Co-circulation of West Nile Virus Variants, Arizona, USA, 2010 - Volume 20, Number 2—February 2014 - Emerging Infectious Disease journal - CDC
Volume 20, Number 2—February 2014
Co-circulation of West Nile Virus Variants, Arizona, USA, 2010
Jessica A. Plante1, Kristen L. Burkhalter1, Brian R. Mann, Marvin S. Godsey, John-Paul Mutebi, and David W. C. Beasley
Author affiliations: University of Texas Medical Branch, Galveston, Texas, USA (J.A. Plante, B.R. Mann, D.W.C. Beasley); Centers for Disease Control and Prevention, Fort Collins, Colorado, USA. (K.L. Burkhalter, M.S. Godsey, Jr., J.P. Mutebi)
West Nile virus (WNV) emerged in the Americas in 1999 after an outbreak of neuroinvasive disease in humans, birds, and horses in New York, New York. The virus spread rapidly across North America and was detected in Arizona in 2003. In 2004, Arizona experienced a large outbreak (214 neuroinvasive cases and 16 deaths, second only to California in that year), followed by ≈50–60 neuroinvasive cases per year during 2005–2008.
An outbreak in 2010 resulted in 107 neuroinvasive cases and 15 deaths, the largest number of cases for a state that year. WNV activity in Maricopa County, which includes the city of Phoenix and surrounding municipalities, where numerous human cases were reported in the town of Gilbert, was investigated by a team from the Centers for Disease Control and Prevention (Fort Collins, CO, USA) working with local and state public health officials. Epidemiologic and entomologic findings from those investigations have been reported (1,2) We describe the molecular and phenotypic characterization of WNV isolates obtained from that outbreak.
As part of the Centers for Disease Control and Prevention investigation, Vero cell culture isolates of WNV were obtained from pools of Culex quinquefasciatus (Say) mosquitoes collected during August 1–9, 2010, at multiple sites in the study areas (Figure 1). Nucleotide sequences (GenBank accession nos. KF704145–KF704159) for the envelope (E) protein–coding regions were determined for 15 strains and subjected to phylogenetic analysis. The AZ10 E gene sequences were distributed in 3 robust monophyletic clusters (designated A, B, C; posterior probabilities 0.99) as determined by using applied relaxed clock Bayesian coalescent analysis (Figure 2, panel A).
Isolates from all 3 clusters were detected from the Gilbert study sites. All AZ10 isolates encoded the E-159 Val→Ala mutation that is characteristic of genotypes described since 2002 (4). The 7 strains in cluster A, which were only obtained from pools collected in Gilbert, also encoded a conservative Leu→Ile mutation at E-312, a surface exposed residue in the putative receptor binding domain III (EIII) known to be a variable site in multiple WNV genetic lineages, including strains of lineage 2 currently circulating in Europe (5–9). The 2 strains in cluster B, collected in Glendale and Gilbert, Arizona, encoded a conservative Ser→Thr mutation at E-275.