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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...