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West Nile Virus infection

Category: Illness or disabilities



Introduction and description

West Nile virus (WNV) is a single-stranded neurotropic RNA virus that causes West Nile fever. It is a member of the family Flaviviridae, specifically from the genus Flavivirus, which also contains the Zika virus, Dengue virus, and Yellow fever virus.  A neurotropic virus is a virus that is capable of infecting nerve cells.

The virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and more recently Central America.  Its range is world-wide as can be seen from the map below. 

There have been human cases and equine cases, and many birds are infected.  The primary hosts of WNV are birds, so that the virus remains within a "bird-mosquito-bird" transmission cycle.  Both the American and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.

West Nile Virus was introduced into the Western Hemisphere during the late summer of 1999, when infected individuals were diagnosed in New York State, and has been causing severe human disease in the USA since that time.  In 2000, and in the USA alone, the epizootic expanded to 12 states and the District of Columbia. From 1999 to 2010, more than 2.5 million people were infected, with over 12,000 reported cases of encephalitis or meningitis and over 1,300 deaths.  By 2006, it had become the most common cause of epidemic viral encephalitis in the United States.

The virus is spreading, partly - it is surmised - because of climate change and the extended range of its hosts. 

WNV is transmitted to humans primarily through the bite of infected mosquitoes, but during the epidemic that spread across North America in 2002, transmission of WNV through blood transfusions and organ transplantation was described for the first time. Individual case reports indicate that WNV can be transmitted also in utero and probably through breast milk. PMID:  15121956

Ticks have also been found to carry the virus. The geographic distribution of the mosquito-borne flaviviruses largely depends on the habitat of the preferred mosquito vector, with Culex mosquitoes transmitting encephalitic flaviviruses mainly in the Northern Hemisphere.

C. tarsalis is a main mosquito vector of WNV in the western United States and can feed on a variety of avian and mammalian species.  Other vectors shown to have competence for both infection and transmission of West Nile virus are C. quinquefasciatus, C. stigmatosoma, C. thriambus, C. pipiens, and C. nigripalpus; to date, over 65 mosquito species have been shown to be infected by WNV.  There are several reports of WNV in Aedes mosquitoes.  The ability to infect various mosquito species, the geographic range of mosquito species, and the ability of mosquitoes to feed on and transmit virus to particular hosts all play a role in WNV vector preference.


The symptoms of WNV can be varied and confusing, initially - backache, aching muscles, joint ache and fever.  Some WNV infections are asymptomatic.

Although the temporal relationship of rhabdomyolysis and neurological WNV illness suggested a common etiology, these patients presented with complex clinical conditions which may have led to development of rhabdomyolysis from other causes. PMID: 16187894


Severe manifestations of WNV infection are far more common in adults than in children, but 105 cases of neuroinvasive WNV disease were reported among children in the United States in 2002.  PMID:  15121956

Many arthropod-borne neurotropic viruses spread to the brain primarily via the blood system by crossing the blood-brain barrier in what is called hematogenous dissemination.  The West Nile virus is no exception.  WNV can lead to meningitis, encephalitis, and acute flaccid paralysis [AFP].  It mimics some symptoms of polio in that AFP is also a symptom of polio.

Many people are suffering from some form of neuropathy, [disease or dysfunction of one or more peripheral nerves] when they are first admitted to hospital, for example in one study:

At initial clinical presentation 93% presented with a significant neurological deficit

  • 49% with weakness,
  • 35% with tremor, and
  • 16% with cranial neuropathy

WNV causes death and coma – in the study mentioned above, seven patients died after initial enrolment in the study, with 5 of those having presented in a coma. [PMID:  24884681]

There is an acute phase, but if people become badly infected the disease resulting can be chronic and can cause severe neurological complications.  Even those initially experiencing fever, could later go on to develop far more serious abnormalities. 

