Lineage 2 West Nile Virus as Cause of Fatal Neurologic Disease in Horses, South Africa
Marietjie Venter , Stacey Human, Dewald Zaayman, Gertruida H. Gerdes, June Williams, Johan Steyl, Patricia A. Leman, Janusz Tadeusz Paweska, Hildegard Setzkorn, Gavin Rous, Sue Murray, Rissa Parker, Cynthia Donnellan, and Robert Swanepoel
Author affiliations: University of Pretoria, Pretoria, South Africa (M. Venter, S. Human, D. Zaayman, J. Williams, J. Steyl, C. Donnellan); National Health Laboratory Services, Pretoria (M. Venter); Onderstepoort Veterinary Research Institute, Pretoria (G.H. Gerdes); National Institute for Communicable Diseases, Johannesburg, South Africa (P. Leman, J.T. Paweska, R. Swanepoel); Chartwell Equine Clinic, Midrand, South Africa (H. Setzkorn); Karoo Veterinary Clinic, Colesburg, South Africa (G. Rous); Witbos Clinic, Midrand (S. Murray); Glen Austin Equine Clinic, Midrand (R. Parker)
Figure 3. Maximum-likelihood analysis of the E-protein region of a West Nile virus isolate, HS101_08 (black diamond), recovered from horses in 2008 compared with isolates obtained from humans and animals from South Africa and other regions of the world. Nucleotide differences between lineage 2 strains included in the alignment are shown in the summarized alignment below the tree, indicating only unique nucleotides. Vertical numbers above the alignment indicate the position of each variable site on the gene fragment. Scale bar indicates nucleotide substitutions per site.
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