Li J, Bhuvanakantham R, Howe J, Ng M-L
Flavivirology Laboratory, Department of Microbiology, 5 Science Drive 2, National University of Singapore, Singapore 117597.
J Gen Virol. 2006 Mar;87(Pt 3):613-622. doi: 10.1099/vir.0.81320-0.
The complete genome of West Nile (Sarafend) virus [WN(S)V] was sequenced. Phylogenetic trees utilizing the complete genomic sequence, capsid gene, envelope gene and NS5 gene/3' untranslated region of WN(S)V classified WN(S)V as a lineage II virus. A full-length infectious clone of WN(S)V with a point mutation in the glycosylation site of the envelope protein (pWNS-S154A) was constructed. Both growth kinetics and the mode of maturation were affected by this mutation. The titre of the pWNS-S154A virus was lower than the wild-type virus. This defect was corrected by the expression of wild-type envelope protein in trans. The pWNS-S154A virus matured intracellularly instead of at the plasma membrane as shown for the parental WN(S)V.
对西尼罗河（萨拉芬德）病毒[WN(S)V]的全基因组进行了测序。利用WN(S)V的全基因组序列、衣壳基因、包膜基因和NS5基因/3'非翻译区构建的系统发育树将WN(S)V归类为II型病毒。构建了包膜蛋白糖基化位点存在点突变的WN(S)V全长感染性克隆（pWNS-S154A）。该突变影响了病毒的生长动力学和成熟模式。pWNS-S154A病毒的滴度低于野生型病毒。通过反式表达野生型包膜蛋白可纠正这一缺陷。与亲本WN(S)V不同，pWNS-S154A病毒在细胞内成熟，而非在质膜上成熟。
