Cerebrospinal fluid

Presently, WNV detection in cerebrospinal fluid or serum by means of IgM or Immunoglobulin M antibody is the most effective clinical diagnosis. The IgM antibody-capture ELISA or enzyme-linked immunoabsorbent assay is described as a method with simplicity, enough sensitivity, and applicability for cerebrospinal fluid and serum samples. Such detection denotes infection in the central nervous system for the IgM antibody is unable to pass through the blood-brain barrier. Specifically, in 90% of the serum samples collected within eight days of symptoms manifestation, IgM will positively be detected.

However, there are two crucial considerations that must be made in the serologic test interpretation. One is the antigenic similarities among faviviruses for vaccination against or previous infections with Japanese encephalitis and other flavivirus-related viral stain may result to positive in WNV IgM antibody test. On the other hand, the specific test, plaque reduction neutralization for flavivirus of anthropod origins, can be employed to differentiate IgM antibody-capture ELISA and other assays’ false-positive results.

This also facilitates serologic cross-reaction differentiation in flaviviruses, but some may still have vague results in cross reaction with a neutralizing body. The elevation of neutralizing antibody titer specific to WNV in the serum of convalescent and acute disease patients is a direct indication of acute infection. Since the IgM antibody exhibits more than six months persistence as majority of the infected individuals were asymptomatic, it is possible that IgM from a previous infection different from the present conditions can still be detected.

West Nile virus, nucleic acid, or any other viral antigen can be detected not only from blood or cerebrospinal fluid but also in tissues and other body fluids. Even though the nucleic acid amplification procedure such as real-time PCR of polymerase chain reaction can be utilized as diagnostic tool, it is not recommended for routine testing due to its low sensitivity. So far, scientists, medical researchers, and doctors are not yet able to develop or formulate a specific drug that would ensure the best treatment for WNV contagion.

Some infected individuals were hospitalized for intensive care and other cases required mechanical ventilation. In connection to this, the mortality rates of WNV victims with greater than 70 years of age in the United States were observed consistently in 2001–2002 at 10% level. Similarly, in New York, patients of ages higher than 75 years were nine times at risk than younger WNV victims. This high risk due to age was attributed to the severity of symptoms and disease complications. Meanwhile, advanced drug treatment for WNV infections is still yet to come, public consciousness can probably alleviate the problem at hand.

Hence, programs on WNV control and prevention require active participation of the community, which can be stimulated by means of information campaign and public education on the transmission, illnesses, neuroinvasive diseases, and complication of WNV infection along with the strategies of control and prevention. As well, the proper use of insecticides and insect repellents can make a great impact on the prevention of WNV infections.


Botha, E. M. , Markotter, W. , Wolfaardt, M. , Paweska, J. T. , Swanepoel, R. , Palacios, G., Nel, L. H. , and Venter, M. (2008). Genetic Determinants of Virulence in Pathogenic Lineage 2 West Nile Virus Strains. Emerging Infectious Diseases, 14 (2), 222-230. Gottfried, K. , Quinn, R. and Jones, T. (2005). Clinical Description and Follow-up Investigation of Human West Nile Virus Cases. Southern Medical Journal, 98 (6), 603-606. Grinev, A. , Daniel, S. , Stramer, S. , Rossmann, S. , Caglioti, S. and Rios, M. (2008). Genetic Variability of West Nile Virus in US Blood Donors, 2002-2005. Emerging Infectious Diseases, 14 (3), 436-444.

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