Genetic Transmission of Wext Nile Virus

THE EMERGENCE OF WEST NILE VIRUS:

A LITERATURE REVIEW

Christopher Allan F. Reballos

INTRODUCTION

The year 1999 was an alarming year when an outbreak of arboviral encephalitis arrived in North America (Nosal and Pellizzari, 2003; Petersen et al, 2002; Scaramozzino et al, 2001). This epidemic spread rapidly across North America, namely United States and into Canada. The detection was first identified among birds and mosquitoes in the year 2001 and by the end of 2002, human infection cases were noted from nearby cities of Canada. It was identified that the human infection is caused by mosquito transmission. Migrating birds are presumed to play a significant role in facilitation of the dispersal of the virus to the mosquito population over distant locations. Though this remains the most significant vehicle for human disease, other possible means are through the blood or organ donation, pregnancy, lactation, needle-stick injury and exposure to infected laboratory specimens. The outbreak is responsible for considerable morbidity and mortality and may cause severe encephalitic, hemorrhagic, hepatic and febrile illness in vertebrates, including humans. Information was gathered from medical literature and the medical surveillance data. Petersen et al (2002) and Jupp (2001) have well documented enzootic activity of the outbreak and in New York City, it was identified to be the West Nile Virus

Genetics of West Nile Virus

West Nile Virus (WNV) is a single-stranded positive polarity RNA virus (Diamond et al, 2003). This etiologic agent of the West Nile encephalitis is a member of the family Flaviviridae (W. Li et al, 2002; Pei-Yong Shi et al, 2001 and 2002; Andersen et al, 1999;Enserinck, 1999), which comprises over 70 viruses sharing common antigenic determinants (Scaramozzino et al, 2001). The family contains eight serosubgroups and nine individual serotypes. This arthropod borne flaviruses are transmitted to vertebrates by mosquito infection or tick vectors. Many viruses that belongs to the family are significant human pathogens, which include the pathogenic viruses Yellow fever virus (YF), Dengue viruses, Tick-borne encephalitis virus (TBE), Japanese encephalitis virus (JE), St. Louis encephalitis virus (SLE).

This single-stranded plus sense non segmented RNA virus has a positive polarity genome of approximately 11,000 nucleotides or 11 Kb (Lanciotti and Kerst, 2001; Lanciotti et al 2000; Pei-Yong et al, 2002). A single, long open reading frame is contained in the genomic RNA of the flavivirus. Both termini of the genomic RNA contain 5’ untranslated region (UTR) and 3’UTR sequences that do not encode viral proteins (Pei-Yong et al, 2001). Viral and cellular proteases translated and co- and posttranslationally processed that encode a single long polyprotein into three structural proteins, namely the capsid (C), premembrane (prM) or membrane (M), and envelope glycoprotein (E) and followed by seven nonstructural proteins NS1, NS2a, NS2b, NS3, NS4a, NS4b, and NS5 in that order. These findings suggest that replacing the genes for the viral structural proteins in a full-length infectious cDNA clone of a flavivirus with the corresponding viral genes of another flavivirus