West Nile virus

West Nile virus (WNV), may cause severe, persistent or fatal disease, although about 80% of infections are asymptomatic. It is found throughout much of Europe, Africa, and North America. In 2006 in the United States, 174 deaths, 1455 cases of West Nile encephalitis/meningitis, and 2612 cases of West Nile Fever were reported to the Center for Disease Control (CDC West Nile). Typical symptoms of classic WN Fever include fever, headaches and body aches, nauses and vomiting, and may include rashes around the torso and swollen lymph glands. In the more serious neuroinvasive cases (encephalitis and meningitis), symptoms may also include neck stiffness, stupor, coma, tremors, muscle weakness, vision loss, numbness and flacid paralysis. Neurological effects may be permanent.

Transmission and Spread of West Nile virus

West Nile virus was first isolated in Uganda in 1937. It first appeared in the Western hemisphere in 1999 in New York. The virus is primarily tranmitted to human by mosquitos. Birds serve as a reservoir, with humans and horses and other mammals acting as incidental, dead-end hosts. Although primarily transmitted by mosquitors, the virus can be transmitted by blood transfusion and organ tranplantation, and pregnant women may pass the infection to their child via intrauterine delivery. WNV virus infects at least 300 bird species, 60 mosquito species, and 30 animal species. Clinical symptoms track closely with the particular strain of the West Nile fever infection [1][2] and two major lineages have been described. Lineage II strains are found primarily in Africa and Madagascar while lineage I strains are widely distributed across North America, Europe and Africa.[3][4] Virus strains found in North America are particularly neuroinvasive. At present, no vaccines or antiviral agents exist for WNV and its spread can, therefore, not be stopped.

Virology and Molecular Biology West Nile Virus

West Nile virus, a flavivirus (family Flaviviridae, genus Flavivirus), is a small, enveloped, single-stranded, positive-sense RNA virus. West Nile virus belongs to the Japanese encephalitis serocomplex (antigenic complex) of flaviviruses and is closely related to Japanese encephatitis virus, Kunjin virus, St. Louis encephalitis virus, Murray valley encephalitis virus, Usutus virus, Cacipacore virus, Koutango virus and Yaounde virus. The West Nile fever RNA encodes for the production of a polyprotein, which is then cleaved into ten proteins. Of these, three are structural proteins, the capsid protein, the membrane protein, and the envelope protein, which together encapsulate and protect the viral RNA by forming a viral particle about 50 nm in diameter. The viral particles multiply in tissue and lymphodes near the site of infection, and travel to the blood via lymphacytes. Viremia is detected early in the infection.

References

1. Beasley, D. W. et al. (2002) Mouse neuroinvasive phenotype of West Nile virus strains varies depending upon virus genotype, Virology, Volume 296, Issue 1, pp 17-23. PMID: 12036314

2. Chambers, T. C. et al. (1998) West Nile virus envelope proteins: nucleotide sequence analysis of strains differing in mouse neuroinvasiveness, J. Gen. Virol., Volume 79, pp 2375-2380. PMID: 9780042.

3. Jia, X.-Y. et al. (1999) Genetic analysis of West Nile New York 1999 encephalitis virus. Lancet, Volume 354, pp 1971-1972. PMID: 10622305.

4. Lanciotti, R. S. et al. (1999) Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States, Science, Volume 286, pp. 2333-2337. PMID: 10600742.