We report an observational study of neurological abnormalities at 1-3 and 8-11 years following WNV infection in the HWNC. We conducted standard neurological examinations at two separate time points to assess changes in neurological status over time.
The majority of patients (86%, 30/35) with encephalitis had abnormal neurological exam findings at the time of the first assessment compared with uncomplicated fever (27%, 3/11) and meningitis (36%, 5/14) cases.   At the time of the second assessment,

·       57% (4/7) of West Nile fever (WNF),

·       33% (2/6) of West Nile meningitis (WNM), and

·       36% (5/14) of West Nile encephalitis (WNE)

 had developed new neurological complications.

The most common abnormalities noted were tandem gait, hearing loss, abnormal reflexes, and muscle weakness. Long-term neurological abnormalities were most commonly found in patients who experienced primary WNV encephalitis. PMID:  25802426


WNV is an enveloped virion containing a single-stranded, positive-sense RNA genome. The genome consists of a single open reading frame of approximately 11 kb with no polyadenylation tail at the 3′ end. Both the 5′ and 3′ noncoding regions of the genome form stem-loop structures that aid in replication, transcription, translation, and packaging.

The 5′ end of the genome encodes the structural proteins, which are necessary for virus entry and fusion as well as encapsidation of the viral genome during assembly. The nonstructural proteins have many diverse functions, which is understandable as the virus has a very limited number of proteins and they must each serve multiple purposes during infection.  The West Nile virus virion is an icosahedral particle with the capsid protein associating with the RNA genome to form the nucleocapsid, which is surrounded by a lipid bilayer. A high proportion of capsid protein localizes to the nucleus, while viral assembly takes place in the cytoplasm, with budding in the endoplasmic reticulum (ER)

Entry of WNV is through receptor-mediated endocytosis after virus attachment to the cell surface.  Within the late endosome, the envelope protein will undergo a conformational change resulting in fusion of the viral lipid membrane with the endocytic membrane and the release of the viral RNA genome into the cell cytoplasm.  . The original viral RNA is replicated by viral and cellular proteins into multiple copies to be used in the production of new virions. The virus travels to the cell surface in an exocytic vesicle and matures as cellular enzymes cleave the prM, resulting in the release of mature virus from the cell surface.

Immature or partially mature flavivirus particles of both DENV and WNV have been shown to account for up to as much as 40% of the total virus population in a given infection. While they were traditionally thought to be non-infectious, several recent studies have shown that immature WNV particles can be highly infectious in vitro and in vivo. Further work remains to be done to determine the role that immature particles play in viral pathogenesis and disease in both vector and mammalian hosts.

Diagnosis and treatment

Diagnosing neurological involvement has proven extremely difficult

Many patients with West Nile neuroinvasive disease (WNND) have normal neuroimaging studies, but abnormalities may be present in areas including the basal ganglia, thalamus, cerebellum, and brainstem. Cerebrospinal fluid invariably shows a pleocytosis, with a predominance of neutrophils in up to half the patients. Diagnosis of WNND depends predominantly on demonstration of WNV-specific IgM antibodies in cerebrospinal fluid. ………….  PMID:  16983682

Metagenomic testing – in those countries where it is offered – can also be used.  The emphasis has been on prevention rather than treatment. 

WNV infection can be diagnosed by detecting WNV-specific antibody in cerebrospinal fluid or serum, or by detecting the virus or viral nucleic acid in cerebrospinal fluid, blood, or tissues. Cornerstones of prevention include personal protection against mosquitoes, including wearing insect repellent, reducing populations of vector mosquitoes, and screening the blood supply for WNV-contaminated blood donations. PMID:  15121956

However, for those with the virus considerable ongoing care is needed to help the patients long after the initial acute phase has passed:

Several recent assessments, …. suggest that patients--even those with apparently mild cases of acute disease--frequently have subjective, somatic complaints following WNV infection. Persistent movement disorders, cognitive complaints, and functional disability may occur after West Nile neuroinvasive disease. West Nile poliomyelitis may result in limb weakness and ongoing morbidity that is likely to be long term. …..the long-term neurological and functional sequelae of WNV infection are likely to represent a considerable source of morbidity in patients long after their recovery from acute illness. PMID: 17516407

