West Nile virus

West Nile Virus (WNV), a flavivirus (family Flaviviridae, genus Flavivirus), was first isolated in Uganda in 1937. It first appeared in the Western hemisphere in 1999 in New York. WNV is a small, enveloped, single-stranded, positive-sense RNA virus tranmitted primarily by mosquitos. Birds serve as a reservoir, with humans and horses acting as incidental, dead-end hosts. Although primarily transmitted by mosquitors, WNV can be transmitted by blood transfusion and organ tranplantation, and pregnant women may pass the infection to their child via intrauterine delivery. Most West Nile virus infections are asymptomatic (80%), but some patients (20%) develop classic West Nile fever and experience high fevers, rashes and severe joint pain often leading to debilitating long-term consequences. A small percentage of West Nile fever patients (< 1%) will suffer neuroinvasive disease, in which the central nervious system becomes infected, perhaps leading to encephalitis, and death occurs in about 0.1% of infections. 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. WNV virus infects at least 300 bird species, 60 mosquito species, and 30 animal species. At present, no vaccines or antiviral agents exist for WNV and its spread cannot be stopped. West Nile virus belongs to the Japanese encephalitis serocomplex 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 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 lymphatics. 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.