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Published online ahead of print on 29 April 2009 as doi:10.1099/vir.0.008656-0
Journal of General Virology 2009;90:1848.

A more recent version of this article appeared on August 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.008656-0
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Virulence variation among isolates of Western equine encephalitis virus in an outbred mouse model.

Christopher H Logue1,6, Christopher F Bosio2, Thomas Welte2, Kimberley M Keene3, Jeremy P Ledermann1, Aaron T Phillips2, Brian J Sheahan4, Dennis J Pierro2, Nicole L Marlenee2, Aaron C Brault5, Catharine M Bosio2, Amber J Singh1, Ann M Powers1 and Ken E Olson2

1 Division of Vector-Borne Infectious Diseases, Centers for Disease Control & Prevention, Fort Collins;
2 Arthropod Borne & Infectious Diseases Laboratory, Colorado State University;
3 Division of Vector-Borne Infectious Diseases, Centers for Disease Control & Prevention;
4 UCD Veterinary Sciences Centre, University College Dublin, Belfield, Dublin 4, Ireland;
5 Center for Vector-Borne Diseases, University of California, Davis

6 E-mail: clogue{at}gmail.com

Little is known about viral determinants of virulence associated with Western equine encephalitis virus (WEEV). Here we have analyzed 6 North American WEEV isolates in an outbred CD-1 mouse model. Full genome sequence analyses showed < 2.7% divergence among the 6 WEEV isolates. However, percent mortality and mean time to death (MTD) varied significantly when mice were subcutaneously injected with 103 pfu of each virus. Two WEEV strains, McMillan (McM) and Imperial 181 (IMP), were the most divergent of the 6 in genome sequence and McM caused 100% mortality by 5 days post infection, whereas IMP caused no mortality. The magnitude of peak viremia was not associated with virulence. McM had significantly higher viral titers in the brain than IMP. Similar differences in virulence were observed when McM and IMP were administered by aerosol, intranasal, or intravenous routes. McM was 100% lethal with an MTD of 1.9 days when 103 pfu of each virus was administered by intracerebral inoculation; in contrast, IMP caused no mortality. The presence of IMP in the brains after different routes of infection and the lack of observed mortality confirmed that IMP is neuroinvasive but not neurovirulent. Based on morbidity, mortality, MTD, severity of brain lesions, virus distribution patterns, routes of infection, and differences in infection of cultured cells, McM and IMP were identified as high and low virulence isolates, respectively. Infectious clones developed from these isolates will be used to generate chimeric viruses that will identify specific viral determinants of neurovirulence in mice.

Received 16 February 2009; accepted 28 April 2009.




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