References and further reading

  • Am J Trop Med Hyg. 2014 Mar;90(3):402-9. doi: 10.4269/ajtmh.13-0206. Epub 2014 Feb 10.  Initial and long-term costs of patients hospitalized with West Nile virus disease.  Staples JE1, Shankar MB, Sejvar JJ, Meltzer MI, Fischer M.
  • Published: 30 November 2004 Emerging flaviviruses: the spread and resurgence of Japanese encephalitis, West Nile and dengue viruses- John S Mackenzie , Duane J Gubler  & Lyle R Petersen  Nature Medicine volume 10, pages S98–S109 (2004)
  • PBS Global Warming The Signs and the Science – about 16 minutes into this video a description is given of an epidemic of WNV in Colorado , about 200,000 people were eventually infected
  • Medigeshi, Guruprasad R.; Hirsch, Alec J.; Streblow, Daniel N.; Nikolich-Zugich, Janko; Nelson, Jay A. (2008-06-01). "West Nile Virus Entry Requires Cholesterol-Rich Membrane Microdomains and Is Independent of αvβ3 Integrin". Journal of Virology. 82 (11): 5212–5219. doi:10.1128/jvi.00008-08. ISSN 0022-538X. PMC 2395215. PMID 18385233
  • Urbanowski, Matt D.; Hobman, Tom C. (2013-01-15). "The West Nile Virus Capsid Protein Blocks Apoptosis through a Phosphatidylinositol 3-Kinase-Dependent Mechanism". Journal of Virology. 87 (2): 872–881. doi:10.1128/jvi.02030-12. ISSN 0022-538X. PMC 3554064. PMID 23115297
  • Colpitts, Tonya M.; Conway, Michael J.; Montgomery, Ruth R.; Fikrig, Erol (2012-10-01). "West Nile Virus: Biology, Transmission, and Human Infection". Clinical Microbiology Reviews. 25 (4): 635–648. doi:10.1128/cmr.00045-12. ISSN 0893-8512. PMC 3485754. PMID 23034323
  • Am J Trop Med Hyg. 2015 May;92(5):1006-12. doi: 10.4269/ajtmh.14-0616. Epub 2015 Mar 23.  Long-term neurological outcomes in West Nile virus-infected patients: an observational study.  Weatherhead JE1, Miller VE1, Garcia MN1, Hasbun R1, Salazar L1, Dimachkie MM1, Murray KO2.
  • Ann Neurol. 2006 Sep;60(3):286-300.  West Nile virus neuroinvasive disease.  Davis LE1, DeBiasi R, Goade DE, Haaland KY, Harrington JA, Harnar JB, Pergam SA, King MK, DeMasters BK, Tyler KL.
  • BMC Infect Dis. 2014 May 9;14:248. doi: 10.1186/1471-2334-14-248.  West Nile virus neuroinvasive disease: neurological manifestations and prospective longitudinal outcomes.  Hart J Jr1, Tillman G, Kraut MA, Chiang HS, Strain JF, Li Y, Agrawal AG, Jester P, Gnann JW Jr, Whitley RJ; NIAID Collaborative Antiviral Study Group West Nile Virus 210 Protocol Team.
  • Clin Infect Dis. 2007 Jun 15;44(12):1617-24. Epub 2007 May 2.  The long-term outcomes of human West Nile virus infection.  Sejvar JJ.
  • Pediatrics. 2004 May;113(5):1375-81.  West Nile virus infection: a pediatric perspective.  Hayes EB1, O'Leary DR.
  • Rev Med Virol. 2006 Jul-Aug;16(4):209-24.  Manifestations of West Nile neuroinvasive disease.  Sejvar JJ1, Marfin AA.
  • Vector Borne Zoonotic Dis. 2005 Fall;5(3):252-7.  Rhabdomyolysis in patients with west nile encephalitis and meningitis.  Montgomery SP1, Chow CC, Smith SW, Marfin AA, O'Leary DR, Campbell GL.


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