Abstract
The complete genome sequence of a Mexican West Nile virus isolate, TM171-03, included 46 nucleotide (0.42%) and 4 amino acid (0.11%) differences from the NY99 prototype. Mouse virulence differences between plaque-purified variants of TM171-03 with mutations at the E protein glycosylation motif suggest the emergence of an attenuating mutation.
Highlights
Since its introduction into North America in 1999, West Nile virus (WNV) has spread rapidly across the continent, and evidence for virus circulation has been detected in the Caribbean and parts of Central America [1]
Analysis of the sequence chromatograms from V1 and V2 passages, and for a polymerase chain reaction (PCR) product obtained from the original brain material, indicated that this reversion was likely to be the result of a mixed virus population, with overlapping “T” and “C” peaks visible at residue 1432 in the sense or antisense sequences for each product
The NY00-grouse3282 sequence differed from New York strain 382-99 (NY99) at only 13 nt (0.11%), and its relationship to TM171-03 was apparently based on 10 nonstructural protein region nucleotide differences from NY99 that were shared with TM171-03 (Table 1)
Summary
Since its introduction into North America in 1999, West Nile virus (WNV) has spread rapidly across the continent, and evidence for virus circulation has been detected in the Caribbean and parts of Central America [1]. To assess the effects of the E-156 Ser→Pro mutation on the virulence of TM171-03, serial 10-fold doses from 1,000 to 0.1 PFU of TM171-03 and four plaque-purified (pp) substrains (TM171-03-pp1 and -pp2 encoding Pro at E-156; TM171-03-pp5 and -pp6 encoding Ser) were inoculated intraperitoneally (i.p.) and intracranially (i.c.) into groups of 3- to 4-week-old female NIH Swiss mice to determine mouse neuroinvasiveness and neurovirulence, as described elsewhere [7] and in accordance with guidelines of the University of Texas Medical Branch Institutional Animal Care and Use Committee.
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