has been speculated, further validation is still required.[2] 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.[3][4][5]


Mosquitoes responsible for viral transmission belong to different families, varying based on geographical location:[6]

  • Culex pipiens: Northern half and West of USA
  • Culex quinquefasciatus: Southeast and West of USA
  • Culex tarsal: West of USA

Pathogenesis

Following inoculation, replication of WNV takes place in Langerhans epidermal dendritic cells, which are antigen-presenting immune cells.[7] 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. Mice models have demonstrated that persistent infection, including CNS infiltration, is also possible; whereby TNF-alpha has been hypothesized to allow viral crossing of the blood-brain barrier (BBB) by promoting endothelial cell permeability.[8][9][10] 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.[11][12][13]

References

  1. ↑ "Emerging Infectious Diseases".
  2. ↑ 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". Emerg Infect Dis. 9 (3): 311–22. doi:10.3201/eid0903.020628. PMC 2958552. PMID 12643825.
  3. ↑ 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". N Engl J Med. 348 (22): 2196–203. doi:10.1056/NEJMoa022987. PMID 12773646.
  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. ↑ Centers for Disease Control and Prevention (CDC) (2002). "Possible West Nile virus transmission to an infant through breast-feeding--Michigan, 2002". MMWR Morb Mortal Wkly Rep. 51 (39): 877–8. PMID 12375687.
  6. ↑ 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.
  7. ↑ 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". J Invest Dermatol. 117 (3): 702–9. doi:10.1046/j.0022-202x.2001.01454.x. PMID 11564180.
  8. ↑ 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". J Exp Med. 198 (12): 1853–62. doi:10.1084/jem.20031223. PMC 2194144. PMID 14662909.
  9. ↑ Samuel MA, Diamond MS (2005). "Alpha/beta interferon protects against lethal West Nile virus infection by restricting cellular tropism and enhancing neuronal survival". J Virol. 79 (21): 13350–61. doi:10.1128/JVI.79.21.13350-13361.2005. PMC 1262587. PMID 16227257.
  10. ↑ 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". Nat Med. 10 (12): 1366–73. doi:10.1038/nm1140. PMID 15558055.
  11. ↑ 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". Virus Res. 111 (2): 194–213. doi:10.1016/j.virusres.2005.04.009. PMID 15885841.
  12. ↑ Monath TP, Cropp CB, Harrison AK (1983). "Mode of entry of a neurotropic arbovirus into the central nervous system. Reinvestigation of an old controversy". Lab Invest. 48 (4): 399–410. PMID 6300550.
  13. ↑ Garcia-Tapia D, Loiacono CM, Kleiboeker SB (2006). "Replication of West Nile virus in equine peripheral blood mononuclear cells". Vet Immunol Immunopathol. 110 (3–4): 229–44. doi:10.1016/j.vetimm.2005.10.003. PMID 16310859.


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