J Gen Virol
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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.008169-0
Journal of General Virology 2009;90:792.

A more recent version of this article appeared on April 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.008169-0
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Smallpox Virus Plaque Phenotypes: Genetic, Geographical and Case Fatality Relationships

Victoria A. Olson1, Kevin L. Karem, Scott K. Smith, Christine M. Hughes and Inger K. Damon

Centers for Disease Control and Prevention

1 E-mail: vao9{at}cdc.gov

Smallpox (Orthopoxvirus variola infection) remains a feared illness >25 years after its eradication. Historically, case-fatality rates (CFRs) varied between outbreaks (<1% to ~40%), reasons for which are incompletely understood. The extracellular enveloped virus (EEV) form of orthopoxvirus progeny is hypothesized to disseminate infection. Investigations with the closely related Orthopoxvirus vaccinia have associated increased comet formation (EEV production) with increased mouse mortality (pathogenicity). Other vaccinia virus genetic manipulations which affect EEV production inconsistently support this association. However, anti-sera against vaccinia virus envelope protect mice from lethal challenge, further supporting a critical role for EEV in pathogenicity. Here we show that increased comet formation phenotypes of a diverse collection of variola viruses associate with strain phylogeny and geographic origin, but not to increased outbreak related CFRs; within clades, there may be an association of plaque size with CFR. The mechanisms for variola virus pathogenicity likely involve multiple host and pathogen factors.

Received 22 October 2008; accepted 16 December 2008.




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