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Volume 10, Number 12—December 2004
Dispatch

Genome Sequence and Attenuating Mutations in West Nile Virus Isolate from Mexico

David W.C. Beasley*Comments to Author , C. Todd Davis*, Jose Estrada-Franco*, Roberto Navarro-Lopez†, Arturo Campomanes-Cortes†, Robert B. Tesh*, Nikos Vasilakis*, and Alan D.T. Barrett*
Author affiliations: *University of Texas Medical Branch, Galveston, Texas, USA; †Comision Mexico-Estados Unidos para la Prevencion de la Fiebre Aftosa y Otras Enfermedades Exoticas de los Animales, Mexico City, Mexico

Main Article

Figure 1

Western blot showing differing mobility of E proteins from nine plaque-purified variants of West Nile virus (WNV) strain TM-171 Mex03. Nucleotide sequencing of strains in lanes 5 to 9 indicated the presence of an “NYS” glycosylation motif at residues 154 to 156 of E, while strains in lanes 1 to 4 encoded “NYP.” Antigens were separated in a nonreducing 5%/10% discontinuous sodium dodecyl sulfate–polyacrylamide gel, transferred to 0.2 μm nitrocellulose and detected with WNV-specific monoclonal ant

Figure 1. Western blot showing differing mobility of E proteins from nine plaque-purified variants of West Nile virus (WNV) strain TM-171 Mex03. Nucleotide sequencing of strains in lanes 5 to 9 indicated the presence of an “NYS” glycosylation motif at residues 154 to 156 of E, while strains in lanes 1 to 4 encoded “NYP.” Antigens were separated in a nonreducing 5%/10% discontinuous sodium dodecyl sulfate–polyacrylamide gel, transferred to 0.2 μm nitrocellulose and detected with WNV-specific monoclonal antibody 7H2 (6).

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